A Practical Approach to

Clinical Echocardiography
 A Practical Approach to
Clinical Echocardiography

Jagdish C Mohan MD DM FASE

Director of Cardiac Sciences
Fortis Hospital
Shalimar Bagh, New Delhi, India

Foreword
Bijoy K Khandheria

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A Practical Approach to Clinical Echocardiography

First Edition: 2014
ISBN978-93-5152-140-2
Printed at:
 Dedicated to
Vineet, my soul-mate for the last thirty-six years
 Foreword

The field of cardiovascular ultrasound continues to explode with an increase in applications and rapid
explosion in technological advances. It was not too long that the world celebrated the 50th anniversary of
cardiac ultrasound. The remarkable progress continues, and the evolution to revolution has yet to see a stop.
With ever-increasing applications and explosion of technology comes the need to transmit this
information in an easy-to-understand, easy-to-digest manner. To this end, Prof Jagdish C Mohan has
exploited the method of making difficult things easy in this book. The book is eminently readable. Strength, weakness
and caveats of every important echo-Doppler observation have been provided. The images and the illustrations are
excellent with extensive labeling for easy understanding. There is less emphasis on bibliography and more on practical
tips. Although there are no separate chapters on transesophageal echocardiography and real-time 3D imaging, these
have been well covered in individual sections wherever appropriate. The same principle has been applied to contrast
echocardiography.
There is little doubt that cardiovascular ultrasound will continue its revolution, and play an important role in the
practice of cardiology as well as medicine. This book compiled by Prof Jagdish C Mohan is a welcome addition to the
various sources of education in this field. It is a must-read book for those wishing to practice the art and science of
cardiovascular ultrasound.

Bijoy K Khandheria MD FACP FAHA FACC FESC FASE

Adjunct Clinical Professor of Medicine
University of Wisconsin, School of Medicine and Public Health
Director, Echocardiography Services
Aurora St Lukes Medical Center, Milwaukee, Wisconsin, USA
Director, Echocardiography Center for Research and Innovation
Aurora Research Institute, Milwaukee, Wisconsin, USA
Past President, American Society of Echocardiography
Former Chair of Cardiovascular Disease, Mayo Clinic, Arizona
Former Professor of Medicine, Mayo Medical School
 Preface

Echocardiography is the most commonly used imaging technique at bedside, in OR, in outpatients and in community
screening. It is highly portable, noninvasive, repeatable, inexpensive and easily accessible. When used appropriately
after some experience, it has inherent internal validation unlike many other imaging modalities. Clinicians using this
technique transcend boundaries of specialties. More and more physicians want to learn and practice it. Despite these
obvious advantages, this modality remains incompletely utilized. There are several learning modules in capsule form
and a multitude of books which claim to make a person expert in short time. In these, either there is over-simplification
or meaningless convoluted and complicated equations and biophysical complexity. At fringes, are clinicians who have
used this technique year after year for assessment of left ventricular function only. Echocardiography represents a
strange mixture of several features which have proven prime-time use and an equally numerous techniques which have
yet to show clinical utility despite extensive research work spanning decades. There is an urgent need to promote that
part of science which has robust validation. What clinicians require needs to be emphasized with clarity. Novices often
get unnerved by the available applications on the systems which are more to stand up to the competition rather than
of tangible clinical value. However, extensive research has shown applicability of a lot of echocardiographic knowledge
and information in day-to-day evidence-based medicine. Quantitative and semi-quantitative protocols are gaining
ground because these make serial follow-up easily. This book is an attempt to make echocardiography simple, practical
and easily usable with reproducible data. Unnecessary and impractical details have been omitted. I would welcome
suggestions to make it more readable and meaningful.

Jagdish C Mohan
 Acknowledgments

I appreciate the contribution of M/s Jaypee Brothers Medical Publishers (P) Ltd., New Delhi, India, in making this
project a success. In particular, Ms Chetna Malhotra Vohra (Senior ManagerBusiness Development) for her belief in
our groups ability to deliver and Saima Rashid (Development Editor) who did very well in making sure we catch-up with
the deadline.
 Contents

Section 1: Fundamentals of Echocardiography

1. Echocardiography: Basic Principles, Technique, Display and Interpretation 3

Ultrasound Physics 3
Ultrasound Beam 7

2. Hemodynamic Evaluation by Echo-Doppler Techniques 24

Hemodynamic Evaluation 24
Doppler Principle for Estimating Velocity 25
Ohms Law of Fluids (The HagenPoiseuille Equation) 27
The Bernoullis Equation 28
Continuity Equation 28
Effective Orifice Area 30
Vena Contracta 31
Pressure Recovery 33
Ventriculovalvular Impedance 34
Proximal Isovelocity Surface Area and Volumetric Measurements 34
Pressure Half-Time 36
Lv Dp/Dt39
Estimation of Pulmonary Artery Pressures and Pulmonary Vascular Resistance 39

Section 2: Valvular Heart Disease

3. Mitral Stenosis 45
Anatomy of the Mitral Valve 45

4. Mitral Regurgitation 64
Functional Morphology of Mr64

5. Aortic Valve Stenosis 83

Anatomy of Trileaflet Aortic Valve 83
Unicuspid Aortic Valve 85
Bicuspid Aortic Valve 85
Quadricuspid Aortic Valve 86
Anatomy of Aortic Stenosis 86
xiv A Practical Approach to Clinical Echocardiography

Planimetry of the Aortic Valve Area on Aortic Stenosis 87

Hemodynamics of Aortic Valve Stenosis 88
Technical Tips 90
Low-gradient, Low-flow Aortic Valve Stenosis 93
Paradoxical Low-flow as with Preserved Ejection Fraction 95
Subaortic Stenosis 95

6. Aortic Valve Regurgitation 98

Hemodynamics of Aortic Regurgitation 98
Functional Anatomy of Aortic Regurgitation 100
Detection of Aortic Regurgitation by Echo-Doppler Techniques 102
Volumetric Severity of Aortic Regurgitation 104
Color Flow Doppler Evaluation of Aortic Regurgitation 104
Aortic Regurgitation Assessment by Vena Contracta 105
Proximal Isovelocity Surface Area Flow Convergence Method 105
Diastolic Flow Reversal in the Descending Aorta and Severity of Aortic Regurgitation 106
Pressure Half-time of Aortic Regurgitation Signal 107
M-mode Color Flow Propagation Velocity 108
Summary of Aortic Regurgitation Assessment by Echo-Doppler Methods 108

7. Tricuspid Valve 110

Functional Morphology of the Tricuspid Valve 110
Conditions Affecting Tricuspid Valve 113
Remodelling in Tricuspid Regurgitation 114
Functional Tr114
Organic Tricuspid Valve Disorders 115
Tricuspid Valve Stenosis 120
Assessment of Severity of Tr121
Vena Contracta 121
Proximal Isovelocity Surface Area Method 122
Anterograde Velocity of Tricuspid Inflow 122
Hepatic Vein Flow in Assessment of Tr123

8. Pulmonary Valve 126

Anatomy of the Pulmonary Valve 126
Pulmonary Valve Disorders 127
Transesophageal Echocardiography in Pulmonary Stenosis 133
Consequences and Associations of Pulmonary Stenosis 134
Assessment of Pulmonary Regurgitation 134
Consequences of Pulmonary Regurgitation 136

9. Evaluation of Prosthetic Heart Valves 138

Ball-in-cage Valve 138
Tilting or Mono-disk Valve 139
 Contents xv

Bileaflet Prosthetic Valves 140

Bioprosthesis141
Hemodynamic Assessment of Prosthetic Valves 141
Technical Considerations 148
Microbubble Formation (Cavitation) 152
Prosthetic Valve Dysfunction 152
Bioprosthetic Degeneration 152
Prosthetic and Paraprosthetic Regurgitation 153
Paraprosthetic Regurgitation 154
Prosthetic Valve Stenosis 155
Tricuspid and Pulmonary Prosthetic Valves 160

Section 3: Systolic and Diastolic Function

10. Left Ventricular Systolic Function 165

Morphology of the Left Ventricle 165
Limitations186

11. Echocardiographic Assessment of Right Ventricular Function:

Methods and Clinical Applications 189
Peculiarities of the Right Ventricle 189
Function Parameters 190
Right Ventricle Diastolic Function and Pressures 193
Tricuspid Annular Peak Systolic Velocity 198
Right Ventricle Strain and Strain Rate Analysis 200

12. Diastolic Function 204

Physiology of Diastole 204
Factors Contributing to Diastole 205
Significance of Diastolic Function 205
Isovolumic Relaxation Time 206
Rapid Filling Phase 207
Deceleration Time of Early Filling Wave (Mitral E- and Pulmonary D-Waves) 207
Diastasis208
Atrial Kick or Contribution 209
Tissue Motion and Diastolic Function 209
Left Atrial Volume and Diastolic Function/Dysfunction 210
How to Perform a Study Focusing on Diastolic Function 211
Mitral Inflow Velocities 212
Mitral Annular Velocities 214
How to Obtain Annular Tissue Velocities 216
Pulmonary Vein Flow and Diastolic Function 218
Mitral Flow Propagation by Color M-Mode 221
Longitudinal Strain, Rotation and Untwisting Rate by Acoustic Speckle Tracking 223
Diastolic Stress Test224
xvi A Practical Approach to Clinical Echocardiography

Section 4: Muscle Mechanics

13. Tissue Doppler Echocardiography: Current Status and Applications 229

Concept of Tdi229
Labeling of Tissue Velocity Waveforms 229
Terms Used in Tissue Doppler Imaging 231
Technical Details of Tdi231
Myocardial Velocities in Short Axis 234
Internal Dependency of Velocities 235
Fundamental Basis of Tdi236
Tissue Doppler Data Processing for Deformation Imaging 238
Clinical Utility of Tdi239
Prognostic Value of Tdi in Diverse Cardiac Disorders 250
Limitations of Tdi251

14. Deformation Imaging: Theory and Practice 257

Myocardial Deformation 257
Descriptive Terms 261
Acoustic Speckle Tracking 262
Velocity Vector Imaging 264
How to Perform Two-Dimensional Strain Imaging? 266
Effects of Ischemia on Regional Deformation Metrics 268
Early Systolic Longitudinal Lengthening (Paradoxical Longitudinal Systolic Strain) 269
Post-systolic Longitudinal Shortening 270
Paradoxical Strain Patterns 272
Right Ventricular Deformation 273
Left Atrial Function by Deformation Imaging 273
Mechanical Properties of the Aorta 274
Three-dimensional/Four-dimensional Deformation Imaging 274
Clinical Applications of Strain and Strain Rate Imaging 276
Limitations277

15. Rotation, Twist and Torsion 280

Fundamentals of Torsion 280
Echocardiographic Methods of Studying Twist 284
Clinical Applications of Torsion 285
Aging and Torsion 286
Aortic Stenosis, Hypertension and Hypertrophic Cardiomyopathy 286
Heart Failure 287
Constrictive Pericarditis 287
Torsion and Cardiac Resynchronization Therapy 288
Acute and Chronic Ischemia 289
Grades of Diastolic Dysfunction and Twist 290
 Contents xvii

Section 5: CHD, Aorta and Pericardium

16. Congenital Heart Disease in Adults 295

Atrial Septal Defect 295
Patent Foramen Ovale 299
Ostium Primum Atrial Septal Defect 299
Sinus Venosus Atrial Septal Defect 300
Common or Single Atrium 300
Ventricular Septal Defect 300
Morphology of Vsd302
Pathophysiology of Vsd302
Ebsteins Anomaly 304
Carpentier Classification of Ebsteins Anomaly 306
Double-Chambered Rv307
Sinus of Valsalva Aneurysms 308
Tetralogy of Fallot 311
Morphological Variants of Tof312
Truncus Arteriosus or Common Arterial Trunk 313
Subaortic Membranous Stenosis 314
Physiology and Pathology 314
Transposition of Great Vessels 315

17. Aorta: Congenital and Acquired Disorders 318

Structure of Aorta 318
Parts of Aorta 318
Functions of Aorta 320
Normal Aortic Measurements and Imaging Views 321
Etiopathogenesis of Aortic Disorders 322
Congenital Disorders of Aorta 322
Aortic Coarctation 324
Aneurysm of Sinus of Valsalva 325
Aortopulmonary Window 329
Truncus Arteriosus 329
Supravalvular Aortic Stenosis 330
Patent Ductus Arteriosus 330
Acquired Aortopathies 331

18. Pericardial Diseases 343

Echocardiographic Anatomy of Pericardium 343
Pericardial Disorders 344
Acute Pericarditis and Pericardial Effusion 345
Cardiac Tamponade 349
Pericardial Cysts and Masses 353
Pericardial Constriction353
xviii A Practical Approach to Clinical Echocardiography

Section 6: Structural Heart Disease

19. Ischemic Heart Disease 363

Myocardial Segment Nomenclature and Coronary Vascular Territory 363
Right Ventricular Segmentation 363
Ischemia and Echocardiographic Imaging 365
Echocardiography in Ihd369
Evaluation of Myocardial Infarction 369
Mechanical Complications of Myocardial Infarction 370
Stress Echocardiography 377

20. Tumors, Masses and Infection 383

Cardiac Manifestations of Masses 383
Cardiac Thrombi and Spontaneous Echo Contrast 384
Cardiac Tumors 385
Echocardiographic Features of Myxoma 387
Papillary Fibroelastoma 388
Malignant Tumors 388
Differential Diagnosis of Cardiac Tumors 389
Infective Endocarditis 389
Points to Remember 392

21. Cardiomyopathies 395

European Classification of Cardiomyopathies 397
Summary of Emf Echocardiographic Features 406

Index 415
 SEction 1
Fundamentals of Echocardiography

Chapters

Echocardiography: Basic Principles, Technique, Hemodynamic Evaluation by Echo-Doppler Techniques

Display and Interpretation
 Chapter Echocardiography: Basic

1
Principles, Technique,
Display and Interpretation

Introduction
Echocardiography is a technique of generating images of
the heart with the help of ultrasound (like skiagraphy is
performed with X-rays). Echocardiography has become
an integral part of clinical examination with its bedside
mobility and utility. Practice of echocardiography
mandates the following steps:
Understanding of ultrasound physics
Knowledge of the instrumentation
Acquisition skills
Interpretative skills
Sound knowledge of cardiovascular anatomy and
physiologies
Adequate knowledge of common cardiac pathology Fig. 1.1: Behavior of the sound waves. Sound wave after striking a
Reporting, storage and retrieval skills. surface gets reflected as well as transmitted into the other medium in a
Ultrasound behaves very differently when it passes different direction (refracted). Total internal reflection without transmis-
sion occurs if it strikes the interface at 90.
through any tissue. Many of the objects and artifacts seen
in ultrasound images are due to the physical properties
of ultrasonic beams, such as reflection, refraction, ULTRASOUND PHYSICS
diffraction and attenuation. Indeed, physical artifacts
are an important element in clinical diagnosis (Fig. 1.1). Sound
Appreciating the phenomena created by ultrasound may Sound is a form of mechanical energy that consists of waves
greatly benefit the patient in terms of increased accuracy of compression and decompression of the transmitting
of interpretation and diagnosis. The ultrasound wave medium, travelling at a fixed velocity (Figs 1.2 and 1.3).
created for sending through the tissues is called incident Sound is an example of longitudinal waves oscillating
wave. This is the wave whose behavior is changed by the back and forth in the direction the sound travels,
tissue. thus consisting of successive zones of compression
4 Section 1: Fundamentals of Echocardiography
Fig. 1.2: Alternating compression and rarefaction of a medium as
sound passes through it.
Fig. 1.4: The concept of pulsed ultrasound. If an interface is closure
to the source of ultrasound, more pulses will be received per second
resulting in better resolution.
(high pressure) and rarefaction (low pressure). The
medium particles, however, show both longitudinal and
transverse oscillations.
Longitudinal oscillations: The oscillating particles
of the medium are displaced parallel to the direction of
motion (direction of energy transfer).
Transverse oscillations: The oscillating particles of the
medium are displaced in a direction perpendicular to the
motion of the wave.
Ultrasound: Sound waves with a frequency of 20000
c/s (20 KHz) are labeled ultrasound. Ultrasound used in
medical diagnosis has a frequency of 110 MHz.13 These
are beyond the capacity of human ear to perceive.
Fig. 1.3: Sound as an oscillating wave of mechanical energy.
Compression is accompanied by high pressure and rarefaction by low
pressure.
Why Use Ultrasound in Medicine?
With higher frequencies (shorter wavelengths), the sound
tends to move more in straight lines like electromagnetic
beams and is reflected like light beams. It is reflected by
much smaller objects (because of shorter wavelengths)
and hence gives good spatial resolution. If the wavelength
of the sound is smaller than the object, no noticeable
diffraction occurs.
wavelength = speed/frequency
Frequency: The frequency of an ultrasound wave
consists of the number of cycles or pressure changes that
occur in one second (Fig. 1.2). The units are cycles per
second or hertz (Hz). Frequency is determined by the
sound source only and not by the medium in which the
sound is travelling.
Propagation speed: Propagation speed is the rate
at which sound can travel through a medium and is
typically considered 1,540 m/s for soft tissue. The speed
is determined solely by the medium characteristics like
density and stiffness. Speed is inversely proportional to
density and incompressibility.
Pulsed ultrasound: Pulsed ultrasound describes a
means of emitting ultrasound waves from a source. To
achieve the depth of resolution required for clinical
uses, pulsed beams are used. Typically, the pulses are a
millisecond or so long and several thousands are emitted
per second (Fig. 1. 4).
Ultrasound interaction with tissue: As a beam of
ultrasound travels through a material, various things
happen to it. A reflection of the beam is called an echo,
 Echocardiography: Basic Principles, Technique, Display and Interpretation 5

Fig. 1.5: The concept of an echo. Fig. 1.6: Soft tissue acoustic interface producing some reflection
and more transmission. If a medium has high acoustic impedance,
stronger reflection will occur.

A B
Figs 1.7A and B: (A) Tissue interfaces with variable acoustic impedance. Higher impedance produces brighter echo due to more reflection
of ultrasound; (B) Refraction: Bending of the sound wave as it enters another medium. Refraction is associated with decreasing speed and
wavelength.

a critical concept in all diagnostic imaging (Fig. 1.5). The
production and detection of echoes form the basis of the
technique that is used in all diagnostic instruments. A
reflection occurs at the boundary between two materials
provided that acoustic impedance of the materials is
different. This acoustic impedance is a product of the
density and propagation speed.
If two materials have the same acoustic impedance,
their boundary will not produce an echo. If the difference in
acoustic impedance is small, a weak echo will be produced
and most of the ultrasound will carry on through the
second medium. If the difference in acoustic impedance
is large, however, a strong echo will be produced. If the
difference in acoustic impedance is very large, all the
ultrasound will be totally reflected. Typically in soft tissues,
the amplitude of an echo produced at a boundary is only a
small percentage of the incident amplitudes (Fig. 1.6).
Strong reflections or echoes show on the ultrasound
image as white and weaker reflections as gray (Figs 1.7A
and B).
A sound wave will undergo certain behaviors when it
encounters a tissue interface. Possible behaviors include:
Reflection off the tissue interface
Diffraction around the interface
Transmission (accompanied by refraction) into the
interface or new medium (Fig. 1.8)
6 Section 1: Fundamentals of Echocardiography
Fig. 1.8: Decreasing wavelength after refraction in the second medium.
Fig. 1.10: Reverberations shown by the curved arrow resulting in a
mirror-image artifact.
Fig. 1.12: Reflection at an angle equal to the angle of incidence
producing less bright echo.
Fig. 1.9: Multiple linear shadows (arrows) in front of mitral prosthesis in
transesophageal echocardiographic (TEE) view due to reverberations.
Fig. 1.11: Reflection from a tissue interface at right angle. There is
stronger reflection resulting in brighter echo. Typically, from posterior
pericardium.
Reflection of sound waves off of surfaces can lead to
one of two phenomenaan echo or a reverberation.
The reception of multiple reflections off of the interface
causes reverberationsthe prolonging of a sound
(Figs 1.9 and 1.10).
Angle of incidence: If a beam of ultrasound strikes the
boundary at right angle, it will be reflected parallel to
the transmitting beam and shall produce stronger echo
(Fig. 1.11). If it strikes a boundary obliquely, the
interactions are more complex than for normal incidence
(Fig. 1.12). The echo will return from the boundary at an
angle equal to the angle of incidence. The transmitted
beam will be deviated from a straight line by an amount
that depends on the difference in the velocity of ultrasound
at either side of the boundary. This process is known as
refraction (Figs 1.1 and 1.7).
 Echocardiography: Basic Principles, Technique, Display and Interpretation 7

Fig. 1.13: Reflection from a large interface is called specular Fig. 1.14: Schematic diagram of an ultrasound beam.
reflection and appears bright while smaller objects (smaller than the
wavelength) produce acoustic scattering.

Reflection is of two types (Fig. 1.13): Frequency % Penetration %

1. Specular reflection: is from a large tissue interface
1 MHz 40 cm
(smooth boundary between media) and produces
2 MHz 20 cm
bright echoes. These signals are intense and angle
3 MHz 13 cm
dependent:
5 MHz 8 cm
2. Acoustic scattering: occurs from smaller objects.
10 MHz 4 cm
Scattering is responsible for tissue texture. The signals
20 MHz 2 cm
are less intense and less angle dependent. These
provide tissue signature to the image.

Attenuation ULTRASOUND BEAM

As sound waves travel through a medium (e.g. tissue or
blood), the intensity weakens or attenuates. The degree
of attenuation is expressed in decibels (dB). Absorption
represents a conversion of sound energy to another
form of energy and is the major reason for attenuation.
Attenuation is greater for high-frequency sounds, which
result in higher absorption and more scatter. Attenuation
coefficient is smallest for the fat and maximum for lungs.
Bones also have very high attenuation coefficient.
Penetration
Depth to which an ultrasound beam travels into a tissue
is called penetration. Besides the tissue characteristic,
penetration is largely dependent upon the frequency of
the ultrasound being applied:
The sound beam is the confined, directional beam of
ultrasound travelling as a longitudinal wave from the
transducer face into the propagation medium. Ultrasound
beams are made of scan lines. These have length (azimuth)
along their long axis and width (elevation) along their
short axis. Beam width should be as narrow as possible to
prevent beam width artifacts and which can be achieved
by using lens. Ultrasound beams are either steered
mechanically or electrically. Both rapidly sweep sound
waves through tissues (Fig. 1.14).
Imaging Using Ultrasound
Image formation requires an ultrasound machine with
appropriate transducers and display, using a cathode-ray
tube or a flat panel.
8 Section 1: Fundamentals of Echocardiography
Fig. 1.15: A schema of an echocardiograph.
Fig. 1.17: Shapes of the transducers.
A basic echocardiography machine has the following
parts (Fig. 1.15):
Transducer probe: Probe that sends and receives the
sound waves
Central processing unit (CPU): Computer that does all
of the calculations and contains the electrical power
supplies for itself and the transducer probe
Transducer pulse controls: Changes the amplitude,
frequency and duration of the pulses emitted from the
transducer probe
Display: Displays the image from the ultrasound data
processed by the CPU
Keyboard/cursor: Inputs data and takes measurements
from the display
Disk storage device (hard, floppy, CD): Stores the acq
uired data.
Fig. 1.16: Transducer and its function.
Transducer
A transducer is a device that converts one form of energy
into another form.
The transducer probe makes the sound waves and
receives the echoes. It is the mouth and ears of the
ultrasound machine (Fig. 1.16).
Ultrasound transducers, or probes, can be categorized
based on their frequency range, low frequency versus
high frequency; and the shape of the probe, curved
versus linear or sector. Linear probes are mostly used
for vascular examination while sector probes are used
for cardiac examination (Fig. 1.17).
Linear array probes are high-frequency probes. High-
frequency probes have less tissue penetration but good
near-field image resolution.
Curved array probes are low-frequency probes and
used mainly for abdominal examination.
Low-frequency probes have greater tissue penetration;
however, resolution is compromised (Fig. 1.18).
Ultrasound transducers have a housing that contains
inside piezoelectric element.
Main component of a transducer is a piezoelectric
element that generates ultrasound waves as it gets
deformed by the applied electrical energy. As returning
ultrasound beam deforms it again, it generates electri
city, which is used to create an image (Fig. 1.19).
Most transducers in use nowadays have synthetic
piezoelectrical ceramics, polymers, composites,
crystals and so forth, with defined electromechanical
coupling and acoustic impedance.
 Echocardiography: Basic Principles, Technique, Display and Interpretation
Fig. 1.18: Relationship between resolution and penetration of various
transducer probes.
Fig. 1.20: Broad bandwidth transducer with a wide range of resonant
frequency.
The new generations of piezoelectric elements have
broad bandwidth for optimal resolution and penet
ration (Fig. 1.20).
Nominal frequency of a transducer depends upon its
resonance frequency.
Damping and electrical energy modulation generate a
wide range of frequencies (broad bandwidth) around
the nominal frequency.
Frequency of a transducer depends upon electrical
pulse frequency.
The piezoelectric element has a very high acoustic
impedance and works like a reflective surface but
material surrounding it works as a dump.
9
Fig. 1.19: Piezoelectric element encased in a housing assembly to
function as a transducer.
Fig. 1.21: Main ultrasound beam flaked by side lobe beams.
The multielement transducer generates a main
ultrasound beam that produces diagnostic images and
accessory beams (side lobes; Fig. 1.21).
Side-lobe beams can produce side-lobe artifacts,
which need to be recognized (Fig. 1.22). Side-lobes may
be minimized by driving the elements at variable voltages
in a process called apodization.
Most transducers have a focal point. Up to the focal
point, there is near field and beyond that there is far
field. Far field has increased distance between scan
lines and hence lower resolution.
Currently, most transducers are fully sampled matrix
array transducers with thousands of elements
10 Section 1: Fundamentals of Echocardiography
Fig. 1.22: M-mode of aortic root and the left atrium behind it. There
is an image of the posterior LV wall seen within the left atrium due to
side lobe error. Note that this image is less echogenic than the original.
Fig. 1.24: Transducer artifact near the apex due to back reflects from
the probe.
[compared to 64256 elements in two-dimensional
(2D) probes] that provide a thick ultrasound beam
(Fig. 1.23).
The probe also has a sound absorbing substance, to
eliminate back reflections from the probe itself; and an
acoustic lens, to help focus the emitted sound waves.
Despite these, there can be back reflects from the
transducer producing transducer artifacts (Fig. 1.24).
The shape of the probe determines its field of view, and
the frequency of emitted sound waves determines how
deep the sound waves penetrate and the resolution of
the image.
Fig. 1.23: A fully sampled matrix transducer with pyramidal field of
view.
Transducers of high frequency have thin piezoelectric
elements that generate pulses of short wavelength.
Beam-forming (link) is a general processing technique
used to control the directionality of the reception or
transmission of a signal on a transducer array.
Developments in transducer technology have resulted
in a reduced transducer footprint, improved side-lobe
suppression, increased sensitivity and penetration, and
the implementation of harmonic capabilities that can be
used for both gray-scale and contrast imaging.
A conventional 2D phased array transducer is com
posed of multiple piezoelectric elements that are elect
rically isolated from each other and arranged in a single
row. Individual ultrasound wave fronts are generated by
firing individual elements in a specific sequence with a
delay in phase with respect to the transmit initiation time.
Each element adds and subtracts pulses to generate a single
ultrasound wave with a specific direction that constitutes
a radially propagating scan line. The linear array can be
steered in two dimensions [vertical (axial) and lateral
(azimuthal)], while resolution in the Z-axis (elevation) is
fixed by the thickness of the image slice, which, in turn, is
related to the vertical dimension of piezoelectric elements.
Three-dimensional echocardiography (3DE) matrix-
array transducers are composed of 3,0009,000 indep
endent piezoelectric elements with operating frequencies
ranging from 2 to 4 MHz and 5 to 7 MHz for transthoracic
echocardiography (TTE) and transesophageal echocar
diographic (TEE), respectively. These piezoelectric
elements are arranged in a matrix configuration within
 Echocardiography: Basic Principles, Technique, Display and Interpretation
Fig. 1.25: The technique of obtaining pyramidal data set with use of a
matrix array transducer.
Fig. 1.27: Axial versus lateral resolution.
the transducer to steer the ultrasound beam electronically.
The electronically controlled phasic firing of the elements
in that matrix generates a scan line that propagates
radially and can be steered both laterally (azimuth) and
in the elevation to acquire a volumetric pyramid of data
(Fig. 1.25).
Multiple-Time Reception and Parallel
Processing of Reflected Beam
Basic imaging by ultrasound uses the amplitude
information in the reflected signal. One pulse is emitted,
the reflected signal, however, is sampled more or less
continuously (99% time is for receiving). As the velocity
of sound in tissue is fairly constant, the time between
11
Fig. 1.26: Parallel processing of multiple reflected beams in several
channels for a single transmitted beam.
the emission of a pulse and the reception of a reflected
signal is dependent on the distance; that is, the depth
of the reflecting structure. The reflected pulses are thus
sampled at multiple time intervals (multiple range
gating), corresponding to multiple depths, and displayed
in the image as depth. Parallel processing for multiple
simultaneous reception of reflected waves improves the
temporal resolution (Fig. 1.26). This parallel processing
could be in ratio of 1:16 or more.
Spatial Resolution
It is the parameter of an ultrasound imaging system that
characterizes its ability to detect closely spaced interfaces
and displays the echoes from those interfaces as distinct
and separate objects. If resolution is better, clarity of the
image is improved. Resolution is of two types:
Axial resolution: Is the minimum required reflector
separation along the direction of propagation required
to produce separate reflections. Good axial resolution is
achieved with short spatial pulse lengths. Short spatial
pulse lengths are a result of higher frequency and higher
damped transducers. Therefore, the higher the frequency,
the better is the resolution (Fig. 1.27). Axial resolution is
also called longitudinal or azimuthal resolution.
Lateral resolution: Is the minimum reflector separation
perpendicular to the direction of propagation required
to produce separate reflections. Good lateral resolution
is achieved with narrow acoustic beams. Wider beams
typically diverge further in the far field and any ultrasound
beam diverges at greater depth, decreasing lateral
12 Section 1: Fundamentals of Echocardiography
Mechanical Index
It is defined as the peak rarefactional pressure (negative
pressure) divided by the square root of the ultrasound
frequency. The used range varies from 0.05 to 1.9.
Technique of Image Acquisition
Fig. 1.28: Improved signal-to-noise ratio with harmonic imaging
compared to fundamental imaging.
resolution. Therefore, lateral resolution is best at shallow
depths and worse with deeper imaging.
Temporal resolution: is the ability to detect that an
object has moved over time. For the purposes of medical
ultrasound, temporal resolution is synonymous with
frame rate. Typical frame rates in echo imaging systems
are 30100 Hz. The temporal resolution or frame rate = 1/
(time to scan 1 frame). The time to scan one frame is equal
to the pulse repetition period number of scan lines per
frame.
Common means of improving frame rate include:
Narrowing the imaging sector, which decreases the
time it takes to scan one frame
Decreasing the depth, which decreases the pulse
repetitive frequency
Decreasing the line density, which requires fewer lines
to scan one frame
Turning off multifocus, which decreases the number of
pulses needed per line.
Focusing
Within transducers, there is a FOCUS that concentrates
the sound beam into a smaller beam area than would
exist otherwise. This area of focus is where one obtains the
best images. The focus is on the monitor, on the vertical
millimeter scale. So when positioning anatomy, make
sure it is in the region of the focus, so best images may be
obtained.
At the start of an echocardiography examination, the
appropriate transducer is selected according to the
type of examination and patients body habitus.
A higher frequency transducer provides better
resolution, but it has a shallower depth of penetration.
For the pediatric population, the transducer frequency
is usually 57.5 MHz, but for adults the transducer
frequency at the start of an examination is usually
22.5 MHz.
In fundamental imaging, echocardiographic images
are created when the transducer receives reflected
beams of the same frequency as the transmitted
beam, but the interface between tissue and blood can
be delineated better with the reception of harmonic
frequencies.
When the only reflected frequency received to
create the ultrasound image is equal to a multiple of
the transmitted frequency, the technique is called
harmonic imaging. Myocardial tissues are able to
generate harmonic frequencies, and harmonic imaging
improves the delineation of the endocardial border
(tissue harmonic imaging). As a result, harmonic
imaging is usually the imaging modality of choice
(Fig. 1.28).
A limitation of harmonic imaging in routine 2D
echocardiography is the increased sparkling quality to
the ultrasound image and the increased thickness of
the endocardial border (Fig. 1.29).
The following should be shown on the screen: The
patients identification, blood pressure at the time of
the examination, and an electrocardiographic tracing.
The examination of an adult patient usually begins
with a depth of 2025 cm and a wide sector (90). This
also gives an idea about any unusual extracardiac
structures. After the initial view, adjust the field depth
to use the entire screen to demonstrate the intended
cardiovascular images.
A zoom or regional expansion selection (RES)
function should be used frequently to visualize a
region of interest. The zoomed image is also better for
 Echocardiography: Basic Principles, Technique, Display and Interpretation
Fig. 1.29: Note thickness of the chordae tendineae in harmonic imag-
ing at 1.3 MHz compared to fundamental imaging at 1.9 MHz. All other
parameters are unchanged.
Fig. 1.31: Time gain compensation (TGC) is mounted on the knob
panel of the echocardiograph.
making measurements, with less intraobserver and
interobserver variability (Fig. 1.30).
When quantitative measurements are made, review
the acquired image in a cine loop format to identify a
frame at a specific timing of a cardiac cycle. Examples
are a midsystolic frame to measure the diameter of the
left ventricular outflow tract, an end-systolic frame to
measure the size of the left atrium and an end-diastolic
frame to measure the wall thickness of the left ventricle.
Improving Temporal Resolution
Specific areas need to be imaged and it may be necessary
to decrease the sector size, which will improve temporal
13
Fig. 1.30: Zoom view of the mitral valve to measure the size of annular
caseoma.
resolution by increasing the frame rate. The gain of the
image is controlled by overall gain and regional gain [by
time gain compensation (TGC)].
Tissue Texture
Hyperechoic areas have a great amount of energy from
returning echoes and are seen as white.
Hypoechoic areas have less energy from returning
echoes and are seen as gray.
Anechoic areas without returning echoes are seen as
black.
Time Gain Compensation
The received ultrasound signal can be amplified by
increasing the gain. Decreased gain yields a black image
and details are masked, while increased gain yields a
whiter image.
TGC will change the gain factor so that equally
reflective structures will be displayed with the same
brightness regardless of their depth (Fig. 1.31).
TGC allows amplification of ultrasound beams from
deeper depths because different amplitudes of ultrasound
signals are produced when received from different depths.
More TGC is required for higher frequency transducers,
which create more attenuation.
Returning ultrasound waves are referred to as signal,
while background artifact is referred to as noise. Increasing
the gain increases the signal-to-noise ratio.
14 Section 1: Fundamentals of Echocardiography
Fig. 1.32: Acoustic shadow (arrow) due to metallic aortic prosthesis.
Compression
Reduces the differences between the smallest and largest
amplitudes of ultrasound images by reducing the total
range without altering the signal ratio.
Side Lobe Artifacts
The probe cannot produce a pulse that travels purely in
one direction. Pulses also travel off at specific angles. These
side lobes are relatively weak and so normally do little
to degrade the image. Their effect is only normally seen
faintly superimposed in fluid filled areas that are anechoic
and so do not obscure the weak side lobe reflections. The
exception is when a side lobe strikes a particularly strong
reflector at 90. In this case, the reflector can appear within
the image.
Partial volume: The slice that makes up the ultrasound
image is 3 dimensional. This typically means that fluid
filled areas, where they are very small or adjacent to
soft tissue will not appear anechoic (black) as would be
expected, but often contain low level echoes which can be
mistaken for debris or even soft tissue.
Acoustic Shadowing
Tissues with high attenuation coefficients like bone or
prosthesis do not allow passage of ultrasound waves.
Therefore any structure lying behind tissue with a high
attenuation coefficient cannot be imaged and will be seen
as an anechoic region (Fig. 1.32).
Fig. 1.33: M-mode echocardiogram through the basal part of the LV.
Structures are identified by motion patterns.
Echocardiographic Display
Reflected ultrasound waves (echoes) are detected, filtered
and amplified electronically by the system and displayed
on the cathode ray tube in the following manner.46
A-mode and M-mode image: Sending and receiving an
ultrasound wave along a single line generates an A-mode
(amplitude-mode) or an M-mode image. In amplitude
mode (A-mode), reflected sound signal is displayed as a
vertical spike (voltage amplitude).
In brightness mode (B mode), the amplitude spike is
replaced by a dot. The dot has a location, certain brightness
and also motion. Dots of a structure or interface have
similar brightness and motion, which can be displayed in
two axes: vertical and horizontal. If there are dots along a
single scan line, it is called M-mode echocardiography.
If dots are along multiple scan lines that are steered in a
predetermined fashion, the morphology of the structure
can be identified when dots are arranged in a plane and
this is called cross-sectional or 2D echocardiography.
Motion imaging mode (M-mode) is a gray-scale
display of amplitude from each depth along a single scan
line over time with a high temporal resolution (Figs 1.33
and 1.34).
2D image is a gray-scale display of amplitude (dots)
from each depth along several scan lines created by
steering the ultrasound beam in an imaging plane. This
provides a real-time tomographic view in the form of a
thin slice with spatial resolution at the cost of temporal
resolution (Figs 1.35 and 1.36).
 Echocardiography: Basic Principles, Technique, Display and Interpretation
Fig. 1.34: M-mode echocardiogram at the level of aortic valve.
Fig. 1.36: Two-dimensional echocardiographic view perpendicular to
the long axis as shown in Figure 1.35.
Fig. 1.38: Longitudinally reconstructed image from a 3D pyramidal
volume. Part of the pyramidal volume is appreciated.
15
Fig. 1.35: Two-dimensional echocardiographic long axis view.
Fig. 1.37: Three-dimensional echocardiographic view with perception
of length, width and depth.
These slices are of less than 1 mm each and can be
sagittal, coronal, transverse or oblique.7
3D image is a colorized-display of amplitude over
depth from several imaging planes in a pyramidal volume
as if tomographic slices in various X, Y and Z planes have
been stitched together (Figs 1.37 and 1.38).
Real-time 3D images are obtained by matrix array
transducers (Fig. 1.39).
Standard Views
Transducers have markings of resonant frequency type of
element array and a light dot or line to indicate reference
or plane of display. The location of transducer while
examining the heart is called a window. Following are the
conventional windows:
16 Section 1: Fundamentals of Echocardiography
Fig. 1.39: Arrangement of piezoelectric elements in a matrix
tansducer shown in a cross-section view.
Fig. 1.41: Short axis image (left lower inset). Right panel shows
position transducer.
Parasternal (anterior chest wall on either side of
sternum between second and 4th intercostal spaces)
Apical (over palpable apex)
Subcostal (below xiphisternum)
Suprasternal (above manubrium sterni in suprasternal
notch)
Transesophageal
Epicardial (during open heart surgery)
Intracardiac
Axis: is the plane in which the ultrasound beam travels
through the heart:
Long axis: When the ultrasound beam travels
longitudinally through the heart (Fig. 1.40).
Short axis: Short axis image is obtained when the
ultrasound beam travels perpendicular to the long axis of
the heart (Fig. 1.41).
Fig. 1.40: Long axis view.
Fig. 1.42: Suprasternal view with transducer placed in the supra
sternal notch and oriented anteriorly to obtain long axis view of aorta.
Views: are window-specific images like apical four-
chamber view or parasternal long axis (PLAX) view or
suprasternal view (Fig. 1.42).
Sequence of an Echocardiographic
Examination
Sequence of an echocardiographic examination is
different in adults and children with suspected congenital
heart disease. In infants and children, the primary window
is subcostal followed by suprasternal with a little use of
parasternal views. In adults, the following sequence of
windows for examination, is usually followed (Fig. 1.43):
Left parasternal window
Apical window
Subcostal window
 Echocardiography: Basic Principles, Technique, Display and Interpretation 17

Fig. 1.43: Echocardiographic windows and the orientation of the transducer.

Fig. 1.44: Parasternal long axis view showing left ventricle (LV); right Fig. 1.45: Long axis view of the right ventricular outflow tract (RVOT)
ventricle (RV); aortic root (AO); left atrium (LA); thoracic aorta (TA); and the pulmonary artery (PA).
mitral valve (MV); aortic valve (AV).

Suprasternal window In the left parasternal view, tilting the transducer

Right parasternal window superiorly and laterally will show the right ventricular
To obtain an image, it is common to rotate, tilt or outflow tract and the pulmonary artery in the long axis
move the transducer in different directions to get the best view (Fig. 1.45).
possible views.

Parasternal Long Axis View Parasternal Short Axis View

In this view, ultrasound beam goes through the long axis From the PLAX view, the transducer is rotated
of the heart. The transducer is placed in the left second to counterclockwise to right angle and tilted up and down
fourth intercostal space close to the sternum. The view and to obtain short axis views at various levels (Figs 1.46
the structures that it shows are depicted in Figure 1.44. to 1.48).
18 Section 1: Fundamentals of Echocardiography
Fig. 1.46: Parasternal short axis view at mid-LV level.
Fig. 1.48: Parasternal short axis view at the level of mitral valve (MV).
Apical Window
The transducer is placed at the palpable apex or just below
and 4 views can be obtained by rotating and tilting it.
1. Apical four-chamber view
2. Apical two-chamber view
3. Apical long axis view
4. Apical five-chamber view.
Apical four-chamber view is obtained when the
transducer is placed at the apex and the reference point
toward the right shoulder (Fig. 1.49).
When the transducer from the apical four-chamber
position is rotated anticlockwise, apical two-chamber
view can be obtained (Fig. 1.50).
Fig. 1.47: Parasternal short axis view at the level of aortic valve.
Fig. 1.49: Apical four-chamber view and the structures shown.
Rotating the transducer clockwise from the apical
four-chamber position shows apical long axis view
(Fig. 1.51).
With inferior tilt of the transducer from the apical four-
chamber view, an apical five-chamber view can be shown
(Fig. 1.52).
Subcostal Window
By placing the transducer in subxiphoid position,
subcostal views can be obtained both like that from
parasternal and apical windows. The transducer needs
to be rotated or tilted. Most standard views like the four-
chamber view (Fig. 1.53) or the short axis views can also be
 Echocardiography: Basic Principles, Technique, Display and Interpretation
Fig. 1.50: Apical two-chamber view with structures shown.
Fig. 1.52: Apical five-chamber view.
obtained from a subcostal transducer position. The sub
costal view can be very helpful in patients with bad image
quality or in patients with suspected pericardial effusion.
To obtain the subcostal four-chamber view, place the
transducer over the center of the epigastrium and tilt it
downward from the suprasternal notch to the left shoulder
of the patient. The image produced will be similar to the
apical four-chamber view. The short-axis subcostal view,
however, is similar to the parasternal view and is ideal for
studying the right side of the heart.
Subcostal four-chamber view is obtained by pointing the
reference point of the transducer toward the left shoulder
with some inferior tilt to the base of probe. By rotating the
transducer, a series of short axis can be obtained (Fig. 1.54).
19
Fig. 1.51: Apical long axis view.
Fig. 1.53: Subcostal four-chamber view (left upper corner) and the
schema (lower left corner).
Main structures examined by subcostal views besides
the cardiac chambers are:
Inferior vena cava
Hepatic veins
Azygous and anomalous pulmonary veins
Abdominal aorta and its branches
The four cardiac chambers, the right ventricular outflow
tract, the aorta, and the vena cava can be visualized in the
subcostal view. Sometimes, it is also possible to visualize
a portion of the abdominal aorta. Pointing the transducer
toward the right side of the patient would result in a good
view of showing the liver and suprahepatic veins as well
as a transverse cross-section of the inferior vena cava
(Fig. 1.55).
20 Section 1: Fundamentals of Echocardiography

Fig. 1.54: Subcostal short axis view showing the entire right heart Fig. 1.55: Longitudinal view of the inferior vena cava (IVC) from the
structures. subcostal view.

Fig. 1.56: Suprasternal long axis view showing aorta and bifurcation of Fig. 1.57: The procedure of TEE in a schematic diagram. The probe
the pulmonary artery. Segmental branches of the left pulmonary artery is flexible and can be rotated and flexed or retroverted with knobs at
(LPA) are also seen. Right pulmonary artery (RPA). the handle.

Suprasternal View Supracardiac variety of anomalous pulmonary venous

drainage
Suprasternal views (Fig. 1.56) are routinely used in
Pulmonary artery bifurcation
children and adult patients to study:
Ascending aorta; arch and its branches; descending
thoracic aorta Transesophageal Echocardiographic Views
Coarctation of aorta
Patent ducts arteriosus The technique of TEE permits visualization of heart
Right and left superior vena cavae without the acoustic interference imposed by the chest
Azygous veins wall, ribs and the lungs. This is achieved by introduction of
 Echocardiography: Basic Principles, Technique, Display and Interpretation 21

a thin-walled probe with tip-mounted multielement 2D or Knob movements (only probe tip moves):
matrix-array 3D (510 MHz) transducer into the esophagus Flex right or left
or the gastric fundus using topical local anesthesia in Anteflex or retroflex
fasting state with or without mild sedation (Fig. 1.57). Its Transducer movements (probe stays still):
distinct advantages over transthoracic echocardiography Rotate angle forward (0180)
(TTE) are: Rotate angle back (1800).
Improved quality with better spatial resolution due to
no acoustic barrier and high-frequency probes Transducer Planes
Better visualization of the TTE blind spots like the left Transverse (0)
atrial appendage, thoracic aorta, pulmonary veins and Longitudinal (90)
so forth Omniplane (0180).
Can be used to monitor patients during invasive inter
ventional procedures without risk of contamination or
Views
interference
Its drawbacks are: High esophageal view
Semi-invasive and hence needs intensive monitoring Midesophageal view
Novel imaging planes need greater technical skills to Transgastric views.
interpret Following are the most common views obtained
Not possible in uncooperative patients or those with during TEE and the structures that are shown according to
esophageal stricture, cervical arthritis, gastric ulcer the standard imaging protocols89 (Figs 1.58 to 1.64):
and so forth. High esophageal views are for visualizing the great
vessels (Fig. 1.65) while the transgastric views are used to
TEE Probe Manipulation study the detailed anatomy of the mitral and aortic valves
including continuous wave (CW) interrogation of the left
Probe movements (entire probe moves): ventricular outflow tract.
Advance or withdraw Details of TEE examinations are shown in respective
Turn right or left chapters.

Fig. 1.58: Transverse midesophageal four-chamber view (4CV). Fig. 1.59: Vertical or Longitudinal midesophageal two-chamber
view (2CV).
22 Section 1: Fundamentals of Echocardiography

Fig. 1.60: Midesophageal long axis view showing aorta, left atrium, left Fig. 1.61: Transverse midesophageal view to show interatrial septum,
ventricle and the mitral valve. aortic valve, atria and the RVOT.

Fig. 1.62: TEE RV inflow view showing tricuspid valve. Fig. 1.63: Midesophageal bicaval view showing inferior and superior
vena cavae and the interatrial septum.

Fig. 1.64: Midesophageal transverse short axis view showing left atrial Fig. 1.65: High esophageal view showing ascending aortic dissection
appendage (LAA). beyond the sinotubular junction.
 Echocardiography: Basic Principles, Technique, Display and Interpretation
References
1. Edelman SK (Ed). Understanding Ultrasound Physics:
Fundamentals and Exam Review, 2nd ed. Woodlands, TX:
ESP; 1994.
2. McGahan JP, Goldberg BB. Diagnostic Ultrasound, Volume
1. New York, NY: Informa Healthcare; 2007.
3. Kremkau FW (Ed). Diagnostic Ultrasound: Principles and
Instruments, 6th ed. Philadelphia, PA: W. B. Saunders;2002.
4. Sites BD, Brull R, Chan VWS, et al. Artifacts and pitfall errors
associated with ultrasound-guided regional anesthesia. Part
I: understanding the basic principles of ultrasound physics
and machine operations. Reg Anesth. 2007;32(5):4128.
5. Edler I, Hertz CH. The use of ultrasonic reflectoscope for
the continuous recording of the movements of heart walls.
1954. Clin Physiol Funct Imaging. 2004;24:11836.
23
6. Joyner CR Jr, Reid JM. Applications of ultrasound in cardi-
ology and cardiovascular physiology. Prog Cardiovasc Dis.
1963;5:48297.
7. Tajik AJ, Seward JB, Hagler DJ, et al. Two-dimensional
real-time ultrasonic imaging of the heart and great vessels:
technique, image orientation, structure identification, and
validation. Mayo Clin Proc. 1978;53:27103.
8. Seward JB, Khandheria BK, Oh JK, et al. Transesopha-
geal echocardiography: technique, anatomic correlations,
implementation, and clinical applications. Mayo Clin Proc.
1988;63:64980.
9. Lang RM, Badano LP, Tsang W, et al. EAE/ASE recom-
mendations for image acquisition and display using three-
dimensional echocardiography. Eur Heart J Cardiovasc
Imaging. 2012;13:1-46.
 Chapter Hemodynamic Evaluation
2
by Echo-Doppler
Techniques
Introduction
Hemodynamics can be defined as the physical factors that
govern blood flow. These are the same physical factors
that govern the flow of any fluid, and are based on a
fundamental law of physics. Pressure, flow and resistance
are all fundamental elements of fluid mechanics. The
relationship between these parameters clearly defines
the behavior of the blood in the heart and vessels of the
human body. Disturbance in flow, intracardiac pressure
and resistance all provide useful information in health and
disease, which can be used to diagnose severity of valvular
stenosis and regurgitation, shunt calculations, assess
the integrity of pulmonary circulation, monitor therapy
and long-term follow-up of asymptomatic patients with
altered pressure-flow dynamics due to structure heart
disease. The valves ensure that blood flows in a single
pathway through the heart by opening and closing in a
particular time sequence during the cardiac cycle and this
mechanism may not be true even in normal conditions.
How much of this valve mechanism is abnormal can be
studied by Doppler hemodynamics. Thus, hemodynamics
is an important part of cardiovascular physiology dealing
with the forces the pump (the heart) has to develop to
circulate blood through the cardiovascular system in
normodynamics and otherwise.
Echocardiography has replaced invasive cardiac
catheterization for various hemodynamic assessments:
cardiac output, valvular pressure gradients, dynamic LV
outflow tract gradient, right heart pressures, constrictive
pericarditis and vascular resistance.
HEMODYNAMIC EVALUATION
1. Hemodynamics: Is an important part of cardiovascular
physiology dealing with the forces the pump (the heart) has
to develop to circulate blood through the cardiovascular
system. Both normotension and normodynamic state
(blood flow within normal range) must be part of the
therapeutic goal.1
2. Flow: Blood in the circulatory system moves from one
point to another driven by a pressure difference at the
two points. It can be expressed as total flow volume in
one cardiac cycle either in systole or diastole or flow rate
(flow/time). Speed with which it moves and the direction
are expressed as velocity. Velocity of flow can be obtained
by using Doppler echocardiography.2 Flow is a product of
velocity and area of flow (Fig. 2.1).
3. Velocity: Velocity basically is the rate of change of the
position of an object with time. For blood, it denotes the
speed and direction of flow (cm/s).
4. Acceleration: Rate of change in velocity is called
acceleration (cm/s2).
5. Force: is a product of mass and acceleration. As the
mass is constant, force and acceleration can be used
interchangeably.
6. Pressure: Force per unit area is called the pressure.
 Hemodynamic Evaluation by Echo-Doppler Techniques 25

Fig. 2.1: Flow through a cylindrical object is expressed by velocity Fig. 2.2: Laminar flow through a cylinder can be either axisymmetric
area. Area is obtained from the two- or three-dimensional gray-scale or asymmetric.
image. For a spherical structure, area = 0.785 (diameter)2.

Fig. 2.3: Laminar flow versus turbulent flow. Fig. 2.4: Doppler equation.

Types of Flow In practice, speed of sound is presumed to be 1,540

m/s, and angle of insonification is kept as close to zero
Flow can be laminar or turbulent. Laminar flow runs in
as possible so that no angle calculation or correction
parallel streamlines, while the turbulent flow is chaotic.
is required. Angle correction has been given up except
It is difficult to apply laws of physics on turbulent flow.
while studying vascular flow. If frequency shift is positive
Estimation of flow using various laws of physics assumes
(received frequency > transmitted frequency), velocity is
that the flow is in streamline (Figs 2.2 and 2.3).
positive toward the transducer and vice versa.
Turbulence and its extent are defined by the Reynolds
number.
Types of Doppler Echo
DOPPLER PRINCIPLE
Types of Doppler are:
FOR ESTIMATING VELOCITY
1. Pulsed wave Doppler
If speed of sound through a medium is known or 2. Continuous wave Doppler
presumed, velocity of flow in it can be determined by the 3. Color Doppler
change in frequency of the moving objects (red blood cells) 4. Tissue Doppler
when compared to the transmitting frequency (Fig. 2.4). 5. Power Doppler
26 Section 1: Fundamentals of Echocardiography
Fig. 2.5: The right heart circulation has low velocity inflow across the
tricuspid valve in diastole and low velocity outflow across the pulmo-
nary valve in systole (approximately 100 cm/s).
Fig. 2.7: Left ventricular outflow tract peak velocity (apical view) by
pulsed wave Doppler and calculation of LVOTvelocitytime integral
(VTI). LVOTVTI (stroke distance), herein, is 18.37 cm. Stroke volume
is obtained when LVOTVTI is multiplied by the cross-sectional area
of the outflow tract.
PW uses a single crystal that sends and receives sound
beam signals.
The crystal emits a short burst of ultrasound at a
certain frequency [pulse repetition frequency (PRF)].
After a certain interval determined by the depth of
interest, it samples the backscatter signals.
The maximal frequency shift that can be determined is
half the PRF or Nyquist limit.
If the velocity exceeds the Nyquist limit, aliasing
occursDoppler spectrum gets cut off at the Nyquist
Fig. 2.6: The left heart circulation shows low-velocity biphasic inflow
across the mitral valve (< 100 cm/s) and low-velocity outflow across
the aortic valve in systole (< 150 cm/s).
frequency and the rest is recorded in the opposite
direction.
CW uses two piezoelectric crystalsone continuously
transmits and another continuously receives.
Useful for high velocities, not limited by the PRF or
Nyquist phenomenon
To get high velocities, one can use the nonimaging
transducer.
The normally functioning valves ensure that blood
flows in a single pathway through the heart by opening
and closing in a particular time sequence during the
cardiac cycle and adequate flow is maintained at low-
flow velocity and driving pressure because valves offer
very little resistance (Figs 2.5 and 2.6). This type of flow is
obtained by PW Doppler.
VelocityTime Integral
For estimation of mean flow, velocity needs to be
multiplied by time to obtain velocitytime integral (VTI).
VTI is also known as stroke distance.2 Stroke distance
when multiplied by cross-sectional area (CSA), provides
volume (Fig. 2.7).
VTI is used to estimate:
Stroke volume (SV) and cardiac output
Regurgitant volumes and regurgitant fractions
Qp:Qs (ratio of left-to-right shunt or pulmonary blood
flow to systemic flow ratio).
Qp:Qs is calculated after obtaining the right
ventricular stroke volume [right ventricular outflow tract

Fig. 2.8: Relationship between flow and driving pressure and
resistance.
Fig. 2.10: An approximate relationship between aortic valve area and
mean transaortic gradient in subjects with normal flow.
(RVOT)-VTI RVOT area], the left ventricular stroke volume
[left ventricular outflow tract (LVOT)-VTI LVOT area] and
then getting their ratio. In subjects with no intracardiac
shunts or valvular regurgitation, Qp = Qs. Absolute
left-to-right shunt can be calculated by multiplying
stroke volume difference by heart rate when the right
ventricular stroke volume is definitely more than the left
ventricular (LV) stroke volume.
Cardiac output (CO) is calculated as: CO = SV heart
rate (L/min).
Normal stroke volume is 45 5 mL/M2. Low flow is
labeled when stroke volume is < 35 mL/M2.
Hemodynamic Evaluation by Echo-Doppler Techniques 27
Fig. 2.9: An approximate relationship between mitral valve area (MVA)
and transmitral mean diastolic gradient in subjects with normal flow.
OHMS LAW OF FLUIDS
(THE HAGENPOISEUILLE EQUATION)
The Ohms law when applied to fluids suggests that
Driving pressure (P) = Flow (Q) resistance (R)
In relating Ohms law to fluid flow,3 the voltage
difference is the pressure difference (P; sometimes
called driving pressure, perfusion pressure or pressure
gradient). For the flow of blood in a chamber or across it,
the P is the pressure difference between any two points
along a given length. There is a linear and proportionate
relationship between flow and driving pressure. This linear
relationship, however, is not followed when pathological
conditions lead to turbulent flow because turbulence
decreases the flow at any given driving pressure. Because
flow and resistance are reciprocally related, an increase in
resistance decreases flow at any given P (Fig. 2.8). Also, at
any given flow along a blood vessel or across a heart valve,
an increase in resistance increases the P.
The resistance (R) is the resistance to flow that is
related in large part to the size of the valve opening or any
other orifice.
Driving pressure or P can be obtained in the heart
using the modified Bernoullis equation.4 Resistance is
the ratio of pressure difference/flow (in Wood units or
dynes.cm.s-5).
There is an approximate relationship between
narrowed valve area and mean gradients (Figs 2.9
and 2.10).
28 Section 1: Fundamentals of Echocardiography
Fig. 2.11: Using Doppler principle, P can be estimated by a
difference in velocities at two points. If the proximal point velocity is
neglected (being very low due to low resistance), the equation is simpl
fied to DP = 4V2 wherein V represents the maximum velocity obtained
at the distal point.
THE BERNOULLIS EQUATION
Doppler echocardiography takes advantage of the
acceleration of flow across a restrictive orifice, and the
relationship defined by the Bernoullis equation between
velocity and pressure, to assess gradients.
Increase in speed of fluid occurs simultaneously with a
decrease in pressure or potential energy (convective flow),
provided there are minimal frictional forces. Within a
fluid flowing horizontally, the highest speed occurs where
pressure is the lowest, and the lowest speed occurs where
pressure is the highest (Fig. 2.11).
It is an approximate relation between pressure,
velocity and elevation, and is valid in regions of steady,
incompressible flow where net frictional forces are
negligible. The Bernoullis equation can not be applied
to normal transvalvular flows because accelerative flow is
more than the convective flow.
The Bernoullis principle is derived from the principle
of conservation of energy. This states that, in a steady flow,
the sum of all forms of mechanical energy in a fluid along
a streamline is the same at all points on that streamline.
This requires that the sum of kinetic energy and potential
energy remain constant. Thus, an increase in the speed of
the fluid occurs proportionately with an increase in both
its dynamic pressure and kinetic energy, and a decrease in
its static pressure and potential energy (Fig. 2.12).
Fig. 2.12: Driving pressure during diastole in an incompetent aortic
valve. The right upper corner shows continuous wave Doppler trac-
ing, which is a replica of P and flow during diastole shown graphi-
cally defining aortic regurgitation. At the onset of regurgitant flow, P is
80 mm Hg, which decreases to 40 mm Hg at the end of flow.
P
Doppler echo measures blood-flow velocities,
which can be converted to pressure gradients by the
Bernoullis equation.
In most clinical situations, flow acceleration and
viscous friction components of the equation can be
ignored.
Flow velocity proximal to a fixed orifice (v1) is much
lower than the peak; so this can be ignored as well.
Pressure gradient (P) across a fixed orifice can then
be calculated with the simplified Bernoullis equation.
Simplified Bernoullis equation:
P = 4v2
Caveats for the Bernoullis Equation
Proximal velocity may not be negligible.
There may be multiple sites across the pathway of
flow, where relationship of kinetic energy to potential
energy changes.
Frictional forces may not be negligible.
Flow may not always be in streamlines.
Accelerative forces may be significant depending upon
the shape of the orifice through which the flow exits.
CONTINUITY EQUATION
One of the fundamental principles used in the analysis
of uniform flow is known as the Continuity of Flow.5

Fig. 2.13: Flow across a pathway is the product of velocity and area.
Unless area changes (changing the velocity), the flow at two points is
constant.
Fig. 2.15: Continuity equation to estimate cross-sectional area (CSA)
at point 2. (Q: Flow volume; VTI: Velocitytime integral).
This principle is derived from the fact that mass is always
conserved in fluid systems regardless of the pathway
complexity or direction of flow.
If steady flow exists in a channel and the principle of
conservation of mass is applied to the system, there exists a
continuity of flow, defined as follows: The mean velocities
at all cross sections having equal areas are then equal,
and if the areas are not equal, the velocities are inversely
proportional to the areas of the respective cross sections
(Fig. 2.13).
Hemodynamic Evaluation by Echo-Doppler Techniques 29
Fig. 2.14: Left heart: The rate at which mass enters the system (mitral
inflow) is equal to the rate at which mass leaves the system (outflow).
This is the equation of continuity. As mass is volume density and the
density of blood is constant, the equation can be applied to the volume
entering and leaving the system. provided there is no sink or sump in
the system.
Thus, if the flow is constant in a reach of channel, the
product of the area and velocity will be the same for any
two cross sections within that reach. This is expressed in
the continuity equation (Fig. 2.14).
If the velocities (or velocitytime integrals) at two
points are estimated by the Doppler equation and area
of one point is known, the area at the other point can be
calculated by the equation of continuity (Fig. 2.15).
Continuity equation is most commonly used to
estimate effective orifice area (EOA) in aortic valve
stenosis. Although it is generally reliable, caveats exist.68
Doppler gradients can overestimate the severity of
aortic stenosis in five circumstances, three of which
involve errors in measurement.
Contamination by mitral regurgitation signal
Dynamic LV obstruction
Use of angle correction
High flow states
Pressure recovery
Limitations of Continuity Equation
While the continuity principle is a fundamental principle
of hydrodynamics, the available data for application in a
given case have a number of error sources and limitations.
Pre-stenotic CSA. For the LVOT, it is assumed that
its shape is circular and its area can be calculated as
r2 or 0.785 D2 (D is the diameter in the parasternal
30 Section 1: Fundamentals of Echocardiography
Fig. 2.16: Estimating aortic valve area in a patient with valvular aortic
stenosis. The velocity ratio of 1/5 is multiplied by the cross-sectional
area of the LVOT assuming it to be circular.
long-axis view and r is the radius or D/2). This is not
strictly true, since the outflow tract is in fact elliptical
in cross-section, and the parasternal long-axis view
shows neither the largest nor the smallest ellipse
diameter (Fig. 2.16).
Furthermore, the true outflow tract diameter is often
underestimated if a tangential long-axis cut of the
outflow tract is recorded, leading to underestimation
of the diameter, radius and ultimately aortic valve area.
This is generally regarded as the most important error
source in the application of the continuity equation.
A possible alternative to the full continuity equation,
therefore, is the velocity ratio, which is the ratio of
peak velocities or velocitytime integrals in the outflow
tract and across the stenosis.
Pre-stenotic flow velocity and VTI. The flow field in the
outflow tract, although laminar, is not homogeneous
and blood flows faster at the septal (anterior) side than
at the posterior side of the outflow tract (see Fig. 2.2).
Moreover, velocities by Doppler are often recorded
at an angle between flow direction and echo beam,
leading to underestimation of velocities.
Furthermore, in atrial fibrillation, different heart
cycle lengths and different preceding heart cycles
make it difficult to find equivalent heart cycles for the
acquisition of peak velocities or velocitytime integrals
in the outflow tract and across the stenotic valve.
If the maximal velocity across the stenotic orifice is
missed by CW Doppler, the continuity equation will
produce erroneous results. The continuity equation,
Fig. 2.17: Relationship between effective orifice area (cross-sectional
area of flow) and geometric or anatomical area. GOA > EOA by a vari-
able proportion called contraction coefficient.
therefore, by no means can correct for a suboptimal
Doppler interrogation of the aortic valve.
Viscous effects cause lower velocities at the edges
of the vena contracta (VC) at low-flow rates, resulting in
a parabolic profile. At higher-flow states, inertial forces
overcome viscous drag, causing a flatter profile. Effective
orifice area itself varies with flow rate as well, with the
smallest areas seen at moderate-flow states. These flow-
dependent factors lead to flow-ratedependent errors in
the Doppler continuity equation.
The continuity equation calculates an effective orifice
area, which by definition is smaller than the geometric
or anatomic orifice area (Fig. 2.17).
EFFECTIVE ORIFICE AREA
Effective orifice area (EOA) is determined using
echocardiography, Doppler and the continuity equation,
and is a reflection of the minimal CSA of the outflow jet (the
vena contracta). EOA is calculated as the product of the
CSA of the LV outflow tract (from its diameter, measured
in the parasternal long-axis view) and the LV outflow tract
velocitytime integral (using PW Doppler from an apical
window), divided by the AV velocitytime integral (using
CW Doppler [CWD] from an apical, right parasternal or
suprasternal window). Unlike gradients, EOA provides an
accurate assessment of stenosis severity independent of
flow in most hemodynamic states.
The ratio between geometric orifice area (GOA)
and EOA, the coefficient of contraction, is somewhat

Fig. 2.18: Comparison of funnel-shaped orifice with that of hole-in-
diaphragm type with similar geometric orifice areas. Effective orifice
area calculated is lower for hole-in-diaphragm type orifice because of
higher velocities and P. This is because greater normal acceleration
is required to bend the flow into the orifice.
Fig. 2.20: Eccentric jet through an orifice have higher velocities and
greater P.
variable, depending on geometrical features (e.g. smooth
or abrupt inlet, Figs 2.18 and 2.19) and also on flow rate,
at least if the latter is low.9 Furthermore, since blood
is a viscous fluid, inaccuracies arise from ignoring the
boundary layer of the fluid in motion.
Eccentric jets exiting from a narrow orifice also have
narrower VC and higher P (Fig. 2.20). This is because of
the greater force required to bend the flow.
The EOA and the corresponding pressure gradients are
deleteriously affected by increasing jet eccentricity. For
the same anatomical size and flow rate, valve morpho
logies producing eccentric jets have greater energy losses
than those that produce concentric jets.10
Hemodynamic Evaluation by Echo-Doppler Techniques 31
Fig. 2.19: Similar geometric area of two different shapes of the orifice.
Elliptical or slit-like shape results in greater P and lower effective ori-
fice area. Contraction coefficient can be as low as 0.60 in such cases.
Fig. 2.21: Site of reattachment of the jet to the wall of receiving
chamber beyond the orifice.
The distance from the VC to the site of pressure
recovery also increases with jet eccentricity.10 Full pressure
recovery only occurs when the jet fully expands to fill the
aorta, that is, at the most distal reattachment site (Fig. 2.21).
VENA CONTRACTA
It is the point in a fluid stream where the diameter of the
stream is the least, and fluid velocity is at its maximum,
such as in the case of a stream issuing out of a narrowed
valve.11 The reason for this phenomenon is that fluid
streamlines cannot abruptly change direction (Figs 2.22
and 2.23).
32 Section 1: Fundamentals of Echocardiography
Fig. 2.22: Vena contracta just beyond the narrow orifice, where
streamlines converge for a variable distance.
Fig. 2.24: Vena contracta measurement in a patient with aortic regur
gitation shown by color flow Doppler in parasternal long-axis view.
The converging streamlines follow a smooth path,
which results in the narrowing of the jet (seen by Doppler
color flow mapping).
Measurement of the VC is useful as it describes the
smallest area of the blood flow jet as it exits a valve. This
corresponds to the EOA calculated for valves using the
continuity equation (Figs 2.23 and 2.24).
Measurement of diameter of VC is useful in assessing
the severity of valvular regurgitations. It is ideally
measured in parasternal long-axis views for mitral and
aortic regurgitation (AR).12 Regurgitation is mild if VC 3
mm and it is severe if VC is 6 mm.13
Even though the measurement of the VC is less
dependent on technical factors, small errors in
measurement can by multiplied due to the relatively small
values of the VC width.
Fig. 2.23: Arrows point to the width of vena contracta of the mitral
regurgitation jet.
Beyond the VC, the fluid expands, and the velocity and
pressure change once again. By measuring the difference
in fluid pressure between the normal section and at the VC,
the volumetric and mass flow rates can also be obtained
from Bernoullis equation.
It is preferable to use a zoom mode to optimize
visualization of the VC and facilitate its measurement.
The color flow sector should also be as narrow as possible,
with the least depth, to maximize lateral and temporal
resolution.
The largest diameter of a clearly defined VC is
measured if possible in two orthogonal planes.
Advantages of Vena Contracta
Simple measure of orifice area
Valuable in eccentric jets as well
Not dependent on pulse repetitive frequency
No correction for angle or convergence walls
Not affected by other valve involvement
If the orifice is fixed, then the size of the VC is indep
endent of driving pressure and flow rate.
Not affected by loading conditions.
Limitations of Vena Contracta
No temporal information
May need biplane or triplane measurement to get it
right in case of eccentric orifices
Multiple jets are a problem
Small errors can make a big difference

Fig. 2.25: Diagrammatic representation of fluid energy (above) and
flow streamlines (below).
In dynamic regurgitant orifice, vena contracta may
change with hemodynamics or during the cardiac
cycle.
The convergence zone is flatter with higher aliasing
velocities and become more elliptical with lower
aliasing velocities. The aliasing velocity is set between
20 and 40 cm/s.
Another limitation regards variation in the regurgitant
orifice during the cardiac cycle. This is particularly
important in mitral valve prolapse, where the
regurgitation is often confined to the latter half of
systole. The precise location of the regurgitant orifice
can be difficult to judge, which may cause an error in
the measurement of the proximal isovelocity surface
area (PISA) radius.
PRESSURE RECOVERY
Pressure recovery occurs because of re-expansion of flow
downstream from the VC of the stenotic jet (Fig. 2.25).
When blood moves through a narrow orifice, pressure or
potential energy is converted to kinetic energy to drive flow
across the orifice. Just beyond the orifice (beyond VC), the
streamlines diverge to attach to the wall and reconvert
some kinetic energy into pressure energy, resulting in
greater pressure drop at the VC, which recovers to some
extent as the jet expands fully. This difference in maximum
pressure loss to net pressure loss is called pressure
recovery (Fig. 2.26).
The pressure recovery phenomenon can be
responsible for Doppler gradients that are substantially
Hemodynamic Evaluation by Echo-Doppler Techniques 33
Fig. 2.26: Pressure recovery beyond an orifice is Pmax Pnet.
higher and valve area that is substantially lower than
those determined invasively.
Key Points
At the VC, velocity is a maximum and pressure is a
minimum. Beyond VC, pressure recovers to some
extent.
Geometry and turbulence are factors that influence
pressure recovery.
Pressure recovery is reduced by turbulence in the
flow field because turbulent dissipation represents
irrecoverable energy loss.
There is increased pressure recovery in patients with
eccentric orifices, eccentric jets, certain types of
bileaflet prostheses and when the receiving chamber
is narrow.
The recovered gradient more accurately reflects the
energy loss across the valve and, therefore, the left
ventricular workload produced by the stenosis.
Pressure recovery phenomenon can explain high
gradients in seemingly normal prosthetic valves
(Fig. 2.27) and certain native orificial narrowings
(Figs 2.28 and 2.29).
Clinical significance of pressure recovery phenomenon
is more in patients with mild or moderate aortic stenosis,
who show very high transaortic gradients due to pressure
recovery. In these patients, energy loss index can be
estimated by measuring aortic diameter (and hence area)
at sinotubular junction and using it along with valve area
calculated by the continuity equation (Fig. 2.30).
34 Section 1: Fundamentals of Echocardiography
Fig. 2.27: Eccentrically placed Medtronic-Hall valve in aortic posi-
tion (arrow) showing peak gradient of > 100 mm Hg. Valve motion is
normal and the patient is asymptomatic.
Fig. 2.29: Supravalvular aortic stenosis in a child with eccentric jet.
Peak gradient of 264 mm Hg (right panel) is due to highly eccentric
orifice and flow.
An energy loss index of 0.5 cm2/M2 indicates severe
stenosis.14
VENTRICULOVALVULAR IMPEDANCE
This Doppler hemodynamic index applies to aortic
valve stenosis. It is used to obtain information about the
hemodynamic load created by a narrowed orifice. It is
a ratio of cuff systolic blood pressure + mean gradient
divided by stroke volume index. A ratio > 4.5 to 5.0 suggests
higher hemodynamic burden and bad prognosis.15
Fig. 2.28: Subaortic stenosis with eccentric orifice in a child with esti-
mated peak gradient of 184 mm Hg. On invasive pressure recording,
peak gradient was 80 mm Hg.
Fig. 2.30: Coefficient of energy loss using a simple formula.
PROXIMAL ISOVELOCITY SURFACE AREA
AND VOLUMETRIC MEASUREMENTS
Proximal isovelocity surface area is a Doppler pheno
menon to estimate orifice area.1618
The PISA method is derived from the hydrodynamic
principle, which states that as blood approaches
a narrow orifice, its velocity increases forming
concentric, roughly hemispheric shells of increasing
velocity and decreasing surface area (Fig. 2.31).

Fig. 2.31: Graphic depiction of flow across a narrow orifice. The red
hemispheres represent proximal isovelocity surface area.
Fig. 2.33: Applying proximal isovelocity surface area method in a
patient with mitral stenosis. Note that the orifice does not have a flat
surface and small angle correction may be needed.
Color flow mapping offers the ability to image one of
these hemispheres that corresponds to the Nyquist
limit of the instrument (Figs 2.32 and 2.33).
If a Nyquist limit can be chosen at which the flow
convergence has a hemispheric shape, flow rate (mL/s)
through the orifice is calculated as the product of the
surface area of the hemisphere (2R2 or 6.28 radius2)
and the aliasing velocity (Va) as 2R2 Va.
Assuming that the maximal PISA radius occurs at the
time of peak flow and peak velocity, the maximal EOA
is derived as: EOA = (6.28R2 Va)/Vmax, where Vmax is
the peak velocity of the jet by CWD.
Hemodynamic Evaluation by Echo-Doppler Techniques 35
Fig. 2.32: Color flow Doppler of mitral regurgitation showing proximal
isovelocity surface area (arrows).
The transiting volume/beat can be estimated as EOA
multiplied by the velocitytime integral of the jet.
Since the PISA calculation provides an instantaneous
peak flow rate, EOA by this approach is the maximal
EOA and may be slightly larger than EOA calculated by
other methods. If it is a regurgitant jet, EOA represents
regurgitant orifice area.
Measurement of PISA by color flow mapping requires
adjustment of the aliasing velocity such that a well-
defined hemisphere is shown. This is generally done
by shifting the baseline toward the direction of flow or
by lowering the Nyquist limit, or both.
If the base of the hemisphere is not a flat surface
(180), then correction for wall constraint should be
performed, multiplying by the ratio of the angle formed
by the walls adjacent to the regurgitant orifice and 180
(Fig. 2.33).
Limitations of PISA Method
It is more accurate for central jets than for eccentric
jets.
The formula is applicable to a circular orifice. However,
in real life, the orifices are more often elliptical or
irregular (Figs 2.34 and 2.35).
If the image resolution allows the flow convergence to
be seen well (using zoom mode), and a Nyquist limit
can be chosen at which the flow convergence has a
hemispheric shape, it is easy to identify the aliasing
line of the hemisphere. However, it can be difficult to
judge the precise location of the orifice and the flow
convergence shape.
36 Section 1: Fundamentals of Echocardiography
Fig. 2.34: Color Doppler jet of aortic regurgitation. Note that the proxi-
mal isovelocity surface area (arrow) is irregular.
Fig. 2.36: Simplified proximal isovelocity surface area method for
calculating mitral regurgitant orifice area (ROA).
Any error introduced is squared, which can markedly
affect the resulting flow rate and ERO.
In patients with normal blood pressure and mitral
regurgitation, a simplified formula can be used if
aliasing velocity is brought to 40 cm/s by shifting the
baseline.19 The formula gives ERO or regurgitant orifice
area by R2/2, where R is the radius of the hemisphere
(Fig. 2.36).
PISA method is much easier to apply in transes
ophageal echocardiography images than in transthoracic
images (Fig. 2.37). Scroll function must be used to define a
cardiac cycle, wherein PISA is seen the best. In about 10%
of the cases, PISA can not be defined although VC can be
easily measured (Fig. 2.38).
Fig. 2.35: Anatomical orifice of aortic regurgitation. Note the triangular
shape, which is more often than not the case.
Fig. 2.37: Proximal isovelocity surface area in a patient with mitral
stenosis in a transesophageal echocardiography view. Clarity of isove-
locity shell boundary and eccentricity are obvious.
An ERO 30 mm2 ( 40 mm2 for mitral) or regurgitant
volume 60 mL indicates severe mitral or aortic
regurgitation.
PRESSURE HALF-TIME
Across any narrow orifice through which blood flows
driven by the perfusion pressure, the P declines slowly
(Fig. 2.39).
Pressure half-time (PHT) is defined as the time needed
for the peak transvalvular pressure gradient to fall to its
half value, in milliseconds. According to the Bernoullis
equation, when pressure is halved, velocity is equal to peak
transvalvular velocity divided by the square root of 2.20

Fig. 2.38: No clear proximal isovelocity surface area delineation in a
patient with severe aortic valve regurgitation.
Fig. 2.40: Pressure half-time in a patient with aortic valve regurgita-
tion. Yellow line indicates deceleration time, 29% of which is pressure
half-time.
Thus, PHT is the time for the peak velocity to reach 0.707
of its initial value (Fig. 2.40). The faster the gradient falls,
the easier the passage of blood through a valve, and vice
versa. Thus, high transvalvular PHT indicates a narrowed
valve area, while low PHT indicates a wide valve area.
Original studies of PHT, initially using catheterization
and then Doppler data, were performed in 1968 and
showed a good correlation between atrioventricular PHT
and effective mitral valve area, relatively insensitive to
changes in heart rate or cardiac output.21 PHT is always
proportionally related to deceleration time (DT).
PHT = 0.29 DT
Hemodynamic Evaluation by Echo-Doppler Techniques 37
Fig. 2.39: Arrow points to the pressure decline in the presence of
aortic regurgitation.
PHT is usually obtained from transmitral and trans
aortic or transpulmonary valve CWD signals to assess the
severity of mitral valve stenosis and aortic/pulmonary
valve regurgitation.22
Mitral Stenosis
The decline of the velocity of diastolic transmitral blood
flow is inversely proportional to mitral valve area (MVA),
and MVA is derived using the empirical formula23
MVA (cm2) = 220/ PHT in milliseconds
PHT is calculated automatically by tracing the
deceleration slope of the E-wave of transmitral flow,
obtained with CWD echocardiography. In patients with
atrial fibrillation, PHT is best measured from a recording
with an adequate diastolic filling period or averaging
different cardiac cycles (Figs 2.41 and 2.42).
If the deceleration slope is bimodal (rapid initial
decline in early diastole followed by slower fall in mid-
diastole), the second (mid-diastolic) slope should be used.
Limitations of Pressure Half-Time in Mitral Stenosis
1. PHT depends not only on EOA but also net atrio
ventricular compliance. Reduced LV compliance (as in
aortic stenosis or aortic regurgitation) can shorten PHT
even in the presence of severe mitral stenosis (Fig. 2.43).
Net left-sided atrioventricular compliance can be
obtained by a formula using EOA by the continuity
equation and the mitral deceleration slope as shown in
Figure 2.43.
38 Section 1: Fundamentals of Echocardiography
Fig. 2.41: PHT estimation along thick line of modal velocity in a
continuous wave Doppler spectrum of transmitral flow. The system
calculates PHT and mitral valve area automatically. (PHT: Pressure
half-time).
Fig. 2.43: Marked disparity between PHT-derived mitral valve area
(2.1 cm2) versus that obtained by two- or three-dimensional planimetry
due to short PHT as a result of markedly reduced net left-sided atrio-
ventricular compliance. (PHT: Pressure half-time).
Sometimes in long-standing mitral stenosis, net left
atrioventricular compliance increases due to enlarged left
atrium, resulting in longer PHT even in the presence of
mild mitral stenosis5 (Fig. 2.44).
2. PHT can not be obtained accurately in the presence
of faster heart rates.
3. PHT method is not valid immediately after
percutaneous mitral valvotomy.
4. PHT method can not be applied to prosthetic mitral
valves.
Fig. 2.42: Mitral valve area by PHT method in the presence of
atrial fibrillation. Heart rate has minimal effect on PHT. PHT can be
obtained either from beats showing long diastole or averaging three
consecutive cardiac cycles in case the rate is controlled. (PHT: Pres-
sure half-time).
Fig. 2.44: Markedly prolonged pressure half-time in a patient with mild
mitral stenosis due to increased atrioventricular compliance.
Aortic Regurgitation Severity
The rate of deceleration of the diastolic regurgitant jet and
the derived PHT reflect both the degree of regurgitation
and the ventricular diastolic pressure. As the degree of
AR increases, the aortic diastolic pressure decreases and
the LV end-diastolic pressure increases. The late diastolic
jet velocity is thus reduced and the PHT, shortened.
A PHT of < 200 milliseconds is consistent with severe AR,
whereas a value of > 500 milliseconds suggests mild AR

Fig. 2.45: Mild aortic valve regurgitation with a pressure half-time of
650 milliseconds.
Fig. 2.47: Pulmonary regurgitation jet by continuous wave Doppler.
A pressure half-time of 80 milliseconds indicates severe pulmonary
regurgitation.
(Figs 2.45 and 2.46). These cut-off values can also be used
in case of prosthetic aortic valve regurgitation.22
The PHT is influenced by chamber compliance in
addition to chamber pressures. For a given severity of AR,
PHT is shortened with increasing left ventricular diastolic
pressure, vasodilator therapy and in patients with a dilated
compliant aorta, or increased in chronic AR. Thus, this
parameter serves only as a complementary finding for the
assessment of AR severity.
Pulmonary Regurgitation
Pulmonary PHT < 100 milliseconds is a good indicator of
hemodynamically significant regurgitation (Fig. 2.47). This
measure is highly reproducible and easily accessible.24
Hemodynamic Evaluation by Echo-Doppler Techniques 39
Fig. 2.46: Severe aortic valve regurgitation with pressure half-time of
100 milliseconds. Rapid deceleration in this case is due to acute aortic
regurgitation.
Tricuspid Stenosis
Although there are similarities between mitral and
tricuspid stenosis, the PHT method has not been as
extensively validated for the calculation of tricuspid valve
area. However, as a general rule, a PHT > 190 milliseconds
is frequently associated with significant stenosis.
LV dP/dt
This is an index that is used clinically to characterize the
contractile ability of the heart. It is believed that maximum
dP/dt is a reasonable index of the initial velocity of
myocardial contraction.24 The maximum left ventricular
dP/dt, which is normally about 1,600 mm Hg/s, tends to
be < 1,200 mm Hg/s in patients with disorders of the left
ventricular myocardium. It is obtained from CW signal of
MR. dP/dt is 32/time taken by velocity to decrease from
one m/s to 3 m/s (Fig. 2.48).
ESTIMATION OF PULMONARY ARTERY
PRESSURES AND PULMONARY
VASCULAR RESISTANCE
The tricuspid regurgitant jet is generally used to estimate
RV systolic pressure via the Bernoullis equation
(4v2, where v is the maximum velocity of the tricuspid
valve regurgitant jet2527 (Figs 2.49 and 2.50). An estimated
right atrial pressure (based on collapsibility of the inferior
vena cava best visualized in the subcostal window)
is added to the peak systolic pressure gradient of the
tricuspid regurgitant flow to obtain RV systolic pressure
40 Section 1: Fundamentals of Echocardiography
Fig. 2.48: Method to estimate LV dP/dt from MR signal. 32/T gives
dP/dt.
Fig. 2.50: Peak and mean pressure gradients obtained from the TR jet
by Bernoullis equation are added to estimated right atrial pressure to
get pulmonary artery systolic and mean pressures.
[which approximates pulmonary artery (PA) systolic
pressure in the absence of pulmonary valve stenosis and
RV outflow tract obstruction]. Although mean PAP can
be estimated by measuring the early diastolic velocity
of the pulmonary insufficiency jet, the correlation
with invasive measures is weak because of difficulty in
accurately visualizing the velocity regurgitant profile at the
pulmonary valve.
TR velocity reflects systolic pressure difference
between RV and RA (Figs 2.49 and 2.50).
4 peak TR velocity2 = RVSP RA
RVSP = 4 peak TR velocity2 + RA
Fig. 2.49: Estimating pulmonary pressures from TR and PR jets.
In the absence of RVOT obstruction, RVSP = PASP.
Doppler measurement by CW closely approximates
pressures measured by simultaneous RA and RV
pressure tracings.
Pulmonary Vascular Resistance
There is a close negative correlation between invasive
pulmonary vascular resistance (PVR) and VTI of the RV
outflow. Similarly, there is a positive correlation between
peak gradient of the TR velocity and the pulmonary
vascular resistance.28 A ratio of TR P/RVOTVTI is a
noninvasive index of PVR (in Wood units). Others have
suggested a ratio of TR velocitymax/RVOTVTI as a reliable
measure of PVR (divide by 10 to get approximate Wood
units, velocity in cm/s). The index has high sensitivity but
relatively modest specificity.29,30
Of the echocardiographic methods used to assess PVR,
equations using the ratio TR velocitymax/RVOTVTI remain
the simplest and the most widely used.
Key Points
This ratio does not work effectively at very high PVR.
Specificity is low.
Instead of RVOT VTI, LVOT VTI can be used with similar
predictability.
Another index of systolic PA pressure/(HR (RVOT VTI)
provides useful estimations of PVR.
An acceleration time (AT) of pulmonary flow Doppler
spectrum < 80 msec has been used as an index of high

Fig. 2.51: Estimation of pulmonary flow acceleration time (AT) and
AT/ejection time.
Fig. 2.53: Estimation of mean and diastolic pulmonary artery
pressures from PR jet velocity.
PVR (> 3 Wood units) (Fig. 2.51). The sensitivity and
specificity of PA AT and AT/ejection time for detecting
right ventricular systolic pressure > 2 SD above normal
are high.25,31
Right atrial pressure can be estimated either from
inferior vena cava size and its respiratory variation or
by right heart E/e.
Doppler assessment of PA pressures may be unfeasible
or may lead to overestimation or underestimation
of pulmonary pressures in up to 40% of individual
patients.
Correlations between the spectral Doppler measures
of right ventricular outflow systolic time intervals
and invasively measured pulmonary artery pressures
appear to be at least as strong as those between
TR velocities and invasively measured pulmonary
pressures.
Hemodynamic Evaluation by Echo-Doppler Techniques 41
Fig. 2.52: Mean pulmonary artery pressure is equal to 4 (peak PR
velocity)2.
Estimating Mean Pulmonary
Artery Pressure (Figs 2.52 and 2.53)
Mean gradient method (adding the right ventricular
right atrial mean systolic gradient to the right atrial
pressure)
Chemla equation (0.61 systolic PA pressure + 2 mm Hg)
Syyed equation (0.65 systolic PA pressure + 0.55 mm Hg)
Masuyama method (4 PR peak velocity2)
There are conflicting data about reliability of
correlation between RV systolic pressure estimated by
Doppler echocardiography and pulmonary pressures
measured via right heart catheterization. When PA
pressures are estimated via echocardiography, they more
often are higher than the pressures measured directly
by catheterization, and although it is clear that Doppler
echocardiography cannot be recommended at this time
for use as the gold standard for diagnosis of pulmonary
hypertension, it remains an excellent screening modality.
References
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ards Committee of the American Society of Echocardiogra-
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3. Pfitzner J. Poiseuille and his law. Anaesthesia. 1976;31(2):
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4. Baumann R, Schwaneberg R. Interpretation of Bernoullis
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42 Section 1: Fundamentals of Echocardiography
5. Flachskampf FA, Weyman AE, Guerrero JL, et al. Influence of
orifice geometry and flow rate on effective valve area: an in
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tic valve disease: a correction to the Bernoulli equation
based on velocity decay in the stenotic jet. J Heart Valve Dis.
2000;9(2):2918.
7. Baumgartner H, Schima H, Tulzer G, et al. Effect of stenosis
geometry on the Doppler-catheter gradient relation in vit-
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8. Niederberger J, Schima H, Maurer G, et al. Importance
of pressure recovery for the assessment of aortic steno-
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area, and direction of the stenotic jet in vitro. Circulation.
1996;94(8):193440.
9. Kadem L, Rieu R, Dumesnil JG, et al. Flow-dependent
changes in Doppler-derived aortic valve effective orifice
area are real and not due to artifact. J Am Coll Cardiol.
2006;47(1):1317.
10. VanAuker MD, Chandra M, Shirani J, et al. Jet eccentricity: a
misleading source of agreement between Doppler/catheter
pressure gradients in aortic stenosis. J Am Soc Echocardi-
ogr. 2001;14(9):85362.
11. Qur JP, Tribouilloy C, Enriquez-Sarano M. Vena contracta
width measurement: theoretic basis and usefulness in the
assessment of valvular regurgitation severity. Curr Cardiol
Rep. 2003;5(2):1105.
12. Hall SA, Brickner ME, Willett DL, et al. Assessment of mitral
regurgitation severity by Doppler color flow mapping of the
vena contracta. Circulation. 1997;95(3):63642.
13. Zoghbi WA, Enriquez-Sarano M, Foster E, et al.; American
Society of Echocardiography. Recommendations for evalu-
ation of the severity of native valvular regurgitation with
two-dimensional and Doppler echocardiography. J Am Soc
Echocardiogr. 2003;16(7):777802.
14. Garcia D, Pibarot P, Dumesnil JG, et al. Assessment of aor-
tic valve stenosis severity: A new index based on the energy
loss concept. Circulation. 2000;101(7):76571.
15. Hachicha Z, Dumesnil JG, Pibarot P. Usefulness of the valvu-
loarterial impedance to predict adverse outcome in asymp-
tomatic aortic stenosis. J Am Coll Cardiol. 2009;54(11):
100311.
16. Enriquez-Sarano M, Miller FA Jr, Hayes SN, et al. Effective
mitral regurgitant orifice area: clinical use and pitfalls of the
proximal isovelocity surface area method. J Am Coll Cardi-
ol. 1995;25(3):7039.
17. Utsonomiya T, Ogawa T, Doshi R, et al. Doppler color flow
proximal isovelocity surface area method for estimat-
ing volume flow rate: effects of orifice shape and machine
factors. J Am Coll Cardiol. 1991;17(5):110311.
18. Schwammenthal E, Chen C, Benning F, et al. Dynam-
ics of mitral regurgitant flow and orifice area. Physiologic
application of the proximal flow convergence method:
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90(1): 30722.
19. Zoghbi WA, Enriquez-Sarano M, Foster E, et al.; American
Society of Echocardiography. Recommendations for evalu-
ation of the severity of native valvular regurgitation with
two-dimensional and Doppler echocardiography. J Am Soc
Echocardiogr. 2003;16(7):777802.
20. Thomas JD, Weyman AE. Doppler mitral pressure half-
time: a clinical tool in search of theoretical justification.
J Am Coll Cardiol. 1987;10(4):9239.
21. Libanoff AJ, Rodbard S. Atrioventricular pressure half-time.
Measure of mitral valve orifice area. Circulation. 1968;38(1):
14450.
22. Lancellotti P, Tribouilloy C, Hagendorff A, et al.; European
Association of Echocardiography. European Association of
Echocardiography recommendations for the assessment
of valvular regurgitation. Part 1: aortic and pulmonary
regurgitation (native valve disease). Eur J Echocardiogr.
2010; 11(3):22344.
23. Baumgartner H, Hung J, Bermejo J, et al.; EAE/ASE. Echo-
cardiographic assessment of valve stenosis: EAE/ASE rec-
ommendations for clinical practice. Eur J Echocardiogr.
2009;10(1):125.
24. Chung N, Nishimura RA, Holmes DR Jr, Tajik AJ. Measure-
ment of left ventricular dp/dt by simultaneous Doppler
echocardiography and cardiac catheterization. J Am Soc
Echocardiogr. 1992;5(2):14752.
25. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echo-
cardiographic assessment of the right heart in adults: a
report from the American Society of Echocardiography en-
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a registered branch of the European Society of Cardiology,
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Echocardiogr. 2010;23(7):685713; quiz 786.
26. Currie PJ, Seward JB, Chan KL, et al. Continuous wave Dop-
pler determination of right ventricular pressure: a simulta-
neous Doppler-catheterization study in 127 patients. J Am
Coll Cardiol. 1985;6(4):7506.
27. Berger M, Haimowitz A, Van Tosh A, et al. Quantitative
assessment of pulmonary hypertension in patients with
tricuspid regurgitation using continuous wave Doppler
ultrasound. J Am Coll Cardiol. 1985;6(2):35965.
28. Abbas AE, Fortuin FD, Schiller NB, et al. A simple method
for noninvasive estimation of pulmonary vascular resist-
ance. J Am Coll Cardiol. 2003;41(6):10217.
29. Haddad F, Zamanian R, Beraud AS, et al. A novel non-in-
vasive method of estimating pulmonary vascular resistance
in patients with pulmonary arterial hypertension. J Am Soc
Echocardiogr. 2009;22(5):5239.
30. Nakatani S, Kyotani S, Kanzaki H, et al. Noninvasive estima-
tion of pulmonary vascular resistance by Doppler echocar-
diography in patients with pulmonary arterial hyperten-
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31. Tossavainen E, Sderberg S, Grnlund C, et al. Pulmonary
artery acceleration time in identifying pulmonary hyper-
tension patients with raised pulmonary vascular resistance.
Eur Heart J Cardiovasc Imaging. 2013;14(9):8907.
 SEction 2
Valvular Heart Disease

Chapters

Mitral Stenosis Tricuspid Valve

Mitral Regurgitation Pulmonary Valve
Aortic Valve Stenosis Evaluation of Prosthetic Heart Valves
Aortic Valve Regurgitation
 Chapter

3 Mitral Stenosis

Introduction
Mitral stenosis remains the commonest stenotic valvular
lesion in young people in the developing world. Most often,
the etiology is rheumatic heart disease, with rare instances
of congenital and acquired cases. Clinical presentation is
typical with symptoms developing early in the developing
countries and in later life in the Western World. Echo
cardiography remains the cornerstone of diagnosis and
choice for therapeutic intervention. Echocardiography
defines the pathological processes like leaflet thickening
and calcification, commissural fusion, chordal thickening
and fusion. Commissural fusion narrows the primary
orifice while the interchordal fusion reduces the secondary
orifice size. Of late, three-dimensional echocardiography Fig. 3.1: The mitral apparatus shown in relation to the left atrium,
(3DE) has contributed to the better understanding of the aortic annulus and the left ventricle.
echocardiographic anatomy. Most guidelines allocate
The mitral apparatus is composed of the left atrial
Class I status to echocardiography for detection of
wall, the annulus, the leaflets, the tendinous chords, the
mitral stenosis, assessment of its hemodynamic severity,
papillary muscles, and the left ventricular walls.13 The
detection of concomitant valve lesions and for definition
valve is located obliquely behind the aortic valve.
of valve morphology. Its use for guiding therapeutic
In its open state, the valvular leaflets are like a funnel
interventions is gaining ground.
extending from the hinge line at the atrioventricular
junction to the free margins. Tendinous cords attach
ANATOMY OF THE MITRAL VALVE the leaflets to two closely arranged groups of papillary
muscles. The interchordal spaces serve as important
Mitral valve is a bileaflet structure housed in a fibrous ring pathways for blood flow (Fig. 3.2). The mitral valve requires
(Fig. 3.1). It guards the inlet of the left ventricle (LV) and all its components, together with the adjacent atrial and
prevents regurgitation of blood into the left atrium (LA). ventricular musculature, to function properly.2
46 Section 2: Valvular Heart Disease

Fig. 3.2: Diagram depicting linearly placed mitral apparatus. Fig. 3.3: Diagram showing shape of the mitral annulus and its relation
to the aortic annulus.

Fig. 3.4: A three-dimensional echocardiographic (3DE) en face view of Fig. 3.5: A 3D cross-sectional view of the mitral valve circumference
the mitral valve showing a D-shaped annulus with scallops (arrows). showing leaflets and the commissures. Small white arrows within the
orifice indicate indentations separating the scallops.

Components of the Valve Apparatus The straight border of the annulus is posterior to
the aortic valve. Expansions of fibrous tissues at either
Leaflets
extreme of the area of continuity form the right and left
Annulus
fibrous trigones. The aortic valve is located between the
Chordae tendineae
ventricular septum and the mitral valve. The annulus
Papillary muscles
functions as a sphincter that contracts and reduces the
Interannular fibrosa
surface area of the valve during systole to ensure complete
Adjacent left atrial and ventricular musculature
closure of the leaflets.

Mitral Annulus Mitral Valve Leaflets

The mitral annulus is a fibrous ring that connects with the Mitral valve consists of a continuous veil inserted around
leaflets. It is not a continuous ring around the mitral orifice the circumference of the mitral orifice (Fig. 3.5). The free
and appears to be more D-shaped, rather than circular edges of the leaflets have several indentations. Two of
(Figs 3.3 and 3.4). these indentations, the anterolateral and posteromedial

Fig. 3.6: Diagram showing en face mitral leaflets with free margin,
rough zone and the clear zone.
commissures, divide the leaflets into anterior and
posterior. These commissures can be accurately identified
by the insertions of the commissural chords into the
leaflets.
Normally, the valvular leaflets are thin, pliable,
translucent and soft. Each leaflet has an atrial and a
ventricular surface. When viewed in profile, two zones can
be distinguished in the anterior leaflet and three zones
in the posterior leaflet according to the insertions of the
tendinous cords.3
In both leaflets, there is a clear zone that is devoid of
chordal attachments (Figs 3.6 and 3.7).
Nearer the free edge, the atrial surface is irregular
with nodular thickenings. This is also the thickest part,
corresponding with the line of closure and the free
margin. Tendinous chords attach to the underside of
this area described as the leaflets rough zone.
The basal zone that is found only in the posterior
leaflet is the proximal area that has insertions of basal
cords to its ventricular surface. Being distant from
the ventricular wall, the anterior leaflet does not have
attachments to basal cords.
In normal valve closure, the two leaflets meet each
other snugly with the rough zone and free edge riding
over each other.
The anterior leaflet is located posterior to the aortic
root and is also anchored to the aortic root, unlike
the posterior leaflet. The anterior leaflet is large and
semicircular in shape. It has a free edge with few or
no indentations. The zones on the anterior leaflet are
referred to as rough and clear zones, according to
Mitral Stenosis 47
Fig. 3.7: Transthoracic parasternal long-axis view in a subject with
mitral stenosis. Rough zone and clear zone are demarcated on the
anterior mitral leaflet due to leaflet thickening.
the chords insertion. These 2 zones are separated by
a prominent ridge on the atrial surface of the leaflet,
which is the line of the leaflet closure. The prominent
ridge is located approximately 1 cm from the free edge
of the anterior leaflet.
The posterior leaflet is the section of the mitral valve
that is located posterior to the commissural areas. It has
a wider attachment to the annulus than the anterior
leaflet. It is divided into 3 scallops by 2 indentations or
clefts. The middle scallop (P2) is larger than the other 2
(called medial and lateral or P3 and P1). The zones on
the posterior leaflets are referred to as rough, clear, and
basal zones, according to the chord insertion.
Chordae Tendineae
The chordae tendineae are small fibrous strings that
originate either from the apical portion of the papillary
muscles or directly from the ventricular wall and insert into
the valve leaflets or the muscle. These 2 types are called
true chordae tendineae and false chordae tendineae,
respectively. The leaflet chordae are the chordae that
insert into the anterior or posterior leaflets. Two types of
chordae tendineae are connected to both leaflets and the
third type to only the posterior leaflet.
Primary or rough zone chords insert into the distal
portion of the leaflets known as the rough zone.
Secondary or strut chords; the chordae that branch
before inserting into the leaflet.
Basal chordae are unique to the posterior leaflet; these
insert into the basal zone of the posterior leaflet, which
is located between the clear zone and the mitral valve
annulus.
48 Section 2: Valvular Heart Disease

Fig. 3.8: Rheumatic mitral stenosis with leaflet thickening and commi Fig. 3.9: Apical four-chamber view showing mitral leaflets directly
ssural fusion viewed from the left atrium. attached to the single papillary muscle (PM) with narrow orifice
(AML: Anterior mitral leaflet; PML: Posterior mitral leaflet; MC: Medial (arrows).
commissure; LC: Leteral commissure).

Pathoanatomy of Mitral Stenosis

The following are the common etiological factors of
mitral stenosis:48
About 99% cases of the mitral stenosis are postinfla
mmatory (rheumatic heart disease) as a sequelae of
poststreptococcal infection (Fig. 3.8).
Congenital (arcade type or parachute mitral valve)
(Fig. 3.9).
Infective endocarditis (due to large obstructive vegeta
tions).
Mitral annular calcification (Fig. 3.10).
Systemic lupus erythematosus.
Postmitral annuloplasty.
Degenerated bioprosthesis with calcification (Fig. 3.11).
Fig. 3.10: Reduced opening of the mitral orifice secondary to mitral Malignant carcinoid.
annular calcification. Rheumatoid arthritis.
Atrial myxoma.
Papillary Muscles and Left Ventricular Wall Ball thrombus (Fig. 3.12).
Gout.
These structures represent the muscular components of Malignant sarcoid.
the mitral apparatus. The papillary muscles normally arise Mucopolysacchridosis.
from the apex and middle third of the left ventricular wall. Anorexiogenic drug-induced valvulopathy.
The anterolateral papillary muscle is normally larger than Radiation-induced valvulopathy.
the posteromedial papillary muscle and is supplied by Typically, rheumatic mitral stenosis is characterized by:4
the left anterior descending artery or the left circumflex Fibrous thickening of the leaflets with shortening and
artery. The posteromedial papillary muscle is supplied retraction (Figs 3.13 and 3.14).
by the right coronary artery. At their bases, the muscles Commissural fusion, which narrows the primary
sometimes fuse or have bridges of muscular or fibrous orifice (Fig. 3.15).
continuity before attaching to the ventricular wall. Fusion Thickening and fusion of the chords reduces the
of papillary muscles results in parachute malformation secondary opening, which is accentuated by papillary
with potential for valvular stenosis. muscle scarring and fusion (Fig. 3.16).
 Mitral Stenosis 49

Fig. 3.11: Degenerated mitral bioprosthesis causing mitral valve Fig. 3.12: Apical four-chamber view showing ball thrombus in the left
obstruction shown in apical four-chamber view. atrium (arrows).

Fig. 3.13: A three-dimensional echocardiographic (3DE) four-chamber Fig. 3.14: Thickening of leaflets with narrow orifice and commissural
view showing thickening of the mitral leaflets in long-axis plane. fusion in cross-section by 3D echo.

Fig. 3.15: Biplane (long-axis and short-axis view) imaging showing Fig. 3.16: Parasternal long-axis view showing narrowed primary
leaflet thickening and commissural fusion causing narrowing of the orifice (yellow arrows) and secondary orifice due to chordal thickening
primary mitral orifice (arrow). and fusion (white arrows).
50 Section 2: Valvular Heart Disease
Fig. 3.17: Calcification involving anterior mitral leaflet and the medial
commissure (thick arrow).
Fig. 3.19: Pathological specimen opened longitudinally in a patient
with mitral stenosis.
Fig. 3.21: Fish-mouth deformity of the mitral orifice seen in 3DE
compared to the pathological specimen (right panel).
Fig. 3.18: Apical long-axis view showing tunnel-type mitral orifice
narrowing.
Fig. 3.20: Fused and thickened chords and leaflets in long-axis view.
(A: Anterior mitral leaflet; P: Posterior mitral leaflet).
Later on, there is dystrophic calcification of the leaflets,
which may extend into the commissures (Fig. 3.17).
Occasionally, there is tunnel-like mitral orifice narro
wing due to minor primary orifice narrowing and
predominant narrowing at insertion of chords to
papillary muscle heads (Fig. 3.18).
There is a close similarity between echocardiographic
appearance and pathological pictures (Figs 3.19 to 3.21).
Hemodynamics of Mitral Stenosis
Normal mitral valve area exceeds 4 cm2 and there is almost
no pressure gradient between the left atrium and the left
ventricle during diastole. Blood flows without much
resistance. As the valve area narrows to < 2cm2, transmitral
pan-diastolic gradient develops with rise in the left atrial
 Mitral Stenosis 51

Fig. 3.22: Depiction of pressure gradients in mitral stenosis Fig. 3.23: Parasternal long-axis view showing three different shapes
(left panel). Right panel shows the continuous-wave (CW) Doppler ve- of the mitral orifice in open position. Pressure gradients are the highest
locity pattern across the mitral valve from which the pressure gradient in the hole-in-diaphragm variety and least in funnel shape.
is obtained by the modified Bernoulli equation.

Table 3.1: Criteria for judging extent of mitral stenosis

Degree of Mitral Stenosis Mean Gradient Mitral Valve Area
Mild mitral stenosis < 5 mm Hg > 1.5 cm2
Moderate mitral stenosis 510 mm Hg 1.01.5 cm2
Severe mitral stenosis > 10 mm Hg < 1.0 cm2
Source: American Society of Echocardiography and European Asso-
ciation of Echocardiography, 2009

Hemodynamics of mitral stenosis are determined by

Fig. 3.24: Flow pattern across the mitral apparatus. Left atrium, mitral
valve and the left ventricle all affect the resistance to flow.
pressure (Fig. 3.22). Mitral stenosis becomes critical when
the valve area narrows < 1 cm2 and mean gradient rapidly
rises.9
Pulmonary hypertension may develop as a result of
(1) retrograde transmission of left atrial pressure, (2)
pulmonary arteriolar constriction, (3) interstitial edema
or (4) obliterative changes in the pulmonary vascular
bed (intimal hyperplasia and medial hypertrophy). As
pulmonary arterial pressure increases, right ventricular
dilation and tricuspid regurgitation may develop.
the following:
Complex anatomical and pathophysiologic features of
the valve apparatus (Fig. 3.23)
Properties of the left ventricle, atrium and pulmonary
vasculature (Fig. 3.24)
The valve and the cardiac chambers have a functional
reserve that becomes exhausted as the stenosis
worsens and/or the compensatory mechanisms of the
chambers fail.
Severity of mitral stenosis is judged by estimating
transmitral gradients and mitral valve area as shown in
Table 3.1.10
Assessment of Severity of Mitral Stenosis
Transmitral pressure gradient:
Estimation of the diastolic pressure gradient is
derived from the transmitral velocity flow curve, using
the simplified Bernoulli equation, that is, DP = 4V2
(Fig. 3.25).
52 Section 2: Valvular Heart Disease
Fig. 3.25: A CW Doppler interrogation of the mitral orifice from apical
view showing velocity profile.
Fig. 3.27: Near equal RR intervals in atrial fibrillation for measurement
of transmitral gradients.
This estimation is reliable, as shown by the good
correlation with invasive measurements.
Use of continuous wave Doppler is preferred to ensure
maximal velocities are recorded. When pulsed-wave
Doppler is used, the sample volume should be placed
at the level or just after leaflet tips.
Doppler gradient is assessed using the apical window
in most cases, as it allows for parallel alignment of the
insonifying beam and mitral inflow.
The ultrasound Doppler beam should be oriented to
minimize the intercept angle with mitral flow to avoid
underestimation of velocities.
Fig. 3.26: A CW Doppler interrogation of the mitral from the apical
window showing a peak gradient of 25 mm Hg while the mean gradient
is only 11 mm Hg.
Color Doppler in apical view is useful to identify
eccentric diastolic mitral jets that may be encountered
in cases of severe deformity of valvular and subvalvular
apparatus. In these cases, the Doppler beam is guided
by the highest flow velocity zone identified by color
Doppler.
Optimization of gain settings, beam orientation and
a good acoustic window are needed to obtain well-
defined contours of the Doppler flow. Maximal and
mean mitral gradients are calculated by integrated
software using the current echocardiographic systems.
Mean gradient is the valid hemodynamic data
for severity. Maximal gradient is of limited value
as it is derived from peak mitral velocity, which is
influenced by net left-sided atrioventricular compli
ance (Fig. 3.26).
Heart rate at which gradients are measured should
always be reported.
In patients with atrial fibrillation, mean gradient should
be calculated as the average of five cycles, with the least
variation of RR intervals and as close as possible to
normal heart rate (Fig. 3.27).
Mitral gradient, although reliably assessed by Doppler,
is not the best marker of the severity of mitral stenosis.
Transmitral pressure gradients are reliable but depend
upon:
Severity of mitral stenosis
Net left-sided atrio-ventricular compliance (mainly
affects peak gradients)
Flow (Fig. 3.28)
 Mitral Stenosis 53

Fig. 3.28: A patient with moderate mitral stenosis with mitral valve Fig. 3.29: Transmitral mean gradient of 15 mm Hg in presence of
area of 1.18 cm2 showing very low mean gradient of 2 mm Hg due moderate mitral regurgitation and mild mitral stenosis (valve area
to reduced flow. Sharp deceleration is due to reduced ventricular 2.0 cm2). Prolonged pressure half-time is due to increased left atrial
compliance. compliance.

Table 3.2: Comparison of various echo-Doppler methods for assessing mitral stenosis
Technique Method Remarks
Direct measurement Measurement in short-axis view Most reliable, operator dependent
Pressure half-time (P ) P = 0.29 Deceleration time Unreliable in conditions with elevated left
*MVA = 220 / P time ventricle end diastolic pressure
Continuity equation assumption blood flow through different In regurgitant lesions reliability decreases
valves is equal
MVA = D2 LVOT 0.785 TVI LVOT TVI MV
PISA (proximal isovelocity surface area) MVA = 2 3.14 r2 V1 Very reliable, operator dependent

Diastolic filling period and heart rate
Associated mitral regurgitation (Fig. 3.29).
The transmitral mean pressure gradient commonly
increases during exercise, regardless of the severity
of stenosis, in accordance with exercise duration and
exercise-induced changes in cardiac output.
Mitral Valve Area
Mitral valve area can be estimated by four different
techniques as shown in Table 3.2.1113
MVA Planimetry
Planimetry using two-dimensional (2D) echocardio
graphy of the mitral orifice has the advantage of
being a direct measurement of MVA and, unlike other
methods, does not involve any hypothesis regarding
flow conditions, cardiac chamber compliance or
associated valvular lesions.
Planimetry has been shown to have the best corre
lation with anatomical valve area. For these reasons,
planimetry is considered as the gold standard measure
ment of MVA.
Planimetry measurement is obtained by direct tracing
of the mitral orifice, including opened commissures on
a parasternal short-axis view (Fig. 3.30).
Careful scanning from the apex to the base of the LV is
required to ensure that the valve area is measured at
the leaflet tips.
The measurement plane should be perpendicular to
the mitral orifice, which has an elliptical shape.
Gain setting should be just sufficient to visualize the
whole contour of the mitral orifice. Excessive gain
setting may cause underestimation of valve area, in
particular when leaflet tips are dense or calcified.
Image magnification, using the zoom mode, is useful
to better delineate the contour of the mitral orifice
(Fig. 3.30).
54 Section 2: Valvular Heart Disease
Fig. 3.30: Planimetery of the mitral valve area in mid-diastole in short-
axis view.
Fig. 3.32: Real-time 3D-echo to obtain mitral valve area at the tip of
leaflets by slicing and dicing.
The optimal timing of the cardiac cycle to measure
planimetry is middiastole (some recommend early
diastole). This is best performed using the cine-loop
mode on a frozen image.12
It is recommended to perform several different measu
rements, in particular in patients with atrial fibrillation
and in those who have incomplete commissural fusion.
Another potential limitation is that the performance
of planimetry requires technical expertise. The meas
urement plane must be optimally positioned at
the mitral orifice. This can be done by 3D-guided
Fig. 3.31: Estimation of mitral valve area by biplane imaging. The cur-
sor can be aligned perpendicular to the narrowest orifice (right panel).
Fig. 3.33: A 3D transthoracic echo. Mitral valve orifice from the left
ventricular side. Mitral orifice can be sliced appropriately.
biplane imaging, which allows the cursor to be
placed at the tip of the leaflets in desired middiastole
(Fig. 3.31).
Real-time 3D echo imaging is useful in optimizing the
positioning of the measurement plane and, therefore,
improving reproducibility.14 It also improves the
accuracy of planimetry measurement when performed
by less-experienced echocardiographers (Fig. 3.32).
The 3D-transthoracic echocardiography (TTE) allows
a 3D acquisition of the entire mitral valve, which can
be sliced along any plane as desired (Fig. 3.33).

Fig. 3.34: Inappropriate short-axis view (right panel) for measurement
of mitral valve area when seen in relation to the shorter anteroposterior
leaflet separation.
Fig. 3.36: Bimodal deceleration slope in third beat of the transmitral
flow. Latter part (white) of the deceleration slope is used to estimate
mitral valve area.
The 3D echo and biplane imaging both have low
temporal resolution as compared to standard 2D echo
cardiography. If adequate time and multiple attempts
are made to obtain valve area, 2D echo still remains the
preferred method in experienced hands.
Planimetry using TTE (either 2D or 3D) is not feasible
in 510% of patients and 3D-transesophageal echo
cardiography (TEE) may represent an interesting
alternative.
It is recommended to measure the distance between
the anterior and posterior mitral leaflets in the LV
parasternal long-axis view in its narrowest area. When
viewing the LV short-axis, planimetry of the mitral valve
Mitral Stenosis 55
Fig. 3.35: Measurement of PHT and hence mitral valve area in
multiple beats in presence of atrial fibrillation. The area varies from
0.8 to 1.0 cm2.
is done making sure that the level of measurement
is the level that has the smallest distance between
anterior and posterior leaflets, which is closest to the
smallest distance obtained from the LV parasternal
long-axis view, and thus serving as the narrowest area
possible by planimetry of the mitral orifice (Fig. 3.34).
Pressure Half-time Method for MVA
Pressure half-time (PHT) is the time interval in
milliseconds between the maximum mitral gradient in
early diastole and the time point where the gradient is
half the maximum initial value.15
The decline of the velocity of diastolic transmitral
blood flow is inversely proportional to valve area (cm2),
and MVA is derived using the empirical formula:15
MVA = 220/PHT
PHT is obtained by tracing the deceleration slope of
the E-wave on Doppler spectral display of transmitral
flow and valve area is automatically calculated by the
integrated software of currently used echo machines
(Fig. 3.35).
Quality of the contour of the Doppler flow, in particular
the deceleration slope, is important. The deceleration
slope is sometimes bimodal, the decline of mitral
flow velocity being more rapid in early diastole than
during the following part of the E-wave. In these cases,
it is recommended that the deceleration slope in
middiastole rather than the early deceleration slope be
traced (Fig. 3.36).
56 Section 2: Valvular Heart Disease
Fig. 3.37: Avoid PHT measurement in short cardiac cycles.
Fig. 3.39: Short PHT and higher mitral valve area in presence of
combined aortic valve disease.18
In the rare patients with a concave shape of the tracing,
PHT measurement may not be feasible.
In patients with atrial fibrillation, tracing should
avoid mitral flow from short diastoles and average
different cardiac cycles (Fig. 3.37).
The PHT method is widely used because it is easy to
perform, but its limitations should be kept in mind
since different factors influence the relationship
between PHT and MVA (Fig. 3.38). Left-sided net
atrio-ventricular compliance (NAVC) is the most
significant factor.1618
PHT effective orifice area
NAVC = 11.6 (peak transmitral gradient)
Fig. 3.38: Mid mitral stenosis with mitral valve area of 1.7 cm2 and
mean gradient of 3.6 mm Hg but PHT of 260 msec.
Concomitant aortic valve disease can reduce left
atrioventricular compliance and PHT becomes shorter
(Fig. 3.39).
Net atrioventricular compliance, derived by Doppler
echocardiography, has been shown to be an important
physiological determinant of pulmonary hypertension
in patients with mitral stenosis.
Routine measurement of net atrioventricular
compliance in all patients with mitral stenosis is
recommended because, in addition to clarifying the
inaccuracies of PHT in calculation of area out of the
46 mL/mm Hg range, it is also a predictor of the left
atrial and pulmonary pressures, exercise capacity and
the need for mitral valve replacement.
Impaired left ventricular diastolic function is a likely
explanation of the lower reliability of PHT to assess
mitral valve area in the elderly.
Continuity Equation for
Calculation of Mitral Valve Area
Continuity equation is not recommended for routine
practice in obtaining mitral valve area. It has many
assumptions, which make it error prone.12 It is also not
reliable in presence of atrial fibrillation, mitral or aortic
regurgitation. Mitral valve area by the continuity equation
can be obtained by dividing the Doppler stroke volume
(from either outflow tract) with the mitral velocity-time
integral (Fig. 3.40).

Fig. 3.40: Error introduced by measurement of the left ventricular
outflow tract (LVOT) in calculation of the mitral valve area by the
continuity equation. LVOT is oval with maximum diameter of 23 mm
and minimum of 17 mm. Calculated area is 0.6 cm2 when LVOT of
17 mm is used, which significantly underestimates the valve area
(0.93 cm2). Estimate of stroke volume is the major factor.
Fig. 3.42: Aliasing velocity of 30 cm/s in transesophageal echocardio-
gram (TEE) long-axis view showing adequate PISA (arrows).
Proximal Isovelocity
Surface Area Method (PISA)
The proximal isovelocity surface area (PISA) method is
based on the continuity principle and assumes that blood
flow converging toward a flat orifice forms hemispheric
isovelocity shells. It has been shown that the PISA method
is accurate and reproducible. This method is useful in
mitral stenosis since the proximal convergence method
can be easily visualized and it may be the only method
available in certain situations (Fig. 3.41).
Mitral Stenosis 57
Fig. 3.41: Arrows point to proximal isovelocity surface area (PISA) in
the left atrium in this apical four-chamber view.
Method
Measure the radius (R) of the hemisphere from the first
aliasing velocity in the left atrium up to the beginning
of narrowest portion of the color jet within the valve in
zoomed mode.
Use an appropriate aliasing velocity (by baseline shift),
which clearly shows hemispheric shape of the PISA.
Estimate the mitral volume flow rate by multiplying
the area of the hemisphere (6.28 R2) with aliasing
velocity. This further needs to be corrected for mitral
leaflet angles/180.
Divide the mitral flow rate thus obtained by the
continuous wave (CW) Doppler peak transmitral
velocity to obtain mitral valve area.
Most systems have in-built capability to obtain these
data.
The PISA method provides an assessment of the
physiologic or effective orifice area at the vena cont
racta, as opposed to the anatomic orifice area measured
by planimetry, which is generally somewhat larger.
Use of lower aliasing velocity results in inadequate
flow convergence shape, ambiguous surface contour
and therefore difficulty in getting a reliable radius
(Fig. 3.42).
One limitation for a wider use of the proximal
isovelocity surface area method (PISA) for the
evaluation of the mitral valve area (MVA) in patients
with mitral stenosis (MS) is the requirement of an angle
correction factor (angle a between the mitral leaflets),
which cannot be obtained using the machines built-in
software and requires a manual measurement.19
58 Section 2: Valvular Heart Disease
Fig. 3.43: Width of vena contracta in two-chamber and four-chamber
views. An average width < 11 mm suggests severe stenosis.
The angle formed by the mitral leaflet only slightly
changes in between patients and use of a fixed angle
value of 100 provides an accurate estimation of the
valve area by the PISA method in patients with mitral
stenosis.19 This simplification would facilitate and
extend the use of the PISA as an additional method for
the assessment of mitral stenosis severity in routine
practice.
The use of color M-mode improves its accuracy,
enabling simultaneous measurement of flow and
velocity.
PISA method has the advantage of being applicable
even in presence of mitral regurgitation.
Miscellaneous Parameters of
Severity of Mitral Stenosis
Mitral valve resistance (ratio of mean gradient/
diastolic flow rate) has been proposed as a flow-indep
endent method of assessing severity. It correlates with
the degree of pulmonary hypertension. However it
has limitations of assessing stroke volume and is not
routinely used in clinical practice.
Estimation of pulmonary pressures (from tricuspid
and pulmonary regurgitation jets) is an indirect clue of
severity or rather the consequence of mitral stenosis.
Shortest distance between the tips of the mitral leaflets
in early diastole in parasternal long-axis view has been
found to correlate with severity of mitral stenosis. A
distance < 10 mm indicates severe stenosis.
Fig. 3.44: Short-axis view showing bilateral commissural fusion
(arrows).
Width of vena contracta in two planes, if < 11 mm,
suggests severe mitral stenosis. From the vena
contracta A (width) and vena contracta B, effective
orifice area can be estimated as p/4 A B (Fig. 3.43).
Morphology of the Mitral Valve
Apparatus in Mitral Stenosis
Evaluation of morphology is a major component of
echocardiographic assessment of mitral stenosis because
of its implications for the type of therapeutic intervention.
Commissural fusion is assessed from the short-axis
parasternal view used for planimetry (Fig. 3.44). Commi
ssural anatomy may be difficult to assess, in particular in
patients with severe valve deformity. Commissures are
better visualized using real-time 3DE 20 (Fig. 3.45).
Commissural fusion is an important feature to
distinguish rheumatic from degenerative MS, to check the
consistency of severity measurements and to study the
effects of therapeutic interventions (Fig. 3.46).
Complete fusion of both commissures generally
indicates severe stenosis. However, the lack of commiss
uralfusion does not exclude significant stenosis in
degenerative aetiology or even rheumatic one, where
restenosis after previous valvotomy may be due to valve
rigidity despite persistent commissural opening.
Echocardiographic examination is used to assess
leaflet thickening and mobility in long-axis parasternal
view (Figs 3.47 to 3.49).
Chordal shortening and thickening are assessed using
long-axis parasternal and apical views (Figs 3.50 and 3.51).
 Mitral Stenosis 59

Fig. 3.45: Asymmetric commissural fusion with dominant medial Fig. 3.46: Splitting of medial commissure with no effect on lateral
commissure fusion. commissure following balloon mitral valvotomy.

Fig. 3.47: Mild leaflet thickening only the tips of the leaflets. Fig. 3.48: Moderate thickening of the leaflets shown in parasternal
long-axis view.

Fig. 3.49: Severe thickening of the leaflets in parasternal long-axis Fig. 3.50: Moderate degree of chordal thickening and shortening.
view. Arrows point to commissures which have no calcium.
60 Section 2: Valvular Heart Disease
Fig. 3.51: Severe chordal thickening and fusion (arrow).
Fig. 3.53: Scoring commissural calcification. Each commissure can
be scored 0-2 depending upon the amount of calcium
Increased echo brightness suggests calcification. The
examination should mention the homogeneity of thick
ening or calcification in short axis (Fig. 3.52).
Extent of mitral valve deformity is expressed in scores
combining different components of mitral apparatus
or using an overall assessment of valve morphology.2122
Scores have been developed, in particular taking into
account the location of valve thickening or calcification
in relation to commissures (Fig. 3.53). No score has been
definitely proven to be superior to another and all have a
limited predictive value with regard to prognosis.
Fig. 3.52: Inhomogeneity and significant (2/2) calcification of the me-
dial commissure (arrow).
Fig. 3.54: Dense spontaneous contrast in the left atrium seen in four-
chamber view.
Concomitant Pathology in Mitral Stenosis
The quantitation of left atrial enlargement helps in
prognostication and deciding therapeutic options.
Left atrial spontaneous contrast, as assessed by TEE,
is a predictor of the thromboembolic risk (Fig. 3.54).
Spontaneous contrast can be graded and may help in
deciding need for anticoagulation.
Transoesophageal echocardiography has a much
higher sensitivity than the transthoracic approach
to diagnose left atrial thrombus, in particular when
 Mitral Stenosis 61

Fig. 3.55: Transthoracic short-axis view demonstrating thrombus in the left atrial appendage (arrow).

A B
Figs 3.56A and B: (A) Transesophageal short-axis view showing large left atrial appendage thrombus (arrows); (B) Combined mitral stenosis
with significant mitral regurgitation as evident from vena contracta of 6 mm width and appreciable PISA (arrows).

located in the left atrial appendage (Figs 3.55 and 3.56).

Associated mitral regurgitation has important
implications for the choice of therapy. Quantitation
should combine semiquantitative and quantitative
measurements. More than mild regurgitation is a
relative contraindication for mitral commissurotomy
(Figs 3.56A and B).
The mechanism of rheumatic mitral regurgitation is
restricted leaflet mobility and retraction. After balloon
mitral commissurotomy, leaflet tear is a frequent cause
of regurgitation (Fig. 3.57).
Mechanism of mitral regurgitation is important in
patients presenting with moderate-to-severe regur
gitation after balloon mitral commissurotomy. A
Fig. 3.57: Apical view showing tear of anterior mitral leaflet (arrow, left traumatic mechanism is an indication to consider
panel) causing severe eccentric mitral regurgitation (right panel).
surgery more frequently than in case of central and/or
62 Section 2: Valvular Heart Disease
Fig. 3.58: Apical view showing combined mitral and tricuspid valve
stenosis.
commissural regurgitation due to valve stiffness
without leaflet tear.
The presence of mitral regurgitation does not alter the
validity of the quantitation of mitral stenosis, except for
the continuity equation valve area.
Other valve diseases are frequently associated with
rheumatic mitral stenosis. The severity of aortic
stenosis may be underestimated because of low flow
(decreased stroke volume). In cases of severe aortic
regurgitation, PHT method underestimates severity of
mitral stenosis.
The analysis of the tricuspid valve should look for
signs of involvement of the rheumatic process. More
frequently, associated tricuspid disease is functional
tricuspid regurgitation although occasionally domi
nant tricuspid valve stenosis may be seen (Fig. 3.58).
A diameter of the tricuspid annulus > 40 mm seems
to be more reliable than quantitation of regurgitation to
predict the risk of severe tricuspid regurgitation and need
for tricuspid annuloplasty.
In summary, mitral stenosis is studied by analysis
of its morphology and commissural calcification, valve
area planimetry and pressure half-time. Transesophageal
echocardiography is employed to rule out left atrial
thrombi before balloon mitral commissurotomy. The 3DE
bridges the gap between novice and expert with regard
to accurately assessing severity. From a standpoint of
therapeutic intervention, mitral valve morphology can
be classified into three groups: flexible valve and mild
subvalvular disease (chordae 10 mm long; Group I),
flexible valve and extensive subvalvular disease (chordae
< 10 mm long; Group II) and calcified valves (Group III).
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 Chapter

4 Mitral Regurgitation

Introduction
Mitral valve regurgitation (MR) is the second commonest
valvular lesion. Incidence is on the rise due to age-related
degenerative valvulopathy and functional regurgitation
secondary to ischemic heart disease and heart failure.
MR could be as a result of structural valve pathology or
due to involvement of the support system of the mitral
valve (MV) complex. Echocardiography plays a pivotal
role in diagnosis, assessing severity and mechanism of
regurgitation, choice of therapy and follow-up of these
patients. Clinical examination misses more than 50% cases
of MR, and echocardiography remains the only bedside
modality for its accurate diagnosis.
Fig. 4.1: Components of mitral valve (MV) apparatus.
FUNCTIONAL MORPHOLOGY OF MR
MV apparatus consists of (Fig. 4.1): Valvular Leaflets
Two leaflets Moving units of the atrioventricular valves are described
Annulus as leaflets. The normal MV has two leaflets (each with
Tendinous chords a thickness about 1 mm) that are attached at their bases
Papillary muscles to the fibromuscular ring and by their free edges to the
Left atrial (LA) musculature adjacent to the valve ring subvalvular apparatus.14 The posterior leaflet has a
Left ventricular (LV) musculature adjoining the origin quadrangular shape and is attached to approximately two
of papillary muscles. thirds of the annular circumference; the anterior leaflet
Complete closure (coaptation) and correct apposition attaches to the remaining one-third (Fig. 4.2).
(symmetrical overlap, usually a minimum of 45 mm) of The posterior leaflet typically has two well-defined
both leaflets is essential in preventing regurgitation. indentations that divide the leaflet into three individual
 Mitral Regurgitation 65

A B
Figs 4.2A and B: Attachment of mitral leaflets to the oval or D-shaped fibrous ring at the peripheri with visible indentations and scallops. The left
panel is a diagram while the right one is a pathological specimen.

Fig. 4.3: Relationship of lateral leaflets to the LA appendage and Fig. 4.4: Diagram showing leaflet coaptation and zone of apposition
anterolateral commissure. (arrow).

scallops identified as P1, P2 and P3.5 The P1 scallop
corresponds to the external, anterolateral portion of the
posterior leaflet, close to the anterior commissure and the
left atrium appendage (Fig. 4.3). The P2 scallop is in the
middle and more developed. The P3 scallop is internal, close
to the posterior commissure and the tricuspid annulus.
The anterior leaflet has a semicircular shape and is in
continuity with the noncoronary cusp of the aortic valve,
referred to as the intervalvular fibrosa. The free edge
of the anterior leaflet is usually continuous, without
indentations. It is artificially divided into three portions
A1, A2 and A3, corresponding to the posterior scallops
P1, P2 and P3.
The commissures define a distinct area where the
anterior and posterior leaflets come together at their
insertion into the annulus (Fig. 4.3).
Sometimes, the commissures exist as well-defined
leaflet segments (commissural scallops), but more often
this area is a subtle region. When the MV is closed, the
line of contact between the leaflets is termed coaptation
line and the region of leaflet overlap is called the zone of
apposition (Fig. 4.4).
66 Section 2: Valvular Heart Disease
Fig. 4.5: Saddle-shaped mitral annulus and systolic contraction (left
lower panel) shown graphically.
Typical length of anterior mitral leaflet is 25 mm and
that of posterior leaflet is about 14 mm.
Mitral Annulus
The mitral annulus constitutes the anatomical junction
between the LV and the LA, and serves as insertion site
for the leaflet tissue. It is oval and saddle shaped. The
anterior portion of the mitral annulus is attached to the
fibrous trigones and is generally more developed than the
posterior annulus. Both parts of the annulus may dilate in
pathologic conditions. The anteriorposterior diameter
can be measured using real-time three-dimensional (3D)
or by conventional two-dimensional (2D) parasternal
long-axis view. The diameter is compared with the length
of the anterior leaflet measured in diastole. Annular
dilatation is present when the ratio annulus/anterior
leaflet is more than 1.3 or when the diameter is more than
35 mm. The presence and extent of annular calcification
is an important parameter. The normal motion and
contraction of the mitral annulus also contributes to
maintaining valve competence. The normal contraction of
the mitral annulus (decrease in annular area in systole) is
25% (Fig. 4.5).
The annulus not only serves as a fulcrum for the
leaflets but also exhibits sphincteric contraction in systole
that decreases the size of the orifice and prevents mitral
regurgitation.
Chordae Tendineae
There are three sets of chordae arising from the papillary
muscles. They are classified according to their site of
Fig. 4.6: Graphic display of posterior mitral leaflet and three types of
chords.
insertion between the free margin and the base of leaflets
(Fig. 4.6).
Marginal chordae (primary chordae) are inserted on
the free margin of the leaflets and function to prevent
prolapse of the leaflet margin.
Intermediate chordae (secondary chordae) insert
on the ventricular surface of the leaflets and relieve
valvular tissue of excess tension. Often two large
secondary or strut chordae can be individualized.
They may be important in preserving ventricular shape
and function.
Basal chordae (tertiary chordae) are limited to the
posterior leaflet and connect the leaflet base and mitral
annulus to the papillary muscle.
Additional commissural chordae arise from each
papillary muscle. Rupture, calcification, fusion or redun
dancy of the chordae can lead to regurgitation.
Mitral regurgitation due to chordal abnormalities also
results from chordae that are abnormally long, abnormally
short, ectopically inserted or ruptured.
Normal MV Competence
MV competence in normal hearts is achieved by:
Systolic reduction in the LV volume (closing force
acting on the leaflets)
LV length shortening letting the leaflets float back
(about 15%)
Interpapillary muscle distance shortening bringing the
leaflets close to each other
Annular diameter shortening in systole
Longitudinal shortening of the papillary muscles
(about 25%)

Fig. 4.7: Orifice of regurgitation due to loss of leaflet tissue in antero-
lateral commissure.
Fig. 4.9: Perforation of the anterior mitral leaflet as the cause of MR
(type I): TEE view.
At end-systole, the anterior MV leaflet is 20% shorter
due to folding at the coaptation point.
Functional Types of MR
Carpentiers functional classification describes leaflet
motion in relation to the mitral annular plane.6
Type 1: Describes normal leaflet motion. Mitral regur
gitation is due to either perforation of the leaflet, such as
trauma or endocarditis, or annular dilatation, usually the
result of left ventricular disease (Figs 4.7 to 4.9).
Type 2: Describes excessive leaflet motion above
the annular plane into the left atrium and is a result of
Mitral Regurgitation 67
Fig. 4.8: Type I mitral valve regurgitation (MR; arrow shows regur-
gitant orifice) due to annular dilatation. Note the chords are thin and
leaflets are normal.
Fig. 4.10: Flail anterior mitral leaflet coapting above the mitral annular
plane with regurgitant orifice (Type II MR).
leaflet prolapse usually the result of degenerative disease
(Fig. 4.10).
Type 3: Describes leaflet restriction and is categorized
into two types; Type 3a, where the restriction is throughout
the cardiac cycle, that is, in systole and diastole (usually
the result of rheumatic valve disease), and Type 3b,
where the leaflet restriction is seen in systole alone
(Fig. 4.11 to 4.14).
Etiology of MR
MR can be primary, wherein valve leaflets are primarily
involved, or secondary in which the valve leaflets are
68 Section 2: Valvular Heart Disease

Fig. 4.11: Apical four-chamber view. Tethering of both leaflets with MR Fig. 4.12: TEE view showing systolic tethering of mitral leaflets below
on color Doppler during systole. Both leaflets coapt below the plane of the annular plane (Type IIIb MR).
the annulus (Type IIIb MR).

Fig. 4.13: Rheumatic MV showing pan-cyclic restriction of the leaflets Fig. 4.14: Type IIIa MR in rheumatic MV disease. Both leaflets are
and the mechanism of Type IIIa MR (arrows) thickened and retracted.

apparently normal. Secondary MR is also called the fibroelastic degeneration, myxomatous valvulopathy and
functional MR. so forth.
Degenerative (60%) Changes in the valves include thickening and stretching
Rheumatic (postinflammatory) (due to disruption of the structural collagen core) of the
Functional and ischemic MR (25%) leaflet tissue. The abnormal leaflets can become twice as
Congenital abnormalities (parachute MV, cleft or hole) extensible (Fig. 4.15).
Infective endocarditis A spectrum from a single segment of one leaflet
Miscellaneous (hypertrophic cardiomyopathy, endo through to all segments of both leaflets may be involved.
myocardial fibrosis, SLE, etc.) The former has been coined fibroelastic deficiency
by Carpentier (Fig. 4.16), whereas the latter describes
Degenerative MV Disease Barlows disease with myxomatous-type leaflets .7
The term degenerative covers a range of abnormalities In fibroelastic deficiency, often the prolapsing segment
and includes Marfans and Ehlers-Danlos syndromes, is relatively normal in appearance; the prolapse being

Fig. 4.15: Elongated MV leaflets in fibroelastic degeneration.
Fig. 4.17: Ruptured free margin chord (arrow) in long axis view.
the result of focal chordal elongation with or without
rupture (Fig. 4.17). At the other end of the spectrum, the
widespread involvement of the majority of the segments
may be observed. This process affects the subvalvular
structures with chordal thinning and elongation. This
results in the affected leaflet segments ballooning into the
left atrium (Figs 4.18 to 4.22).
Features of fibroelastic deficiency are:
Elongated leaflets
Long and thin chords
Rupture of chords
Annular dilatation
The posterior leaflet is the most frequent area to
develop thickening and become flail. Mechanical stress
on the degenerative chords may lead to rupture. If this
Mitral Regurgitation 69
Fig. 4.16: Flail A2 segment due to fibroelastic deficiency causing se-
vere MR (arrows).
involves the primary chords, there may be total eversion of
the leaflet free edge into the left atrium. This is described
as a flail segment and is inevitably associated with
severe regurgitation (Fig. 4.23). Flail segment needs to be
differentiated from the prolapse wherein there is prot
rusion of the body of the segment with tip lagging behind
although coaptation reaches superior to the annular plane.
The same disease process can result in focal regions of
thickening with retraction and restriction.
A striking feature of the patient with Barlows disease
(billowing MV) is the size of the valve apparatus:
The leaflets are usually thick, bulky, elongated and
distended
The chords are thickened and elongated, often mesh-
like in nature
Annulus is dilated and enlarged (Fig. 4.24).
Herein, the body of the leaflet scallops protrude into
the left atrium with coaptation point staying behind at the
annular plane.
Mitral Valve Prolapse (MVP)
MVP is defined as failure of leaflet coaptation due to
partial or complete systolic displacement of mitral leaflets
beyond the annulus in the left atrium(> 2 mm). It includes
Barlows syndrome as well as floppy MV due to fibroelastic
deficiency and other connective tissure disorders.8
The prolapse is often multisegmental, and involves
both leaflets in up to 40% of patients (Figs 4.25 and 4.26).
Prolapse needs to be assessed in parasternal long-axis
view and not in apical views wherein the annulus is saddle
shaped.
70 Section 2: Valvular Heart Disease

A B
Figs 4.18A and B: Prolapse of flail A2 segment with tip in the left atrium.

Fig. 4.19: Apical four-chamber view displaying elongated chords and Fig. 4.20: Isolated single segment (A2) thickening in fibroelastic defi-
flail A2 segment (arrow). ciency shown in diastole.

Fig. 4.21: Redundant chords seen during diastole. Fig. 4.22: Unsupported A2 segment in short axis in diastole (arrow).
Lack of chordal support allows it float back in closed position.

Fig. 4.23: Schematic diagram showing flail A2 due to rupture of
primary chord.
Fig. 4.25: Multisegment prolapse of MV in TEE view.
Fig. 4.27: Rheumatic MV showing thickening and restriction of the
leaflets. Note tethering of the posterior leaflet and short chords in
apical four-chamber view.
Mitral Regurgitation 71
Fig. 4.24: Bulky leaflets (scallops) of the MV in Barlows syndrome.
Fig. 4.26: The MR due to incomplete coaptation between P1 and A2
due to myxomatous valve prolapse in TEE commissural view.
Rheumatic MR
In the developing world, rheumatic MR is one of the
commonest lesions in the young people. The mechanism
of MR is deficiency of the leaflets due to thickening and
restriction, causing malcoptation (Figs 4.27 and 4.28). In
addition, chordal thickening and shortening along with
papillary muscle scarring may cause pan-cyclic tethering
especially of the posterior leaflet. Commissural calcium
can also prevent coaptation.
Functional and Ischemic MR
Functional mitral regurgitation is defined as a disorder
of regional or global left ventricular remodeling in which
anatomically normal leaflets fail to coapt adequately.9 The
abnormal closure pattern is one of apical tethering of one
or both leaflets (Figs 4.29 to 4.31).
72 Section 2: Valvular Heart Disease
Fig. 4.28: Rheumatic MR in apical view. Note thickened and retracted
leaflets with no displacement of coaptation point.
Fig. 4.30: Schematic diagram showing functional MR due to apical
tethering of leaflets.
Pathological tethering and concomitant regurgitation
occur when an imbalance is present between closing and
tethering forces (Figs 4.32 and 4.33).
Tethering forces are increased when increased traction
on the leaflets exists through a combination of annular
dilation, infarct expansion and spherical remodeling of
the left ventricle.
Closure forces (due to left ventricular contraction) are
reduced as a consequence of left ventricular systolic
dysfunction.
Functional mitral regurgitation may paradoxically
decrease in midsystole10 or even disappear though
transmitral pressure is at its peak because of greater
closing force (Figs 4.34 and 4.35).
Fig. 4.29: Graphic depiction of the apical long axis view showing
normal coaptation of both leaflets at the plane of mitral annulus.
Fig. 4.31: Graphic depiction of normal coaptation (upper panel) and
malcoaptation causing effective regurgitant orifice (lower panel).
Tethering of leaflets pulls down the coaptation point
into the LV cavity and away from the annular plane and
causes MV deformity. Mitral valve deformation can be
assessed by the tenting area and the tenting height from
the parasternal long-axis view at midsystole.11
The degree of tethering and hence degree of MR is
gauged by:
Tenting height (distance between the midmitral
annulus point to coaptation point). Tenting height of
10 mm indicates severe MR.
Tenting length (distance between the tip of the papillary
muscle to the base or hinge-point of opposite leaflet)
Tenting area. Tenting area has good correlation with
effective regurgitant orifice area (Figs 4.36 and 4.37).
 Mitral Regurgitation 73

Fig. 4.32: A depiction of tethering and closing forces acting upon Fig. 4.33: TEE long-axis view showing sea-gull deformity of the anteri-
the leaflets. (AML: Anterior mitral leaflet; PML: Posterior mitral leaflet; or mitral leaflet due to tethering: effaced and tethered posterior leaflet.
PM: Papillary muscle).

Fig. 4.34: A CW Doppler spectrum of functional MR showing Fig. 4.35: A CW Doppler spectrum of functional MR. Arrows point to
decreased density of the envelope during midsystole. sudden cutoff of MR signal due to closing forces overpowering tether-
ing forces in midsystole.

Fig. 4.36: Schematic depiction of the tenting area. Fig. 4.37: Parasternal long-axis view showing tenting length (arrow in
direction) and tenting area in functional MR.
74 Section 2: Valvular Heart Disease

Figs 4.38A and B: (A) Graphic depiction of three different types of AML tethering and their relationship to success of mitral ring annuloplasty;
(B) Schematic diagram showing mitral regurgitation during systole.

Hemodynamics of MR
As systole begins, the LV volume decreases, mitral annulus
contracts, interpapillary muscle distance decreases and
the chords stretch as the mitral leaflets coapt at the annular
plane. Normally, hardly any blood regurgitates into the
left atrium during systole. Mitral regurgitation is said to be
present when a part of LV stroke volume is received by the
left atrium through a regurgitant orifice (Fig. 4.38B).
Total amount of blood flow that goes to the LA per
beat is called regurgitant volume.13 Regurgitant volume
normalized to total LV stroke volume is regurgitation
fraction (Fig. 39).
The orifice through which regurgitant volume enters
Fig. 4.39: Regurgitant fraction is ratio of mitral stroke volume-aortic
the LA is called effective regurgitant orifice area.14 There
stroke volume/mitral stroke volume. can be more than one such orifice of different shape and
also of dynamic nature. Mitral valve repair may also result
A tenting area 2.5 cm2 suggests presence of severe in two orifices that leak to some extent. All these parameters
functional MR. are used to judge severity of MR.15 Total LV stroke volume
Indicators of severity of functional MR are: can be obtained by 2D or 3D echocardiographic volumetry.
LA diameter Forward stroke volume can be obtained from LV outflow
Tenting length tract flow using the formula of volume = area velocity
Tenting height or depth time integral. Following Tables 4.1 and 4.2 provide
Tenting area criteria for volumetric severity of MR:
Asynchronous contraction of the mitral annulus (as in Points to Remember:
left bundle branch block) The regurgitant volume (RV) depends upon the
Loading conditions regurgitant orifice and the systolic pressure gradient
Type of anterior mitral leaflet (AML) tethering, which between LV and LA.
has been categorized into three types,12 predicts success of The observed degree of MR depends on hemodynamic
mitral annuloplasty (Fig. 4.38A). conditions at the time of examination.16 Any increase

Table 4.1: Regurgitant volume and regurgitant orifice area to
assess severity of organic mitral valve regurgitation (MR)
Quantification of Organic MR based upon regurgitant volume
(RV)
Absent: RV 0
Mild: RV 30 mL (ERO 20 mm ) 2
Moderate: RV 30-59 (ERO 21-39 mm ) 2
Severe: RV 60 mL (ERO 4m2)
Fig. 4.40: Reverse Sabre-shaped CW Doppler spectrum of acute
MR. Rapid rise of LA pressure cuts-off the late systolic signal due to
noncompliant atrium causing a large V wave (arrow).
Fig. 4.42: Severe functional MR (shown by large tenting area, right
panel), causing huge enlargement of the LA and aneurysmal dilatation
of right upper pulmonary vein (left panel).
in preload or afterload, and any decrease in myocardial
contractility, causes LV dilatation, enlargement of the
mitral annulus and an increase in effective regurgitant
orifice (ERO) area.
Mitral Regurgitation 75
Table 4.2: Regurgitant volume and regurgitant orifice area to
assess severity of functional mitral valve regurgitation (MR)
Quantification of Functional MR based upon regurgitant
volume (RV)
Absent: RV 0
Mild: RV 15 mL (ERO 10 mm2)
Moderate: RV 1529 mL (ERO 1119 mm2)
Severe: RV 30 mL (ERO 20 mm2)
Grigioni et al. Circ. 2001
Fig. 4.41: Schematic diagram displaying CW Doppler spectrum of
acute MR. Large V wave of LA pressure cuts-off the ascending limb
obliquely.
In acute MR, the atrium is noncompliant and therefore
mechanical energy generated by the left ventricle
causes an increase in intra-atrial pressure (Figs 4.40
and 4.41).
In chronic MR, the atrium is more compliant, and
therefore mechanical energy generated by the ventricle
causes volume overload and atrial enlargement rather
than an increase in intra-atrial pressure (Fig. 4.42).
In severe MR, transthoracic echocardiography
(TTE) shows left atrial and ventricular enlargement
(Fig. 4.42).
LV systolic motion may be increased in the
compensatory phase of chronic MR.
Peak mitral flow velocity is increased and flow in the
pulmonary veins during systole may be reversed in
severe MR.17 These are supportive signs of severe MR
(Fig. 4.43).
Occasionally, diastolic MR may accompany systolic
MR due to elevated LV diastolic pressure (Fig. 4.44).
76 Section 2: Valvular Heart Disease
Fig. 4.43: Large mitral E velocity and velocitytime integral suggestive
of severe MR.
Fig. 4.45: Large color jet area and depth of presumably severe MR.
Methods to Assess Severity of MR
There are several indirect clues to the severity of MR like
LA and LV enlargement, dense continuous wave (CW)
Doppler spectrum, pulmonary vein systolic flow reversal,
increased mitral flow E wave velocity (> 1.50 m/s) in
absence of mitral stenosis, visible size of regurgitant
orifice, tenting area and tenting height and en face view of
the MV during systole in 3D.
However, in clinical practice, following methods are
routinely used:
Fig. 4.44: Diastolic MR (arrow) along with functional systolic MR.
Fig. 4.46: Mild MR by color jet area. The jet is shorter without PISA
and narrower.
Color Flow Jet Area in LA
Not long back, at default Nyquist limits, MR color jet
area in the LA was predominantly used to assess severity
of MR. A color jet area < 4 cm2 indicated mild MR and
that > 8 cm2 suggested severe MR. Later on, jet area > 10
cm2 was considered evidence of severe MR (Fig. 4.45).
Nowadays, color jet area is used to ballpark MR but
more refined methods are used for estimating severity.
Beyond doubt, a small and thin jet area close to the MV
indicates mild MR (Fig. 4.46) and swirling jet as shown in
Figure 4.45 is suggestive of severe MR.

Fig. 4.47: Two contrasting jet areas at nearly similar Nyquist limits.
Even though ERO is bigger in right panel, its jet area is smaller.
Fig. 4.49: With similar vena contracta width, eccentric jet (right panel)
shows smaller jet area due to Koanda effect.
There are a few caveats for color jet flow area as
criterion for assessing MR severity:
Most frequent but inaccurate way of assessing severe
MR (Figs 4.47 and 4.48)
Size and depth of the jet color area are frequently used
criteria for semiquantitation even though these are
dependent upon many technical and hemodynamic
factors
Color jet area is smaller in eccentric jets compared to
central jets (Fig. 4.49)
In acute MR, color jet area is misleading
Mitral Regurgitation 77
Fig. 4.48: Left panel shows an apparently larger ERO with smaller
color flow jet compared to that in right panel.
Fig. 4.50: Width of vena contracta in apical view (arrows).
Jet area is usually low in presence of elevated LA
pressure.
Color jet flow area is used to detect MR but not quantify
it except in certain emergency situations.
Vena Contracta Width
Measurement of the vena contracta is useful as it describes
the smallest area of the blood flow jet as it exits a valve
(Fig. 4.50). This corresponds to the effective orifice area
calculated for valves using the continuity equation.18
It is preferable to use a zoom mode to optimize
visualization of the vena contracta and facilitate its
78 Section 2: Valvular Heart Disease
Fig. 4.51: Commissural view showing a very large vena contracta.
This view is not recommended for measuring vena contracta width.
measurement. The color flow sector should also be as
narrow as possible, with the least depth, to maximize
lateral and temporal resolution, Nyquist limit of
3070 cm/s and to be measured in views perpendicular to
the commissures (Figs 4.51 and 4.52).
The largest diameter of a clearly defined vena contracta
is measured if possible in two orthogonal planes and
averaged over several cardiac cycles.
Advantages of Vena Contracta
Simple measure of orifice area
Valuable in eccentric jets as well
Not dependent on pulse repetitive frequency
No correction for angle or convergence walls
Not affected by other valve involvement
If the orifice is fixed then the size of the vena contracta
is independent of driving pressure and flow rate
Not affected by loading conditions
Limitations of Vena Contracta Width
No temporal information (as needed in MVP and
hypertrophic cardiomyopathy)
May need biplane or triplane measurement to get it
right in case of eccentric orifices
Multiple jets are a problem
Small errors can make a big difference
In dynamic regurgitation, orifice vena contracta may
change with hemodynamics or during the cardiac cycle
Fig. 4.52: Best lateral resolution in parasternal long axis view for
measuring width of vena contracta as the jet is perpendicular to the
commissures.
The convergence zone is flatter with higher aliasing
velocities and becomes more elliptical with lower
aliasing velocities. The aliasing velocity is set between
20 and 40 cm/s.
Another limitation is with regard to variation in the
regurgitant orifice during the cardiac cycle. This is
particularly important in MVP where the regurgitation
is often confined to the latter half of systole. The precise
location of the regurgitant orifice can be difficult to
judge, which may cause an error in the measurement
of the proximal isovelocity surface area (PISA) radius.
The 3D echo derived vena contracta measured in more
than one axis when seen en face is a better method.19
Even though the measurement of the vena contracta
is less dependent on technical factors, small errors in
measurement can by multiplied due to the relatively small
values of the vena contracta width.
MR Severity and Width of Vena Contracta
Mild 3 mm
Moderate 3.16.9 mm
Severe > 7 mm
The above criteria are applicable only for holosystolic
MR with preferably circular regurgitant orifice.5,13
Proximal Isovelocity Surface Area (PISA)
Volumetric Measurements for Severity of MR
The PISA method is a Doppler phenomenon to estimate
orifice area.

Fig. 4.53: Schema for proximal isovelocity surface area (red hemi-
spheres).
The PISA method is derived from the hydrodynamic
principle, which states that, as blood approaches
a narrow orifice, its velocity increases, forming
concentric, roughly hemispheric shells of increasing
velocity and decreasing surface area (Fig. 4.53).
Color flow mapping offers the ability to image one of
these hemispheres that corresponds to the Nyquist
limit of the instrument. Apical four-chamber view is
the most appropriate for visualization.
If an Nyquist limit can be chosen at which the flow
convergence has a hemispheric shape, flow rate (mL/s)
through the orifice is calculated as the product of the
surface area of the hemisphere (2pR2 or 6.28 radius2)
and the aliasing velocity (Va) as 2pR2 Va) Figure 4.54.
Assuming that the maximal PISA radius occurs at
the time of peak flow and peak velocity, the maximal
ERO is derived as ERO = (6.28R2 Va)/Vmax where
Vmax is the peak velocity of the jet by continuous wave
Doppler
The transiting volume/beat can be estimated as ERO
multiplied by the velocity time integral of the jet. Since
the PISA calculation provides an instantaneous peak
flow rate, ERO by this approach is the maximal ERO
and may be slightly larger than ERO calculated by
other methods. If it is a regurgitant jet, ERO represents
regurgitant orifice area.
Measurement of PISA by color flow mapping requires
adjustment of the aliasing velocity such that a
well-defined hemisphere is shown. This is generally
done by shifting the baseline toward the direction of
flow, or by lowering the Nyquist limit or both.20
Mitral Regurgitation 79
Fig. 4.54: Measuring PISA radius (10 mm) at aliasing velocity of
33 cm/s and calculating flow rate and ERO of MR.
Presence of flow convergence at default Nyquist limit
of 5060 cm/sec indicates significant MR.
Functional MR can not only be biphasic but can also
be only early systolic in some cases (Fig. 4.55). In both
these instances, estimation of regurgitant volume is
inaccurate.
Limitations of PISA Method
It is more accurate for central jets than for eccentric jets.
The formula is applicable to a circular orifice.21
However, quite often, the orifices are elliptical or
irregular or elongated along the coaptation line as in
functional MR (Fig. 4.56).
If the image resolution allows the flow convergence
to be seen well (using Zoom mode), and an Nyquist
limit can be chosen at which the flow convergence has
a hemispheric shape, it is easy to identify the aliasing
line of the hemisphere. However, it can be difficult to
judge the precise location of the orifice and the flow
convergence shape.
Any error introduced is squared, which can markedly
affect the resulting flow rate and ERO.
In patients with normal blood pressure and MR, a
simplified formula can be used if aliasing velocity is
brought to 40 cm/s by shifting the baseline (Fig. 4.57).
The formula gives ERO or regurgitant orifice area by
R2/2 wherein R is the radius of the hemisphere.22
PISA method is much easier to apply in transeso
phageal echocardiographic (TEE) images than in
transthoracic images.23 Scroll function must be used to
80 Section 2: Valvular Heart Disease

Fig. 4.55: Early systolic functional MR. Both vena contracta and PISA overestimate severity of MR in such cases.

Fig. 4.56: Irregular PISA shape not conforming to the hemispheric or Fig. 4.57: Modified PISA method to estimate ERO in those with normal
hemi-elliptical method. systolic blood pressure and holosystolic MR.

define a cardiac cycle wherein PISA is seen the best. In

about 10% of the cases, PISA cannot be defined although
VC can be easily measured.
An ERO > 40 mm2 or an regurgitant volume 60 mL
indicates severe organic mitral regurgitation. Half of these
values are criteria for severity of functional MR.

Pulsed-Wave Doppler
Velocity for Assessing Severity of MR
In the absence of mitral stenosis, a peak mitral E
velocity > 1.5 m/s suggests severe MR (Fig. 4.58).
A dominant mitral A wave practically rules out severe
MR.
Fig. 4.58: A CW interrogation of mitral orifice in pure MR. Inset picture Mitral flow velocitytime integral/aortic timevelocity
shows lack of mitral stenosis. A peak mitral E velocity of 175 cm/s is integral ratio > 1.4 indicates severe MR. This ratio
suggestive of severe MR.
< 1 indicates mild MR.

Fig. 4.59: Mid- and late systolic MR in presence of MV prolapse.
Nearly first half of systole does not display regurgitant jet.
Fig. 4.61: Triangular CW spectrum of MR due to slow rise and fall of
LV pressure in systolic dysfunction.
Reduction in pulmonary venous systolic waveform
velocity occurs with increasing severity of MR. In
severe cases, systolic wave gets reversed or blunted.
This sign lacks specificity because atrial fibrillation and
diastolic dysfunction both can blunt systolic wave.
CW Doppler Interrogation in MR
MR velocity does not provide estimate of severity of MR
Density of CW jet roughly correlates with severity of
MR
A CW spectrum can display holosystolic versus non-
holosystolic MR (Fig. 4.59). Non-holosystolic jets have
smaller RV
Mitral Regurgitation 81
Fig. 4.60: A CW Doppler spectrum of acute MR. Left panel shows flail
AML due to endocarditis.
In acute MR, CW spectrum of MR becomes triangular
with early systolic peaking (Fig. 4.60).
True triangular CW spectrum can also occur due to
severe LV systolic dysfunction (Fig. 4.61).
In summary, evaluation of MR requires careful study
of 2D/3D echocardiographic morphology of the MV
complex, quantitation by measuring vena contracta
and flow convergence method and use of supportive
signs to corroborate the severity of MR. As functional
MR is dynamic and can be non-pansystolic, temporal
information should be obtained by Doppler or color
Doppler M-mode. The report should state if possible
whether the mechanism is primarily organic or functional,
localized remodeling or generalized LV dysfunction as
this has potential bearing on management. However, the
two are not always mutually exclusive as severe MR, due
initially to localized remodeling, may lead over time to
global ventricular dilation.
A holistic approach should be used with integration
of all available information rather than relying on a single
parameter.
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20. Chaliki HP, Nishimura RA, Enriquez-Sarano M, et al.
A simplified, practical approach to assessment of severity
of mitral regurgitation by Doppler color flow imaging with
proximal convergence: validation with concomitant cardi-
ac catheterization. Mayo Clin Proc. 1998;73:92935.
21. Fukuda S, Tran H, Greenberg NL, et al. Geometry of the
proximal isovelocity surface area in mitral regurgitation
by 3-dimensional color Doppler echocardiography: differ-
ence between functional mitral regurgitation and prolapse
regurgitation. Am Heart J. 2008;155:2318.
22. Pu M, Prior DL, Fan X, et al. Calculation of mitral regurgitant
orifice area with use of a simplified proximal convergence
method: initial clinical application. J Am Soc Echocardiogr.
2001;14:1805.
23. Tribouilloy C, Shen WF, Qur JP, et al. Assessment of
severity of mitral regurgitation by measuring regurgitant jet
width at its origin w\ith transesophageal Doppler color flow
imaging. Circulation. 1992;85:124853.
 Chapter

5 Aortic Valve Stenosis

Introduction
Aortic valve guards the left ventricular outflow tract
(LVOT) and is responsible for unidirectional flow into the
aorta. It is a three-leaflet valve with three components:
annulus, leaflets and commissures. In individuals with
normal aortic valves, the valve area is 3.04.0 cm2. As
aortic stenosis develops, minimal valve gradient is present
until the orifice area becomes less than half of normal. The
pressure gradient across a stenotic valve is directly related
to the valve orifice area and the transvalvular flow.
Aortic valve stenosis (AS) is the commonest valve
disorder encountered in clinical practice. Typically, severe
aortic stenosis is the one with a peak transaortic velocity
of 4 m/s, mean gradient of 40 mm Hg and aortic valve Fig. 5.1: Diagram showing cross-section of the aortic valve.
area (AVA) of 1.0 cm2. However, AS is a diverse disorder
wherein flow, pressure and area frequently do not
match. A number of factors affect the total hemodynamic
ANATOMY OF TRILEAFLET AORTIC VALVE
burden imposed by AS on the left ventricle (LV). There is
no gold standard for AVA. Comorbidities that affect flow The aortic valve functions to prevent the regurgitation
and pressure are frequent. Conventional assessment of of blood from the aorta into the LV during ventricular
AS with echocardiography could be erroneous because diastole and to allow the appropriate flow of blood from
of geometric assumptions and Doppler phenomena like the LV into the aorta during ventricular systole. The aortic
pressure recovery. Functional anatomy of the aortic valve valve has three principle components13 (Figs 5.1 and 5.2).
complex is important for decision making. Understanding 1. Annulus
the true nature of AS helps in better management of 2. Cusps
patients. 3. Commissures.
84 Section 2: Valvular Heart Disease
Fig. 5.2: Three-dimensional echocardiographic cross-section at the
aortic valve showing right cusp (RC), noncoronary cusp (NCC) and
the left cusp (LC).
(IAS: Inter-atrial septum; RA: Right atrium; LA: Left atrium).
Fig. 5.4: Transthoracic echocardiography short-axis view showing
right (R), left (L) and the noncoronary cusp (NC) of the aortic valve.
Note that the noncoronary cusp is slightly larger than the other two.
The Annulus
The aortic valve annulus is a fibrous structure lying at the
level of the junction of the aortic valve and the ventricular
septum, which is the nadir of the aortic valve complex.
This area provides structural support to the aortic valve
complex. The annulus is shaped like a crown and extends
to the level of the aortic sinuses. It attaches to the aortic
media distally and the membranous and muscular
ventricular septum proximally and anteriorly (Fig. 5.3).
Fig. 5.3: Relationship of aortic annulus to ventricular septum and the
mitral annulus.
(RPA: Right pulmonary artery; LVOT: Left ventricle outflow tract).
Aortic Cusps
There are three aortic valve cusps, each semilunar in
appearance. A small dilatation of the proximal aorta is
associated with each cusp (sinus of Valsalva or aortic
sinus). Their association with the respective coronary ostia
identifies them: left, right and posterior (or noncoronary).
In the normal human heart, the left and right coronary
arteries originate from the left and right aortic sinuses.
In about 10% of cases, coronary artery origins occur
above the sinotubular junction. The aortic sinuses share
the same histological characteristics of the aortic wall:
tunica intima, tunica media and tunica adventitia;
however, the bases of the left and right sinuses are primarily
composed of ventricular musculature, whereas the base
of the noncoronary sinus is solely fibrous tissue. This is a
consequence of the shared fibrous skeleton between the
aortic and mitral valve structures.
The right and left cusps are usually equal in size, with
the posterior cusp being slightly larger (Fig. 5.4).
Each cusp has two free edges, both shared with the
adjacent cusps. At the center of each free edge is a small
fibrous bulge named the nodule of Arantius. These nodules
are located at the contact site of valve cusp closure. The
rim of each valve cusp is slightly thicker than the cusp
body and is known as the lunula. The lunulae of adjacent
cusps slightly overlap each other at the time of valve
closure, serving a role of increased valve support. The

Fig. 5.5: Lunulathicker free margin of cusp; nodule of Arantius
slight nodularity in the centre of the free margin.
lunula can have fenestrations, most often located adjacent
to the commissures; however, these are also not of clinical
consequence (Fig. 5.5).
Commissures
Each cusp is attached to the wall of the aorta by the outward
edges of its semicircular border. The level at which this
attachment occurs is known as the sinotubular junction
and is the functional level of the aortic valve orifice. A line
of demarcation known as the supra-aortic ridge identifies
the sinotubular junction.
The small spaces between each cusps attachment
point are called the aortic valve commissures. The three
commissures lie at the apex of the annulus and are equally
spaced around the aortic trunk. The commissures are
composed of collagenous fibers oriented in a radial fashion
that penetrate into the aortic intima and are anchored
in the media of the aorta. This configuration provides
optimal support to valvular structure, with stress on the
valve cusps being transmitted into the aortic wall. The
commissure between the left and posterior cusp is located
at the right posterior aspect of the aortic root, whereas the
commissure between the right and noncoronary cusp is
located at the right anterior aspect of the aortic root.
Etiology of Aortic Stenosis
Congenital aortic stenosis
Calcification of bicuspid valve in middle age
Aortic Valve Stenosis 85
Fig. 5.6: Unicuspid aortic valve in diastole showing single commissure
(left) and during systole (right). The ring-in-ring appearance is typical
of unicuspid valve.
Postinflammatory fibrocalcific disease (rheumatic)
Degeneration of aging valve
Calcification of unicuspid valve
Other rare causes like ochronosis, alkaptonuria, lupus,
and so on.
UNICUSPID AORTIC VALVE4
Unicuspid aortic valve is a congenital valvular defect
with an incidence of 0.02% in the general population. It
is commonly associated with clinically significant aortic
stenosis, usually manifesting during the third decade
of life. All valves are unicommissural with the posterior
commissural attachment. The free edge of the valve
extends from the single commissure without further
communication with the aorta (Figs 5.6 and 5.7).
An estimated 50% of individuals with unicuspid aortic
valve have associated ascending aortic dilatation. This
is a rare cardiac anomaly presenting at a young age with
clinically significant aortic stenosis.
BICUSPID AORTIC VALVE5
Bicuspid aortic valve is the most common congenital
cardiac anomaly, occurring in 12% of the population,
with a 2:1 male predominance. Evidence exists of familial
clustering, with the incidence as high as 10% in some
families. Bicuspid aortic valve may be clinically silent
but can lead to early development of aortic stenosis or
aortic insufficiency, most commonly in the fifth and sixth
86 Section 2: Valvular Heart Disease
Fig. 5.7: Unicuspid aortic valve in transthoracic short-axis view in
diastole (left panel) and aortic dilatation shown in transesophageal
long-axis view (right panel).
Fig. 5.9: Bicuspid aortic valve with conjoined leaflet made of fused
right and noncoronary cusps. High raphe (arrow) is shown.
decades of life. Conditions associated with bicuspid aortic
valve include:
Patent ductus arteriosus
Williams syndrome
Turner syndrome
Coarctation of aorta
Aortic root dilatation and ascending aortic aneurysm
The larger leaflet is referred to as the conjoined leaflet
(Fig. 5.8).
Two commissures (or hinge points) are present; usually,
neither is partially fused. The presence of a partially fused
commissure, which has also been called a high raphe,
probably predisposes toward eventual stenosis. At least
half of all congenitally bicuspid valves have a low raphe,
which never attains the plane of the attachments of the
Fig. 5.8: Bicuspid aortic valve with conjoined leaflet due to fusion of
left and noncoronary cusps.
two commissures and never extends to the free margin of
the conjoined cusp (Figs 5.9 and 5.10).
Valve leaflet orientation and morphology can vary.
Fusion along the right or left leaflets is less commonly
associated with stenosis. Fusion along the right and
noncoronary leaflets is more frequently associated with
pathological changes of stenosis.
QUADRICUSPID AORTIC VALVE
The incidence of quadricuspid aortic valve (QAV) is
estimated at 0.01250.033% in the general population.6
Seven different subtypes of QAV have been identified, with
the most common being three cusps of equal size with a
fourth smaller cusp (Fig. 5.11).
Quadricuspid valve most commonly occurs as an
isolated defect but has been associated with patent
ductus arteriosus, EhlersDanlos syndrome, hypertrophic
obstructive cardiomyopathy and subaortic stenosis (SAS).
Aortic valvular insufficiency is commonly observed in this
anomaly. It occurs secondary to a central orifice formed
from malcoaptation of the four valvular leaflets.7
ANATOMY OF AORTIC STENOSIS
Aortic valve stenosis is the functional narrowing of the
orifice of the aortic valve due to the following pathology:8
Thickening of the leaflets from base to free margins
Shortening of the leaflets
Commissural fusion (Figs 5.12 and 5.13)
Dystrophic calcification (Fig. 5.14)
Hypoplastic annulus in congenital aortic stenosis
The congenitally stenotic aortic valve may be acomm
issural, unicommissural, bicuspid or rarely, congenitally

Fig. 5.10: Bicuspid aortic valve in three-dimensional echocar
diographic. The conjoined leaflet (CL) is due to fusion of noncoro-
nary cusp with left cusp without raphe. The commissures are marked
(arrows).
Fig. 5.12: Transthoracic short-axis view showing commissural fusion
with calcification (left) and pathological specimen (right).
Fig. 5.14: Bicuspid aortic valve with stenosis, A is pathological
specimen while B is three-dimensional echocardiographic picture.
Aortic Valve Stenosis 87
Fig. 5.11: Transesophageal echocardiographic short-axis view showing
quadricuspid aortic valve (arrows).
Fig. 5.13: Pathological specimen of the rheumatic aortic valve stenosis
(left) and short-axis view on en face aortic valve (right).
quadricuspid/quadricommissural.9 The presence of one,
two or four cusps instead of three is associated with
abnormal valve hemodynamics and produces greater and
earlier leaflet damage (Fig. 5.14).
PLANIMETRY OF THE AORTIC VALVE
AREA IN AORTIC STENOSIS
Planimetry is the tracing out of the opening of the aortic
valve in a still image obtained during echocardiographic
acquisition during ventricular systole, when the valve is
supposed to be open. While this method directly measures
the valve area, the image may be difficult to obtain due to
artifacts during echocardiography, and the measurements
are dependent on the effort undertaken to manually
trace the perimeter of the open aortic valve right at its tip
88 Section 2: Valvular Heart Disease
Fig. 5.15: Planimetry of the aortic valve area (AVA) in transthoracic
short-axis view in mid-systole.
(Fig. 5.15). Craniocaudal motion of the leaflets causes
echo dropouts. Because of these reasons, planimetry of
aortic valve is not routinely performed.
Major limitations are:
Difficulty in obtaining oblique cuts to profile the orifice
in two-dimensional (2D) echocardiography
Heavy calcification hampering border detection
Phasic cranial motion of the cusps during systole
Inability to get minimal cross-sectional area due to
slice thickness artifact.
Usually, transesophageal echocardiography (TEE)
is better than transthoracic echocardiography (TTE) for
planimetry of AVA.10 However, accuracy of 2D TEE method
may also be limited by difficulties in obtaining the correct
cross-sectional view at the level of the edges of the aortic
cusps.11
Planimetry of AVA by TTE/TEE is difficult and less
accurate than the continuity equation for assessing the
severity of aortic stenosis. It is usually over-estimated
(because it is geometric area and not flow cross-sectional
area) but can be used in noncalcific mild or moderate AS.
Some have reported good success in obtaining valve area
in severe cases and irregular valves by three-dimensional
(3D) TTE12 (Fig. 5.16).
Development of real-time 3D TEE has allowed
volumetric data acquisition of the aortic valve, from which
the true orthogonal 2D cut plane of the aortic cusps can
be extracted for the accurate determination of the AVA
(Fig. 5.17). This method has more accuracy but is time-
consuming.
Fig. 5.16: Three-dimensional transthoracic echocardiography planim-
etry of mild aortic stenosis.
HEMODYNAMICS OF AORTIC
VALVE STENOSIS
Normal AVA in adults is 34 cm2, and in children it is
about 1.7 cm2/m2. With development of orificial narro
wing, valve offers resistance to transvalvular flow. To
maintain transvalvular flow, the LV generates greater
pressure during systole (Fig. 5.18). This results in develo
pment of transaortic pressure gradients (P). P incr
eases with increasing severity of aortic stenosis but in a
curvilinear fashion (Fig. 5.19). The presence of an obstr
uction results in both turbulent flow and increased
velocity, two characteristics readily detected by Doppler
echocardiography.13,14 Because of the large gradient,
the pressures within the LV rise significantly and left
ventricular hypertrophy results. AVA is relatively flow-
independent and hence preferred over the velocity and
pressure gradients for judging severity of AS.15
Complete assessment of the degree of aortic stenosis
requires:
Measurement of the transvalvular flow
Determination of the transvalvular pressure gradient
Calculation of the AVA
Calculation of energy loss coefficient
Calculation of valvuloarterial impedance
Conventionally, severity of AS is judged by the above
parameters using criteria shown in Table 5.1:16,17
Stroke volume (SV) is measured by multiplying LVOT
cross-sectional area by the velocitytime integral of the
outflow. SV should be indexed for body surface area
(Fig. 5.20).
 Aortic Valve Stenosis 89

Fig. 5.17: Three-dimensional volumetric data of the left ventricular outflow tract used to extract multiple cross-sectional views of the aortic valve.
Minimum valve area from middle row images can be considered true anatomical area.

Fig. 5.18: Development of transaortic gradients in aortic valve ste- Fig. 5.19: Curvilinear relationship between aortic valve area and P.
nosis is by virtue of greater pressure developed by the left ventricle.
Three different types of P are shown.
90 Section 2: Valvular Heart Disease

Table 5.1: Relationship of transvalvular velocities, P and aortic TECHNICAL TIPS

valve area for judging severity
The most common windows used for recording peak
Severity of Aortic Stenosis
aortic systolic velocity are the apical, suprasternal and
Velocity (m/s) Valve Area (cm2) right parasternal. A comprehensive Doppler exami
Mild 2.63.0 (mean G < 25) > 1.5 nation for aortic stenosis requires that the ascending
Moderate 3.04.0 (mean G 2540) > 1.01.5 aorta be examined from all possible windows in order
to align the beam parallel to the jet (Figs 5.22 and 5.23).
Severe > 4.0 (mean G > 40) 1.0
A potential source for error is mistakenly interpreting
(G: Gradient). the profile of mitral regurgitation for that of aortic
stenosis in apical windows. However, AS signal begins
LVOT diameter is measured from parasternal long-axis after the isovolumic contraction and is slightly delayed
view in mid-systole and area is estimated by assuming (Fig. 5.24).
it to be circular (Fig. 5.21). The CW spectrum profile can help in differentiating
Transaortic flow rate is calculated by dividing SV by mild aortic stenosis from the severe one. As the severity
systolic ejection time. increases, peak of P gets delayed and occurs in later
Aortic valve area is calculated by dividing SV by aortic part of systole (Figs 5.25 and 5.26).
velocitytime integral (Fig. 5.21). Whenever there is doubt about the quality of
Valve resistance is calculated by dividing mean parasternal long-axis measurement of the LVOT
transaortic gradient by transaortic flow rate.18 or there is associated aortic or mitral regurgitation
Substituting the Doppler-derived SV by SV directly (making continuity equation nonapplicable), it is
obtained with real-time 3D echocardiography, which prudent to use a dimensionless index of ratio of LVOT
considerably simplifies the calculation, overcomes peak velocity to transaortic peak velocity (Figs 5.27
many potential sources of error, and does not depend and 5.28). An index of 0.25 usually denotes severe
on the quality of the parasternal acoustic window.19 aortic valve stenosis. However, in low-flow situations,
Echo-2D underestimates the LVOT area, which may it may not differentiate true from pseudostenosis.
explain the tendency of Echo-2D to estimate a smaller The weakest aspect of area calculation is the variability
AVA than Echo-3D. in measurement of LVOT area, because it involves
Stroke volume index is the only independent predictor squaring the LVOT dimension. The other weak point
of the difference in AVA between invasive and is some flow-dependency of the AVA by the continuity
noninvasive assessments. equation.20

Fig. 5.20: Measurement of LVOT diameter from parasternal long-axis Fig. 5.21: Aortic valve area by continuity equation is calculated as
view and LVOT velocitytime integral from apical view using pulsed stroke volume divided by velocitytime integral across the aortic valve.
wave Doppler with a small sample volume placed just proximal to flow
acceleration zone. (LVOT: Left ventricular outflow tract).
 Aortic Valve Stenosis 91

Fig. 5.22: CW interrogation of aortic valve flow jet by apical window Fig. 5.23: Incompletely formed aortic Doppler spectrum (upper panel)
(left) and suprasternal window (right). Note that the P is higher by compared to fully formed CW velocity spectrum (lower panel) from
14 mm Hg when measured from the suprasternal window. apical windows. There is a difference of 80 mm Hg in P.

Fig. 5.24: Combined CW signals of mitral regurgitation and subaortic Fig. 5.25: CW profiles of varying degree of aortic valve stenosis (AS).
stenosis. Note that the signal of aortic valve stenosis (AS) is delayed.

Fig. 5.26: Comparison of CW Doppler spectrum of mild versus severe Fig. 5.27: Measurement of dimensionless index from the apical
aortic valve stenosis (AS). window. Upper panel shows left ventricular outflow tract velocity and
the lower panel shows aortic velocity profile.
92 Section 2: Valvular Heart Disease

Fig. 5.28: In the presence of severe aortic regurgitation (AR), dimensionless index (DI) is 0.21 despite left ventricular outflow tract peak velocity
of 118 cm/s. This suggests significant aortic valve stenosis in the presence of AR.

Fig. 5.29: Diaphragm-like aortic valve orifice (arrow) and narrow Fig. 5.30: Method of estimating energy loss index.
ascending aorta; two common causes of higher transaortic velocity
and P.

Geometry of the aortic orifice, inflow and the size of
aorta all affect estimation of the AVA by the continuity
equation (Fig. 5.29).
It has been suggested that estimation of energy loss
index (ELI) is a better guide for severity and prognosis
of AS than the AVA.21 Figure 5.30 shows the method
to estimate ELI. Energy loss index takes into account
the pressure recovery (Fig. 5.31). The valves with the
greatest pressure recovery have the least energy loss.
Another method to assess hemodynamic burden of
aortic stenosis is estimation of ventriculovalvular
impedance (VVI). VVI is the ratio of arterial systolic
pressure + mean transaortic gradient divided by the
SV index.22 A value of > 4.5 is significant VVI. VVI takes
into account the hemodynamic load on the LV
imposed by systemic hypertension and also corrects
for the lower P seen in patients with low flow
(reduced SV index). It is possible to use VVI regardless
of ejection fraction (Fig. 5.32).
Percent stroke work loss calculated as mean systolic
pressure gradient divided by mean ventricular
systolic pressure 100% is also a good parameter of
AS severity.
A simplified continuity equation that provides AVA
is a product of dimensionless index and LVOT cross-
sectional area (Fig. 5.33).

Fig. 5.31: Just beyond the orifice, P is maximum, which gradual-
ly decreases near sinotubular junction due to conversion of kinetic
energy into pressure energy. If the flow distally is turbulent due to di-
lated aorta, less pressure recovery occurs as some energy is lost to
tissues as heat.
Fig. 5.33: Modified continuity equation for estimating aortic valve area.
Flow (area velocity) is constant across a stream if there is no sump
or sink.
If dynamic obstruction creates difficulty in estimating
LVOT SV, the right ventricular outflow tract SV can be
used as the numerator.
LOW-GRADIENT, LOW-FLOW AORTIC
VALVE STENOSIS
Low-gradient low-flow aortic stenosis is characterized by
AVA 1.0 cm2, mean gradient 30 mm Hg and SV index
35 mL/m2 (Figs 5.34 to 5.36).
Aortic Valve Stenosis 93
Fig. 5.32: Systolic aortic pressure recovers in divergence zone with
decrease in mean gradient. Combination of systolic aortic pressure
and mean transaortic gradient represents the pressure load to be
overcome by the left ventricle (LV) during ejection. When this is divided
by the stroke volume index, it is akin to total resistance faced by the LV.
Flowchart 1: Representation of low-flow low-gradient aortic stenosis
Types of Low-Gradient Low-Flow
Severe Aortic Valve Stenosis
Schematic diagram of low-flow low-gradient AS is shown
in Flowchart 1.
Calculation of AVA by continuity equation is flow-
dependent and in presence of low flow, one estimates
much smaller AVA due to boundary effects.
About 30% of all patients have AVA in the severe range
with low flow or low gradients or both.
Low-flow low-gradient AS may truly have severe AS
with resultant myocardial failure (true AS) or may
have more moderate degrees of AS and unrelated
myocardial dysfunction.23,24
In patients with true AS, increased flow (as with
dobutamine infusion) across a fixed valve orifice
results in increased transvalvular flow velocity and
94 Section 2: Valvular Heart Disease
Fig. 5.34: Low-gradient and low-flow aortic valve stenosis with mean gradient of 17 mm Hg and stroke volume of 20 mL/M2.
Fig. 5.35: Calculated aortic valve area of 0.5 cm2 in a patient with
pseudosevere aortic valve stenosis (AS) with a peak transaortic veloc-
ity of 212 cm/s. CW Doppler pattern (left panel) shows early systolic
peaking suggesting that the AS is not severe.
gradients, without a change in calculated valve area
(Fig. 5.37A and B).
In the setting of pseudo-AS, the augmented flow results
in only a mild increase in transvalvular gradient and an
increase in valve area by 0.2 cm2.
As many as 30% of patients with low-flow low-gradient
AS fail to augment SV by at least 20% with dobutamine
infusion; these patients are denoted as having no
Fig. 5.36: Low-flow (stroke volume index30 mL/m2) despite ad-
equate left ventricular outflow tract diameter.
contractile reserve.23,24 Such patients have higher
operative mortality.
Majority of patients with low-gradient low-flow AS
have significant valve stenosis.
The differentiation between true and pseudo-AS may
be improved by using other noninvasive parameters,
such as the projected valve area at a normal flow rate,
an echocardiographic method that attempts to control
 Aortic Valve Stenosis 95

A B
Figs 5.37A and B: (A) Baseline left ventricular outflow tract and transaortic velocities and calculated aortic valve area at baseline at heart rate
of 69/min in a low-flow, low-gradient aortic valve stenosis (AS) patient. (B) At 20 g/kg/min dobutamine infusion and heart rate of 113/minute.
There is 20% increase in stroke distance and 27% increase in transaortic velocity without any change in aortic valve area suggesting that it is
true severe AS despite a mean gradient of 24 mm Hg at rest.

for the variable augmentation of transaortic flow
induced by dobutamine.25
There is a good correlation between calcium and
severity. Calcified valves usually have severe AS.
Planimetry, when possible, can accurately tell about
anatomical area, which in general is no greater than
20% when compared to the effective orifice area.
PARADOXICAL LOW-FLOW AS WITH
PRESERVED EJECTION FRACTION
As many as 35% of patients with severe AS (AVA
< 0.6 cm/m2) and preserved ejection fraction (> 50%)
have paradoxically low flow, defined as a SV index of
< 35 mL/m2.26
The mechanism of the paradoxically low flow in the
face of preserved ejection fraction likely relates to high
afterload, and the reduced SV in this setting is an early
marker of intrinsic myocardial dysfunction.
Such cases can be identified by small LV cavity with
marked hypertrophy (Fig. 5.36).
Paradoxical low-flow AS has variable prognosis.
3D TTE or TEE Planimetry of AVA may better define the
severity of AS in these patients.
SUBAORTIC STENOSIS
Discrete fixed SAS has hemodynamic consequences like
valvular AS (Figs 5.38 to 5.40). It is known for its sometimes
rapid hemodynamic progression in childhood. In contrast
to children, fixed SAS progresses slowly in adulthood.
Discrete subaortic membrane accounts for 810% of all
cases of LVOT obstruction in children.27,28
There are three types of SAS identified by echocar
diography:
1. Discrete membranous ring
2. Discrete fibromuscular stenosis
3. Diffuse tubular stenosis
Pathoanatomically, it is of four types:29
1. Short segment SAS
2. Long segment SAS
3. Posterior displacement of infundibular septum
4. Accessory tissue of membranous septum obstructing
the LVOT
SAS presents as a membranous or fibromuscular ring
below the aortic valve, either in isolation or in association
with other congenital anomalies such as ventricular septal
defect, patent ductus arteriosus, coarctation of the aorta,
bicuspid aortic valve, abnormal left ventricular papillary
muscle, atrioventricular septal defect and persistent
superior left vena cava.
The jet from the narrowed subaortic tract damages the
aortic cusps and causes regurgitation, which is present in
20% of the cases.
Aortic regurgitation is a common consequence of
discrete SAS and the prevention of progressive aortic
regurgitation by early operation has been advocated.
Hemodynamically, SAS is characterized by unusually
higher gradients due to hole-in-diaphragm or tubular
architecture with much greater pressure recovery.
96 Section 2: Valvular Heart Disease
Fig. 5.38: Membranous subaortic stenosis (arrow) shown in parasternal
long-axis view with peak velocity exceeding 7 m/s and mild aortic valve
regurgitation (right panel).
(RVOT: Right ventricular outflow time; AO: Aortic; LV: Left ventricle;
LA: Left atrium).
Fig. 5.40: Long subaortic stenosis with a peak velocity of 7.6 m/s.
However, hemodynamic severity is not the only
criterion for intervention. Symptoms and onset of aortic
regurgitation should dictate operation.
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12. Gutirrez-Chico JL, Zamorano JL, Prieto-Moriche E, et al.
Real-time three-dimensional echocardiography in aortic
stenosis: a novel, simple, and reliable method to improve
accuracy in area calculation. Eur Heart J. 2008;29(10):1296
1306.
13. Otto CM. Aortic stenosis. In: Valvular Heart Disease. Phila-
delphia, PA: WB Saunders Company; 1999. pp. 179217.
14. Weyman AE, Scherrer-Crosbie M. Aortic stenosis: physics
and physiologywhat do the numbers really mean? Rev
Cardiovasc Med. 2005;6(1):2332.
15. Bermejo J, Antoranz JC, Burwash IG, et al. In-vivo analysis
of the instantaneous transvalvular pressure difference

-flow relationship in aortic valve stenosis: implications of
unsteady fluid-dynamics for the clinical assessment of dis-
ease severity. J Heart Valve Dis. 2002;11(4):55766.
16. Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006
guidelines for the management of patients with valvular
heart disease: A report of the American College of Cardi-
ology/American Heart Association Task Force on Practice
Guidelines (writing committee to revise the 1998 Guide-
lines for the Management of Patients with Valvular Heart
Disease): Developed in collaboration with the Society of
Cardiovascular Anesthesiologists: Endorsed by the Soci-
ety for Cardiovascular Angiography and Interventions and
the Society of Thoracic Surgeons. Circulation. 2006;114:
e84231.
17. Baumgartner H, Hung J, Bermejo J, et al.; American Society
of Echocardiography; European Association of Echocardi-
ography. Echocardiographic assessment of valve stenosis:
EAE/ASE recommendations for clinical practice. J Am Soc
Echocardiogr. 2009;22(1):123; quiz 101.
18. Ford LE, Feldman T, Chiu YC, Carroll JD. Hemodynamic
resistance as a measure of functional impairment in aortic
valvular stenosis. Circ Res. 1990;66(1):17.
19. de la Morena G, Saura D, Oliva MJ, et al. Real-time three-
dimensional echocardiographyin aortic stenosis: a novel,
simple, and reliable method to improve accuracy inarea
calculation. Eur Heart J. 2008;29:12961306.
20. Kadem L, Rieu R, Dumesnil JG, et al. Flow-dependent
changes in Doppler-derived aortic valve effective orifice
area are real and not due to artifact. J Am Coll Cardiol. 2006;
47(1):1317.
21. Garcia D, Pibarot P, Dumesnil JG, et al. Assessment of aor-
tic valve stenosis severity: A new index based on the energy
loss concept. Circulation. 2000;101(7):76571.
Aortic Valve Stenosis 97
22. Hachicha Z, Dumesnil JG, Pibarot P. Usefulness of the
valvuloarterial impedance to predict adverse outcome
in asymptomatic aortic stenosis. J Am Coll Cardiol. 2009;
54(11):100311.
23. deFilippi CR, Willett DL, Brickner ME, et al. Usefulness of
dobutamine echocardiography in distinguishing severe
from nonsevere valvular aortic stenosis in patients with
depressed left ventricular function and low transvalvular
gradients. Am J Cardiol. 1995;75(2):1914.
24. Monin JL, Monchi M, Gest V, et al. Aortic stenosis with
severe left ventricular dysfunction and low transvalvu-
lar pressure gradients: risk stratification by low-dose
dobutamine echocardiography. J Am Coll Cardiol.
2001;37(8):21017.
25. Blais C, Burwash IG, Mundigler G, et al. Projected valve
area at normal flow rate improves the assessment of steno-
sis severity in patients with low-flow, low-gradient aortic
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Aortic Stenosis) Study. Circulation. 2006;113:71121.
26. Clavel MA, Ennezat PV, Marchaux S, et al. Stress echocar-
diography to assess stenosis severity and predict outcome
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stenosis and preserved LVEF. JACC Cardiovasc Imaging.
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27. Rohlicek CV, del Pino SF, Hosking M, et al. Natural history
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28. Freedom RM, Pelech A, Brand A, et al. The progressive na-
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29. Foker JE. Outcomes and questions about discrete subaortic
stenosis. Circulation. 2013;127(14):144750.
 Chapter
6 Regurgitation
Introduction
Aortic regurgitation (AR) is characterized by regurgitation
of blood from the aorta to the left ventricle (LV) during
diastole and is attributable to diverse congenital and
acquired abnormalities of the aortic valve or the wall of
the aortic root. Pure AR (no element of aortic stenosis)
has multiple causes, some of which directly affect the
aortic valve (50% of all) and others of that are due to
problems with the aorta without direct involvement of the
aortic valve. Unlike aortic stenosis, which essentially is
always a slowly progressing chronic condition, AR may
develop acutely (acute AR) or over a prolonged period
(chronic AR). Quantitation of AR, its mechanism of
occurrence, associated hemodynamic load and need for
intervention can be assessed by use of echocardiography.
HEMODYNAMICS OF AORTIC
REGURGITATION
Diastolic reflux through the aortic valve is called AR.
Aortic regurgitation leads to left ventricular (LV) volume
overload. An increase in systolic stroke volume (SV) and
low diastolic aortic pressure produce an increased pulse
pressure. The LV becomes larger and more compliant, with
greater capacity to deliver a large SV that can compensate
for the regurgitant volume. The resulting hypertrophy is
necessary to accommodate the increased wall tension that
results from LV dilation.
Aortic Valve
The severity of AR is dependent on the diastolic valve
area, the diastolic pressure gradient between the aorta and
LV, and the duration of diastole (Figs 6.1 to 6.3).
During the early phases of chronic AR, the LV ejection
fraction is normal or even increased (due to the increased
preload and the FrankStarling mechanism). As AR
progresses, LV enlargement surpasses preload reserve on
the FrankStarling curve, with the ejection fraction falling
to normal and then subnormal levels. The LV end-systolic
volume rises and is a sensitive indicator of progressive
myocardial dysfunction.1
Eventually, the LV attains its maximal diameter and
compliance starts falling. Diastolic pressure begins to
rise, resulting in symptoms. Increasing LV end-diastolic
pressure may also lower coronary perfusion gradients,
causing subendocardial myocardial ischemia. The LV
gradually transforms from an elliptical to a spherical
configuration.
Common causes of AR are:
Congenital bicuspid or quadricuspid valve (Fig. 6.4)
Subarterial ventricular septal defect or aneurysm of
sinus of Valsalva (Figs 6.5 and 6.6)
Rheumatic heart disease (Fig. 6.7)
Systemic hypertension
Infective endocarditis (Fig. 6.8)
Marfan syndrome (Fig. 6.9)
Rheumatoid arthritis
Ankylosing spondylitis
Behcets disease
 Aortic Valve Regurgitation 99

Fig. 6.1: In diastole, both mitral and aortic valves are open in aortic Fig. 6.2: Transaortic diastolic P is the driving force in aortic regur
regurgitation, causing left ventricle volume overload. gitation.

Fig. 6.3: Three-dimensional transthoracic echocardiographic view of Fig. 6.4: Congenital bicuspid aortic valve in diastole showing regur
the aortic valve with diastolic regurgitant area. Viewed from the left gitant orifice.
ventricle. (RVOT: Right ventricle outflow tract; RCC: Right coronary
cusp, NCC: Noncoronary cups; LCC: Left coronary cups; RA: Right
atrium; LV: Left atrium).

Fig. 6.5: Three-dimensional transthoracic echocardiographic showing Fig. 6.6: Subannular pseudoaneurysm (red arrow) results in
ruptured aneurysm of sinus of Valsalva reducing support to the decreased support to aortic annulus causing aortic regurgitation.
annulus and creating regurgitant orifice (red arrow).
100 Section 2: Valvular Heart Disease

Fig. 6.7: Short, thickened and deficient leaflets (arrows) in rheumatic Fig. 6.8: Vegetations on aortic leaflets (arrows) with incomplete
heart disease affecting aortic valve without causing stenosis. coaptation in infective endocarditis.

Fig. 6.9: Dilated aortic root in Marfan syndrome resulting in a Fig. 6.10: Apical long-axis view. Aortic dissection flap prolapsing into
regurgitant aortic valve orifice (arrows). the left ventricular outflow tract and causing aortic regurgitation.

EhlersDanlos syndrome FUNCTIONAL ANATOMY OF

Whipples disease AORTIC REGURGITATION
Systemic lupus erythematosus
Takayasus disease There are three main mechanisms of AR.3,4
Giant cell arteritis Type 1: Dilatation of the aortic root (Fig. 6.11)
Aortic dissection (Fig. 6.10) Type 2: Excess cusp motion, including cusp prolapses
Subaortic aneurysm and free edge fenestrations, with good cusp tissue quality
Other causes of annuloaortic ectasia (Fig. 6.11) (Fig. 6.12)
Aortic root dilation may be present in up to 25% of Type 3: Poor cusp tissue quality, including cusp
patients with AR due to bicuspid valve, hypertension or retraction, extensive cusp calcifications ( Grade III) and/
connective tissue disorders.2 or endocarditis (Fig. 6.13).

Fig. 6.11: Parasternal long-axis view showing dilated aortic root with
stretched out annulus causing malcoaptation of the aortic leaflets.
Fig. 6.13: Parasternal long-axis view showing cusp retraction with
calcification (type 3 aortic regurgitation).
Fig. 6.15: Parasternal long-axis view showing whole cusp prolapse of
the posterior leaflet.
Aortic Valve Regurgitation 101
Fig. 6.12: Parasternal long-axis view showing flail aortic cusps with
excessive mobility (arrows). Type 2 aortic regurgitation.
Fig. 6.14: Parasternal long-axis view showing partial prolapse of the
right cusp (arrow).
Cusp prolapse is further categorized into three groups.
1. Flail cusp (eversion of the cusp into the left ventricular
outflow tract (LVOT); Fig. 6.12)
2. Partial or distal cusp prolapse (Fig. 6.14)
3. Whole cusp prolapse (Fig. 6.15).
Type 1 AR is identified when the dimensions of any
components of the aortic root, including the aortic
annulus, the sinuses of Valsalva and the sinotubular
junction exceed the upper limits of published normal
values.
Type 2 AR is considered in the presence of an eccentric
AR jet and either a cusp prolapse or a cusp fenestration.
Cusp prolapse is considered whenever the free edge of one
or more the aortic cusps overrode the plane of the aortic
annulus (Fig. 6.12).
102 Section 2: Valvular Heart Disease
Fig. 6.16: Measurement of aortic annulus, root, sinotubular junction
and ascending aorta in parasternal long-axis view in mid-systole.
Type 3 AR is considered whenever the quality or
quantity of the cusp tissue is judged to be poor. Thickened
and rigid valves with reduced motion, valves whose leaflet
tissue have been destroyed by endocarditis and severely
calcified valves are included in this category.
The degree of calcification of the aortic valve is scored
as follows:
Grade I: no calcification
Grade II: isolated small calcification spots
Grade III: bigger calcification spots interfering with
cusp motion
Grade IV: extensive calcifications of all cusps with
restricted cusp motion
In addition to the anatomical evaluation of the aortic
valve, the aortic root diameter (valve annulus, aortic
sinuses, sinotubular junction and proximal ascending
aorta) measurements are performed in mid-systole by
inner edge-to-inner edge (Fig. 6.16).
DETECTION OF AORTIC REGURGITATION
BY ECHO-DOPPLER TECHNIQUES
Diastolic reflux through the aortic valve has direct and
indirect clues (Fig. 6.17).
Three key areas require attention in echocardiographic
examination.
Structural details of the aortic valve and its apparatus
Severity of AR as judged by the total volume of
regurgitation
Hemodynamic load of AR on the LV (LV size, function
and geometry)
Fig. 6.17: Diagram showing the concept of aortic regurgitation. The re
gurgitant jet can be central or be directed toward anterior mitral leaflet
or interventricular septum.
M-Mode Echocardiography
As structural details of the aortic valve are seen much
better with two-dimensional (2D)/three-dimensional
(3D) imaging, M-mode echocardiography is rarely used
for assessment of AR.5,6 It is more of historical interest.
M-mode echocardiography shows diastolic fluttering
of the anterior mitral leaflet (AML), which is a finding
of diagnostic significance. It results from the AR jet
hitting the AML, and may be seen in cases of AR of
even mild degree.
In severe cases, the AML may fully close from the
impact of the jet; this finding may serve as an indication
for valve surgery. Premature mitral valve closure
occurs more frequently in acute AR.
Diastolic flutter of the interventricular septum may
also be seen in some patients.
Aortic root and LV dimensions can be increased by
leading edge-to-leading edge method. In experienced
hands, these measurements are valid.
M-mode echocardiography may show systolic anterior
motion of the anterior mitral valve leaflet or chordae.
Two-Dimensional Echocardiography
The parasternal long-axis view is classically used to measure
the LVOT, the aortic annulus and the aortic sinuses.
Leaflet thickening and morphology can be visualized
from this window as well as from the parasternal short-
axis view and the apical five-chamber view. Sometimes,
2D transthoracic echocardiography may not allow correct
identification of the anatomy and causes of AR. In this

Fig. 6.18: Parasternal long-axis view showing reverse doming of the
anterior mitral leaflet in diastole due to impinging aortic regurgitation
jet (white arrow) with partial mitral valve closure.
Fig. 6.20: Parasternal short-axis view showing anatomical regurgitant
area.
situation, 3D echo could provide better delineation of the
aortic valve morphology. In some cases, transesophageal
echocardiography is needed particularly for assessing the
mechanisms and causes of AR as well as the aortic root
dimensions.
Several 2D echo findings can be observed in AR.
If the regurgitant jet impinges on the anterior mitral
valve leaflet, a reverse doming (concavity toward
the ventricular septum) of the anterior leaflet can be
observed on the parasternal long-axis view (Fig. 6.18).
As a result, the leaflet presents a high-frequency
Aortic Valve Regurgitation 103
Fig. 6.19: Color flow jet of aortic regurgitation impinging upon the
anterior mitral leaflet (arrow) resulting in closure of the mitral valve in
diastole (parasternal long-axis view).
fluttering during diastole and its opening can be
compromised (Fig. 6.19).
The M-mode echo can confirm the fluttering motion of
the anterior leaflet.
It can also appear on the mitral valve chordae or the
interventricular septum. Its absence cannot rule out
the diagnosis of AR and a pseudofluttering can be
observed in atrial fibrillation and in hyperkinetic
circulatory states.
The M-mode echo is also helpful in demonstrating
the premature mitral valve closure as a sign of severe,
usually acute, AR.
Anatomical regurgitant orifice can be seen quite often
in short-axis view (Fig. 6.20). The orifice provides direct
clue to the severity. It is usually larger than the effective
regurgitant area measured by the color Doppler flow
convergence method. Aortic Regurgitation is usually
severe if the planimetric area exceeds 0.5 cm2. However,
it may vary in phases of diastole. Early diastolic area
provides the largest size while the end-diastolic is the
smallest.
Presence of aortic valve vegetation, a flail aortic leaflet,
aortic cusp retraction and shortening, or aortic root
abnormalities are discernible with reasonable ease.
Determination of LV dimensions and systolic function
is central to the decision regarding the timing of
surgery. In asymptomatic subjects, LV end-systolic
internal dimension 50 mm and/or ejection fraction
< 0.55 are usual indications for surgery.
104 Section 2: Valvular Heart Disease
Fig. 6.21: Concept of aortic regurgitant volume. Systemic stroke
volume can be estimated at mitral orifice and total stroke volume in
left ventricular outflow tract. The difference provides the regurgitant
volume.
Fig. 6.23: Eccentric aortic regurgitation jet due to perforation (arrow).
Presence of diastolic mitral regurgitation indicates markedly elevated
left ventricle diastolic pressure.
VOLUMETRIC SEVERITY OF
AORTIC REGURGITATION
The total forward volume across a regurgitant orifice is
the sum of systemic SV and regurgitant volume.
Hence, regurgitant volume can be obtained by
calculating the difference between the total SV
(regurgitant valve) and systemic SV (competent valve).
R Vol = SV regurgitant valve SV competent valve.
In AR, the regurgitant volume corresponds to the
difference between the LVOT SV (total) and the mitral
inflow volume (competent valve, Fig. 6.21).
Fig. 6.22: Parasternal long-axis view in a patient with mitral stenosis
and aortic regurgitation. Note the central jet of aortic regurgitation.
In both, effective regurgitant area is calculated as
R Vol divided by timevelocity integral (TVI) of the
regurgitant jet velocity recorded by continuous wave
(CW) Doppler (EROA = R Vol/TVI regurgitant jet).
Regurgitant fraction is expressed as regurgitant flow
divided by total flow.
Regurgitant volume can be obtained by combined
Doppler and 2D/3D volumetry of the LV.
In presence of multivalvular regurgitation, it is not
possible to use this simple formula.
COLOR FLOW DOPPLER EVALUATION OF
AORTIC REGURGITATION
It is a semiquantitative method to assess AR.
Parasternal long- and short-axis views are used
because of better axial resolution.
Color jet area and length do not correlate with severity
of AR and should not be used.
Central jets are found in rheumatic heart disease
(Fig. 6.22), while eccentric jets occur in prolapse or
perforation (Fig. 6.23).
Height of AR jet/ LVOT height can be used as a criterion
for judging severity of AR.7 A ratio of > 0.65 indicates
severe AR ( Fig. 6.24).
Measuring jet height in LVOT is different from
measuring vena contracta. Jet height is measured in
divergence zone when jet is expanding. Jet expansion
may be erratic in eccentric flow jets.

Fig. 6.24: Aortic regurgitation jet height is nearly two-thirds of the left
ventricular outflow tract height, indicating severe aortic regurgitation.
Fig. 6.26: Eccentric jet of severe aortic regurgitation (arrow) in a
patient with bicuspid aortic valve.
AORTIC REGURGITATION ASSESSMENT
BY VENA CONTRACTA
For AR, imaging of the vena contractathe regurgitant jet
as it traverses the aortic orifice or the effective regurgitant
areais obtained from the parasternal long-axis view
(Fig. 6.25).
To properly identify the vena contracta, the three
components of the regurgitant jet should be visualized
(convergence zone, vena contracta and divergence
zone).
A narrow color sector scan coupled with the zoom
mode is recommended to improve measurement
accuracy.
Aortic Valve Regurgitation 105
Fig. 6.25: Arrows point to the vena contracta with convergence in
aorta and divergence in the left ventricular outflow tract.
Vena contracta represents the smallest flow diameter
at the level of the aortic valve in the LVOT, immediately
below the flow convergence region (Fig. 6.25).
It provides, thus, an estimate of the size of the effective
regurgitant orifice area (EROA) and is smaller than the
regurgitant jet width in the LVOT.8
Using a Nyquist limit of 50 to 60 cm/s, a vena contracta
width of < 3 mm correlates with mild AR, whereas a
width of > 6 mm indicates severe AR.
The measurement of the vena contracta is affected by
several factors as the presence of multiple jets. In this
situation, the respective widths of the vena contracta
are not additive.
The concept of vena contracta is based on the assum
ption that the regurgitant orifice is almost circular. The
orifice is, however, often elliptical or irregular, which
changes the width of the vena contracta in different
views (Fig. 6.26).
3D color Doppler echo has been shown to be a useful
tool in the visualization of the actual shape of the
regurgitant orifice and could be used to measure the
vena contracta.9 With 3D echo, an EROA of < 20 mm2
and an EROA of > 60 mm2 have been proposed to
define mild AR and severe AR, respectively (Fig. 6.27).
PROXIMAL ISOVELOCITY SURFACE AREA
FLOW CONVERGENCE METHOD
The assessment of the flow convergence zone is less often
performed in AR than in mitral regurgitation.
Imaging of the flow convergence zone is obtained from
the apical three- or five-chamber or parasternal long-
axis or upper right parasternal views (Fig. 6.28).
106 Section 2: Valvular Heart Disease
Fig. 6.27: Three-dimensional transthoracic echocardiographic color
flow jet area of aortic regurgitation at its narrowest orifice. Note the
irregular shape.
Fig. 6.29: Transesophageal echocardiographic long-axis view show
ing aortic regurgitation jet through eccentric orifice. Vena contracta is
small but proximal isovelocity surface area is large.
The area of interest is zoomed, the sector size is reduced
as narrow as possible to maximize frame rate and the
Nyquist limit is adjusted to obtain a clearly visible,
round and measurable proximal isovelocity surface
area (PISA) radius.10
The color flow velocity scale is shifted toward the
direction of the jet. The PISA radius is measured from
a stop frame as the distance between the regurgitant
orifice and the first aliasing in early diastole (closest to
the peak of regurgitant velocity).
When imaged from the apical window, the PISA
method significantly underestimates AR severity in the
Fig. 6.28: Apical view showing proximal isovelocity surface area
(arrows) with a hemispheric appearance.
presence of eccentric AR jets. In this situation, imaging
the flow convergence zone from the parasternal long
axis improves the accuracy of the PISA method.
For central AR jets, the apical view remains the most
appropriate.
The PISA method has several limitations. First, it is not
feasible in a significant percentage of patients with AR
due to interposition of valve tissue and difficulty in
correctly identifying the flow convergence zone.
Nonplanar flow convergence zones that invalidate the
hemispheric assumption are potential causes of either
under- or over-estimation of AR severity by the PISA
method (Fig. 6.29).
Grading of the severity of AR classifies regurgitation
as:10
Mild: EROA < 10 mm2 and regurgitant volume < 30 mL
Moderate: EROA 10 to 29 mm2 and regurgitant volume
30 to 59 mL
This can be further subdivided into mild-to-moderate
(EROA 10 to 19 mm2) and moderate-to-severe (EROA
20 to 29 mm2).
Severe: An EROA 30 mm2 or a regurgitant volume of
60 mL indicates severe AR.
DIASTOLIC FLOW REVERSAL IN THE
DESCENDING AORTA AND SEVERITY OF
AORTIC REGURGITATION
Aortic regurgitation can lead to diastolic flow reversal in
the aorta (Figs 6.30 and 6.31), which can be assessed by
several Doppler techniques.

Fig. 6.30: Color Doppler flow reversal in descending thoracic aorta.
(LCCA: Left common carotid artery; LSCA: left subclavian artery).
Fig. 6.32: Pulsed wave Doppler interrogation of the descending tho
racic aorta showing an end-diastolic velocity of 60 cm/s in a pattern of
pan-diastolic flow reversal.
The flow reversal is best imaged in the upper descending
aorta at the aortic isthmus level using a suprasternal
view by using pulsed Doppler (Fig. 6.31).
The sample volume is placed just distal to the origin of
the left subclavian artery and it is aligned as much as
possible along the major axis of the aorta.
The Doppler filter is decreased to its lowest setting to
allow detection of low velocities (< 10 cm/s).
With milder degrees of regurgitation, there is a brief
reversal of flow limited to early diastole. As the degree
of the regurgitation increases, the duration and the
velocity of the reversal flow increases.11
It becomes sustained throughout diastole at velocities
exceeding 20 cm/s in severe AR11 (Fig. 6.32).
Aortic Valve Regurgitation 107
Fig. 6.31: Pan-diastolic flow reversal just below the left subclavian
artery by pulsed wave Doppler. The late rise in diastolic velocity is due
to change in effective regurgitant orifice area.
Fig. 6.33: Holodiastolic flow reversal in abdominal aorta.
Significant holodiastolic reversal in the abdominal
aorta is also a sensitive sign of severe AR (Fig. 6.33).
However, in the case of reduced aortic compliance
(advancing age) or in the presence of increased heart
rate, the duration and velocity of flow reversal may be
increased.
In severe acute AR, diastolic velocity decreases quickly
with no end-diastolic velocity due to equalization of
aortic and LV diastolic pressures.
PRESSURE HALF-TIME OF
AORTIC REGURGITATION SIGNAL
The rate of deceleration of the diastolic regurgitant jet and
the derived pressure half-time reflect both the degree of
108 Section 2: Valvular Heart Disease
A B
Figs 6.34A and B: In panel A, CW spectra of aortic regurgitation. In
panel B, pressure half-time is much shorter due to severe aortic re
gurgitation.
Fig. 6.36: CW Doppler spectrum in acute aortic regurgitation. Pres
sure half-time is < 100 ms and end-diastolic forward flow (arrows) is
also seen due to left ventricle end-diastolic pressure exceeding aortic
diastolic pressure.
regurgitation and the ventricular end-diastolic pressures.12
As the degree of AR increases, the aortic diastolic pressure
decreases and the LV end-diastolic pressure increases
(Figs 6.34A and B).
The late diastolic jet velocity is thus reduced and the
pressure half-time shortened. A pressure half-time of
< 200 ms is consistent with severe AR, whereas a value of
> 500 ms suggests mild AR (Fig. 6.35).
The pressure half-time is dependent upon chamber
compliance in addition to chamber pressures.
For a given severity of AR, pressure half-time may be
further reduced by elevated LV diastolic pressures
Fig. 6.35: Comparing mild aortic regurgitation (left panel) with severe
aortic regurgitation (right panel). The right panel shows hardly any
pressure gradient in end diastole, indicating markedly left ventricle
elevated diastolic pressure.
or prolonged in patients with increase in peripheral
resistance or who have a dilated aorta with increased
aortic compliance.
It tends to normalize with chronic LV adaptation to AR.
Hence, its sensitivity and specificity in detecting severe
AR are modest.
Accurate measurement of pressure half-time is also
dependent on obtaining an adequate spectral envelope
of the regurgitant jet.
In acute severe AR, pressure half-time is markedly
shortened, the CW spectrum of AR may become
triangular and diastolic forward flow may be seen in
end-diastole (Fig. 6.36).
M-MODE COLOR FLOW
PROPAGATION VELOCITY
Although not commonly used, M-mode color flow
propagation velocity 80 cm/s has been suggested as a
useful criterion to detect severe AR.13
SUMMARY OF AORTIC
REGURGITATION ASSESSMENT
BY ECHO-DOPPLER METHODS
Minimum information that needs to be provided while
reporting on a patient with AR is shown below.1416
Possible etiology should be mentioned after studying
the valve anatomy and function.
Severity or grade of AR should be mentioned by an
integrated multiparametric approach using jet width,

vena contracta, pressure half-time, flow reversal in
thoracic aorta and PISA method whenever feasible.
Eccentricity of jet and its origin should be recorded.
Density of signal is not a useful criterion.
Size of aortic root and ascending aorta should be
reported.15
Consequences of AR that need to be reported are
LV dimensions and volumes, and ejection fraction.
Global longitudinal strain is fast emerging as a useful
prognostic factor.
Right heart size, function and pulmonary pressures
along with indexed left atrial volume should form part
of the report.
3DE EORA may become a useful index once the
technique is standardized.16
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7. Perry GJ, Helmcke F, Nanda NC, et al. Evaluation of aortic
insufficiency by Doppler color flow mapping. J Am Coll
Cardiol. 1987;9(4):9529.
8. Tribouilloy CM, Enriquez-Sarano M, et al. Assessment of
severity of aortic regurgitation using the width of the vena
contracta: A clinical color Doppler imaging study. Circula-
tion. 2000;102(5):55864.
9. Fang L, Hsiung MC, Miller AP, et al. Assessment of aor-
tic regurgitation by live three-dimensional transthoracic
echocardiographic measurements of vena contracta area:
usefulness and validation. Echocardiography. 2005;22(9):
77581.
10. Tribouilloy CM, Enriquez-Sarano M, Fett SL, et al. Applica-
tion of the proximal flow convergence method to calculate
the effective regurgitant orifice area in aortic regurgitation.
J Am Coll Cardiol. 1998;32(4):10329.
11. Tribouilloy C, Avine P, Shen WF, et al. End diastolic flow
velocity just beneath the aortic isthmus assessed by pulsed
Doppler echocardiography: a new predictor of the aortic
regurgitant fraction. Br Heart J. 1991;65(1):3740.
12. Samstad SO, Hegrenaes L, Skjaerpe et al. Half time of the
diastolic aortoventricular pressure difference by continu-
ous wave Doppler ultrasound: a measure of the severity of
aortic regurgitation? Br Heart J. 1989;61(4):33643.
13. Onbasili OA, Tekten T, Ceyhan C, Ercan E, Mutlu B. A new
echocardiographic method for the assessment of the sever-
ity of aortic regurgitation: color M-mode flow propagation
velocity. J Am Soc Echocardiogr. 2002;15(12):145360.
14. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. American
Society of Echocardiography. Recommendations for evalu-
ation of the severity of native valvular regurgitation with
two-dimensional and Doppler echocardiography. J Am Soc
Echocardiogr. 2003;16(7):777802.
15. Kang JW, Song HG, Yang DH, et al. Association between
bicuspid aortic valve phenotype and patterns of valvular
dysfunction and bicuspid aortopathy: comprehensive eval-
uation using MDCT and echocardiography. JACC Cardio-
vasc Imaging. 2013;6(2):15061.
16. Ewe SH, Delgado V, van der Geest R, et al. Accuracy of
three-dimensional versus two-dimensional echocardio
graphy for quantification of aortic regurgitation and vali-
dation by three-dimensional three-directional velocity-
encoded magnetic resonance imaging. Am J Cardiol.
2013;112(4):5606.
 Chapter
7 Tricuspid Valve
introduction
Tricuspid valve disorders are common although more
often of functional nature. Organic tricuspid valve disease
can be either similar to that which affects the mitral valve
or unique to it. Tricuspid valve disorders are mostly
congenital and rheumatic although carcinoid, anorexi
genic valvulopathy, infective endocarditis, myxomatous
degeneration also afflict this valve. Functional tricuspid
valve disorders secondary to long standing pacing leads in
the right ventricle are subject of recent interest. Functional
disorders are usually secondary to left-sided disease
and help in assessment of pulmonary arterial and the
right ventricular pressures. Both functional and organic
disorders have impact on prognosis that can be altered
by appropriate management. The most common cause
of tricuspid regurgitation is not a primary disease but
rather an impaired valve coaptation caused by a dilation
of the right ventricle and/or of the tricuspid annulus.
The tricuspid valve is a complex structure that, unlike
the aortic and mitral valve, is not possible to visualize in
one cross-sectional view using either transthoracic or
transesophageal two-dimensional echocardiography
(2DE; i.e. imaging all three leaflets and their attachment
in the annulus simultaneously). Conversely, three-
dimensional echocardiography (3DE) allows users to
visualize the whole tricuspid valve apparatus from any
perspective and is currently gaining prominence.
FUNCTIONAL MORPHOLOGY OF THE
TRICUSPID VALVE
The tricuspid valve complex consists of (Figs 7.1 to 7.4):
Three leaflets (anterior, posterior and septal)
The chordae tendinae
Two or three discrete papillary muscles (large variation)
Fibrous tricuspid annulus
Right atrial and right ventricular myocardium
Successful valve function depends on the integrity and
coordination of these components.13
The anterior leaflet is the largest, whereas the posterior
leaflet is notable for the presence of multiple scallops. The
septal leaflet is the smallest and arises medially directly
from the tricuspid annulus above the interventricular
septum. The anterior papillary muscle provides chordae
to the anterior and posterior leaflets, and the medial
papillary muscle provides chordae to the posterior and
septal leaflets.3
The septal wall gives chordae to the anterior and septal
leaflets (there is no formal septal papillary muscle as with
the anterior and posterior (medial) papillary muscles).
In addition, there may be accessory chordal attachments
to the right ventricular free wall and to the moderator
band. These multiple chordal attachments are important
mediators of tricuspid valve regurgitation (TR), as they
impair proper leaflet coaptation in the setting of right
ventricular dysfunction and dilation (Fig. 7.5).
 Tricuspid Valve 111

Fig. 7.1: Schematic diagram showing tricuspid valve apparatus laid Fig. 7.2: Schema showing en face view of the tricuspid annulus with
open longitudinally. leaflets and posterior relationships.

Fig. 7.3: 2D echocardiographic four-chamber view (left panel) compared with anatomical specimen (right panel). (AL: Anterior leaflet; SL: Septal
leaflet; MS: Membranous interventricular septum; AML: Anterior mitral leaflet).

The septal aspect of the tricuspid annulus is considered algorithms have been based on the dimension of the base
to be analogous to the intertrigonal portion of the mitral of the septal leaflet.
annulus in that it is relatively spared from annular Tricuspid valve is the most apically placed valve with
dilation. Because of this property, tricuspid annular sizing the largest orifice. Position of septal attachment of the
112 Section 2: Valvular Heart Disease

Fig. 7.4: 3D echocardiographic en face view (left panel) compared with anatomical specimen (right panel) seen from above. (MV: Mitral valve;
PL: Posterior leaflet; IVC: Inferior vena cava; SVC: Superior vena cava; RAA: Right atrial appendage).

Fig. 7.5: Aberrant chords (right panel) contrasted with normal arrangement (left panel).
 Tricuspid Valve 113

Fig. 7.6: Attachment of the septal (anterior) mitral leaflet is superior Fig. 7.7: Atrioventricular discordance shown in four-chamber view.
(white arrow) to that of tricuspid septal leaflet (yellow arrow). The right ventricle is identified by the position of the septal leaflet of
the tricuspid valve as well as by the moderator band.

parasternal short-axis view) systematically underestimate

the actual tricuspid annulus size. Role of annular dilatation
centers around the right ventricular (RV) free wall portion
of the annulus as the primary lesion.

CONDITIONS AFFECTING
TRICUSPID VALVE
Functional Tricuspid Regurgitation (FTR)
Idiopathic FTR
Hypertensive FTR
Diastolic TR
Organic TR and TS (Anatomically abnormal valves)
Rheumatic
Fig. 7.8: 3D shape of the tricuspid annulus which is elliptical and sad- Infective endocarditis
dle-shaped. Ebsteins anomaly
Floppy (prolapse)
valve compared to that (anterior mitral leaflet) on the Congenital (non-Ebsteins)
left side helps in identification of the morphological right Carcinoid
ventricle (Figs 7.6 and 7.7). The longitudinal height of this Trauma
difference is about 10 mm. Connective tissue disorder (Marfans)
The tricuspid annulus shows a nonplanar structure Rheumatoid arthritis
with an elliptical saddle-shaped pattern having two high Radiation therapy
points superiorly and two low points oriented inferiorly The Carpentiers classification remains the most
that is best seen in midsystole.4 The normal TV annulus commonly used functional classification:5
is saddle shaped, with the highest points located in an Type I: leaflet perforation (infective endocarditis) or
anteriorposterior orientation and the lowest points in a more frequently by annular dilatation
medio-lateral orientation (Fig. 7.8). Type II: prolapse of one or more leaflets (tricuspid
The tricuspid annulus shape is not circular but oval valve prolapse)
both in normal-sized and in dilated annulus. Currently Type III: restricted motion as the consequence
used tricuspid annulus diameters measured with 2DE of rheumatic disease, significant calcifications, toxic
(both measured in apical four-chamber view and in valvulopathy, FTR.
114 Section 2: Valvular Heart Disease
REMODELLING IN TRICUSPID
REGURGITATION
TR leads to RA and RV dilatation, a dilated and pulsatile
inferior vena cava and hepatic vein, a dilated coronary
sinus and systolic bowing of the interatrial septum toward
the LA. Absence of these changes suggests milder degree
of TR. Imaging the vena cava and its respiratory variation
also provides an evaluation of RA pressure. Although not
specific, a rapid anterior motion of the interventricular
septum at the onset of systole (paradoxical ventricular
septal motion) is a sign of RV volume overload due to
severe TR.
Annulus diameter measured in apical four-chamber
view (> 2.1 cm/M2) can both be the cause or effect of TR
and also the threshold for intervention.6
FUNCTIONAL TR
One of the commonest observations during echocar
diographic examinations is the presence of FTR. Nearly
5060% of young adults exhibit mild TR and its prevalence
increases with age. Up to 15% of normal people have
moderate TR. Usually, substantial redundancy of leaflet
tissue prevents TR in normal tricuspid valves (ratio
leaflets/annular length > 1.45; Fig. 7.9). Tricuspid leaflets
length (septal + anterior leaflets) can be easily measured
and ratio to systolic annulus diameter is calculated to
assess valvular coverage of annulus in systole.
FTR is characterized by structurally normal leaflets
and is due to the deformation of the valvulo-ventricular
Fig. 7.9: Apical four-chamber view showing coaptation of the tricuspid
valve (arrows). Note striking coaptation distance due to redundancy
of the leaflets.
complex.6 While mild FTR is frequent and usually benign,
patients with severe FTR may develop progressive
ventricular dysfunction and incur increased mortality.
FTR is dependent on annular dilatation, with
significant TR occurring with > 40% dilatation. A central
zone of leaflet malcoaptation is consistent with annular
dilatation demonstrating the dependence on the 3 leaflets
coapting simultaneously (Fig. 7.10).
FTR often appears in conjunction with left-sided valve
disease and left ventricular (LV) dysfunction despite the
presence of a structurally normal tricuspid valve. This is
usually associated with elevated right ventricular systolic
pressure.
Idiopathic FTR (due to ageing, atrial fibrillation etc) is
characterized by (Fig. 7.11):
Dilated annulus
Incomplete valve coverage
Conical right ventricular shape with basal dilatation
only
No leaflet tethering
Decreased RV systolic function
Hypertensive FTR is characterized by (Figs 7.12
and 7.13):
Annular dilatation
Spherical or elliptical RV dilatation
Leaflet tethering
Apparently normal RV systolic function due to volume
overload.
Hypertensive FTR is predominantly due to valve
deformation with tenting and only modest annular
enlargement. Valvular tenting and leaflet tethering are
linked to RV elongation and deformation (Fig. 7.13).
Fig. 7.10: Dilated annulus causing central malcoaptation responsible
for tricuspid valve regurgitation (TR) (arrows). A 3DE en face view in
systole.

Fig. 7.11: Idiopathic functional tricuspid regurgitaion characterized by
incomplete coaptation without leaflet tethering (2DE picture on left side
and the schematic diagram on the right side).
Fig. 7.13: Hypertensive functional tricuspid regurgitation in mitral
stenosis (MS) showing symmetrical leaflet tethering and tenting height
of 12 mm.
With FTR, the annulus becomes larger, more
planar and circular. Anterior leaflet is responsible for
compensating for an increase in orifice area as a result of
annular dilatation.7 Patients with annular dilatation but
no TR have longer leaflets, specifically the anterior leaflet
(Fig. 7.14).
Diastolic TR can occur in certain conditions, e.g., heart
block, atrial flutter, severe pulmonary regurgitation, and
restrictive cardiomyopathy, due to reversal of pressure
gradient between RA and RV during diastole (Figs 7.15
and 7.16).
Tricuspid Valve 115
Fig. 7.12: Hypertensive functional tricuspid regurgitaion is charac
terized by leaflet tethering (left panel) with definite tenting height and
area (right panel).
Fig. 7.14: Apical four-chamber view showing dilated annulus with
elongated anterior leaflet as a compensatory mechanism.
ORGANIC TRICUSPID VALVE DISORDERS
Tricuspid valve is examined in different views to obtain
complete anatomic information. Parasternal long-axis
view of the RV inflow is obtained by tilting the probe
inferomedially and rotating it slightly clockwise from
the parasternal long-axis view of the LV. This incidence
reveals the anterior tricuspid leaflet (near the aortic valve)
and the posterior tricuspid leaflet. Parasternal short-axis
view, at the level of the aortic valve, apical four-chamber
view and subcostal four-chamber view visualize the septal
and the anterior tricuspid leaflets (Fig. 7.17).
116 Section 2: Valvular Heart Disease
Fig. 7.15: Diastolic TR (arrows) along with systolic TR in presence of
first degree AV block.
Fig. 7.17: Various views used to study the tricuspid valve.
Fig. 7.19: Para-sternal long axis view in diastole showing doming of
the mitral valve with narrowed orifice. There is thickening of the aortic
valve with significant aortic regurgitation.
Fig. 7.16: Diastolic TR (arrows) along with systolic TR in restrictive
cardiomyopathy and atrial fibrillation.
Fig. 7.18: Apical four-chamber view showing rheumatic tricuspid and
mitral stenosis (left panel) and tricuspid regurgitation (left panel).
Thickening of both leaflets with doming is obvious.
Most patients with rheumatic tricuspid valve disease
present with TR or a combination of stenosis and
regurgitation.8 Rheumatic TS does not occur as an isolated
lesion, but it often accompanies mitral and aortic valve
disease (Figs 7.18 and 7.19).
Rheumatic involvement of the TV is less common
(25%) than that of left-sided valves. Regurgitation is a
consequence of deformity, shortening and retraction of
one or more leaflets of the TV as well as shortening and
fusion of the chordae tendinae and papillary muscles.9 The
2DE usually detects thickening and the distortion of the
leaflets but cannot provide a comprehensive assessment
of extension of valve apparatus involvement (Fig. 7.20).
The full-volume data set from apical approach usually
provides a comprehensive assessment of the whole
TV apparatus, which can be examined from different

Fig. 7.20: Modified RV inflow view showing tethered and thickened
leaflets causing free flow TR (right panel).
Fig. 7.22: 3DE en face view in systole showing regurgitant orifice and
in diastole showing fusion of all three commissures with narrowed
tricuspid diastolic orifice.
perspectives.10 The en face view of the TV obtained
by RT-3DE allows the visualization of the commissural
fusion, which is helpful to establish a correct diagnosis of
rheumatic aetiology of TV regurgitation (Figs 7.21 to 7.23).
The 3D TEE produces an en face view of all the three
valve leaflet/cusps simultaneously. This allows more
detailed morphological assessment of each individual
leaflet/cusp as well as coaptation between leaflets.
Involvement of subvalvular apparatus is identified and
better characterized. There is improved delineation of the
Tricuspid Valve 117
Fig. 7.21: 3DE en face view from the ventricular aspect in diastole.
Tricuspid leaflets are thickened and commissures are patent; the
orifice is wide open compared to severe mitral stenosis with narrow
orifice and thick leaflets.
Fig. 7.23: Nodular thickening of the mitral valve leaflets as well as the
septal leaflet of the tricuspid valve. A cleft is seen in the anterior tricus-
pid leaflet. Arrows point to the three commissures.
spatial relationship between valve, subvalvular apparatus
and the endocardium of surrounding chambers (Fig. 7.23).
In the carcinoid disease, the valve appears thickened,
fibrotic with markedly restricted motion during cardiac
cycle11 (Fig. 7.24). The RT-3DE can show the regions of
ineffective leaflet coaptation and the lack of commissural
fusion.
Tricuspid valve infective endocarditis is rare and
accounts for 510% of infective endocarditis.12 Its
predispositions are congenital heart disease, insertion of
118 Section 2: Valvular Heart Disease
Fig. 7.24: Thickened and shortened tricuspid valve leaflets in Carci-
noid heart.
Fig. 7.26: Large vegetations on ventricular surface of the tricuspid
leaflets (arrow) in a patient on hemodialysis.
a central venous catheter, placement of a pacemaker or
implantable defibrillator, a history of intravenous drug use
and hemodialysis (Figs 7.25 and 7.26).
Pulmonary embolism occurs in 75100% cases of
tricuspid valve endocarditis.
Degenerative Tricuspid Valve Disease
Three types of tricuspid changes can be visualized:
1. Billowing valve
2. Prolapsing valve
3. Flail tricuspid valve
Fig. 7.25: Vegetation on the tricuspid valve (arrow) in presence of
central intravenous line.
Fig. 7.27: Apical four-chamber view showing flail anterior leaflet
(white arrow) with severe TR (right panel).
Tricuspid prolapse is generally associated with mitral
valve prolapse and is defined as a midsystole posterior
leaflet displacement beyond the annular plane. The
coaptation line is behind the annular plane. Tricuspid
prolapse most often involves the septal and anterior
tricuspid leaflets. The most common phenotype of
tricuspid prolapse is diffuse myxomatous degeneration
(Barlows disease). A flail tricuspid leaflet is observed when
the free edge of a leaflet is completely reversed in the RA
(Fig. 7.27), usually as a consequence of ruptured chordae
(degenerative TR, infective endocarditis, trauma).

Fig. 7.28: Thickened mitral and tricuspid valve leaflets with normal
thickness of chords in a case with degenerative MR.
Fig. 7.30: Ebstein anomaly. Apical four-chamber view showing normal
insertion of the anterior leaflet along the free wall and rudimentary
displaced septal leaflet along the interventricular septum.
Fibroelastic degeneration also occurs in tricuspid
valve, albeit much less common as the chamber pressures
are low. However, it has morphological features and
hemodynamic consequences similar to that seen in mitral
valve (Fig. 7.28).
Ebstein anomaly is a congenital heart defect in which
the septal leaflet of the tricuspid valve is displaced toward
the apex of the right ventricle of the heart. The annulus
of the valve is still in the normal position.13 However, the
valve leaflets are, to a varying degree, attached to the walls
and septum of the right ventricle. There is subsequent
Tricuspid Valve 119
Fig. 7.29: Apical four-chamber view showing large anterior leaflet and
apically displaced septal leaflet of the tricuspid valve.
Fig. 7.31: Modified long axis view of the right heart structures showing
displacement of posterior (along free wall) and the septal leaflet result-
ing in an atrialized chamber.
atrialization of a portion of the morphologic right
ventricle (which is then contiguous with the right atrium).
This causes the right atrium to be large and the anatomic
right ventricle to be small in size (Fig. 7.29).
Typically, there are anatomic abnormalities of the
tricuspid valve, with enlargement of the anterior leaflet
of the valve. The other leaflets are described as being
plastered to the endocardium (Figs 7.30 and 7.31).
About 50% of individuals with Ebstein anomaly have
an associated shunt between the right and left atria, either
an atrial septal defect or a patent foramen ovale.
120 Section 2: Valvular Heart Disease
Fig. 7.32: Rudimentary tricuspid valve leaflets (arrows) with normal
annular attachment and grossly incomplete coverage of the orifice.
Fig. 7.34: Extreme form of tricuspid valve dysplasia showing markedly
dilated annulus with hardly any leaflet tissue.
Fig. 7.36: Apical four-chamber view showing congenital tricuspid
stenosis (arrows). The mitral valve is normal and presence of right
ventricular hypertrophy is due to associated pulmonary stenosis.
Fig. 7.33: Normally attached but thin and flail tricuspid valve leaflet
causing unguarded orifice.
Fig. 7.35: Parasternal four-chamber view showing aneurysmally
dilated right atrium, thrombus (arrow), spontaneous contrast and
hardly any valvular tissue.
Ebstein anomaly typically has TR as the hemodynamic
lesion. However, rarely combined tricuspid regurgitation
with tricuspid stenosis can also occur.
Non-Ebstein anomalies of the tricuspid valve due
to tricuspid valve dysplasia are not rare.14,15 These
are associated with TR and varying degree of right ventri
cular dysfunction and atrial fibrillation subsequently
(Figs 7.32 to 7.35).
TRICUSPID VALVE STENOSIS
Tricuspid valve stenosis (TS) is an uncommon echocar
diographic and pathological lesion and is rarely diagnosed
clinically. The common etiologies are:
Rheumatic (99% of all)
Congenital (Figs 7.36 to 7.38)

Fig. 7.37: Congenital parachute tricuspid valve causing TS.
Fig. 7.39: 3DE en face view showing narrowed orifice of the tricuspid
valve (on left side with) commissural fusion.
Carcinoid
Infective endocarditis
Right atrial myxoma
Anorexic drug abuse
Postsurgical (restrictive annuloplasty)
Trans-tricuspid valve gradients are indicative of
TS although there is no validated cutoff to define TS.
Morphological features with reduced orifice, doming
of the leaflets and commissural fusion usually suggest
presence of TS, which are better appreciated by real-time
3D echocardiography (Fig. 7.39).
Tricuspid Valve 121
Fig. 7.38: Congenital TS with hypoplastic tricuspid annulus. Concavity
of the interatrial septum suggests raised right atrial pressure.
ASSESSMENT OF SEVERITY OF TR
Color Flow Mapping
Color flow jet of TR can be used to estimate rough
severity of TR like that in mitral regurgitation.16 However,
the jet area is dependent upon several hemodynamic
factors besides the machine settings. Hence it is not
recommended to grade severity of TR based upon the jet
area in the right atrium.17 However, if the jet is small and
close to the leaflets, it is likely to be mild TR and if the color
jet fills most of the right atrium and swirls, it is likely to be
severe (Figs 7.40 and 7.41)
VENA CONTRACTA
Vena contracta (VC) or the narrowest jet width just
beyond the regurgitant orifice is a good index of severity
of TR and is usually measured in apical four-chamber
view. A VC width of > 7 mm suggests severe TR while
< 6 mm is indicative of mild or moderate TR.18 Mild
and moderate cannot be distinguished by width of VC
(Fig. 7.42). Geometry of the regurgitant orifice is
complex and 2D VC does not have good correlation with
3DE regurgitant orifice area. Proposed 3DE new criteria
for estimating TR severity based on VC area or 3DE
color Doppler regurgitant orifice are: < 0.5 cm2 for mild;
0.50.75 cm2 for moderate and > 0.75 cm2 for severe.19
122 Section 2: Valvular Heart Disease
Fig. 7.40: Color flow jet area of TR filling nearly 50% of the right atrium
but no swirling although vena contracta is wide (13 mm) suggestive
of severe TR.
Fig. 7.42: Apical four-chamber view showing TR color flow jet.
Although VC is 10 mm (suggestive of severe TR). Effective regurgitant
orifice area by PISA method is only 7 mm2 indicative of mild TR.
PROXIMAL ISOVELOCITY
SURFACE AREA METHOD
Proximal isovelocity surface area (PISA) method is rarely
used in clinical practice and it is not sure if the regurgitant
jet proximal to the orifice actually makes hemi-spheric
shells in case of the tricuspid valve:
It is usually performed in the four-chamber view.
The area of interest is optimized by lowering imaging
depth and the Nyquist limit to ~1540 cm/s.
Radius of the PISA is measured at midsystole using the
first aliasing (Fig. 7.43).
Fig. 7.41: Large TR color Doppler jet area occupying > 2/3 of the right
atrium. However in view of narrow vena contracta (4 mm) and small
radius of PISA, it is unlikely to be severe.
Fig. 7.43: PISA radius of 5 mm at aliasing velocity of 28.9 cm/sec
should suggest mild TR although the vena contracta width is 7 mm.
Qualitatively, a TR PISA radius > 9 mm at a Nyquist
limit of 28 cm/s alerts to the presence of significant TR,
whereas a radius of < 5 mm suggests mild TR17
An effective regurgitant orifice area (ERO) of 40 mm2
or a regurgitant volume of 45 mL indicates severe TR.
There is a good chance of underestimation of the TR
severity by this method (Figs 7.42 and 7.43).
ANTEROGRADE VELOCITY OF
TRICUSPID INFLOW
The severity of TR will affect the early tricuspid diastolic
filling. In the absence of tricuspid stenosis, the peak

Fig. 7.44: Peak early diastolic tricuspid valve velocity of 200 cm/s
(right panel) in a patient with no TS (left panel), suggesting severe TR.
Fig. 7.46: Marked blunting of antegrade systolic waves (arrows) in
hepatic vein in TR. Blunting lacks specificity.
E velocity increases in proportion to the degree of TR.
Tricuspid inflow Doppler tracings are obtained at the
tricuspid leaflet tips. A peak E velocity 1 m/s suggests
severe TR (Fig. 7.44).
HEPATIC VEIN FLOW IN
ASSESSMENT OF TR
In normal individuals, the pattern of flow velocity in
hepatic veins consists of antegrade systolic (S), transient
flow reversal as the TV annulus recoils at the end of
systole, antegrade diastolic (D) and a retrograde A wave
(AR) caused by atrial contraction (Fig. 7.45).
With increasing severity of TR, there is a decrease in
hepatic vein systolic velocity. In severe TR, systolic flow
Tricuspid Valve 123
Fig. 7.45: Normal hepatic vein flow pattern.
Fig. 7.47: Dense CW Doppler envelope of severe TR.
blunting or reversal occurs (Fig. 7.46). The sensitivity of
flow reversal for severe TR is 80%. Thus the absence of
systolic flow reversal does not rule out severe TR. Blunted
systolic hepatic vein flow can be observed in case of
abnormal right atrial and RV compliance, atrial fibrillation
and elevated right atrial pressure from any cause. Blunting
of hepatic flow may thus lack specificity.17
Continuous Wave Doppler
Interrogation for TR Signal
Density of the continuous wave (CW) envelope of the
TR jet can be a guide to TR severity.
A dense TR signal with a full envelope indicates more
severe TR than a faint signal (Fig. 7.47).
124 Section 2: Valvular Heart Disease
Fig. 7.48: Severe TR with triangular shape of the CW spectrum in
systole due to elevated right atrial pressure. Early diastolic velocity of
120 cm/s and dense envelope suggest severe TR.
Fig. 7.50: CW Doppler signal alternans of TR.
The CW Doppler envelope may be truncated (notch)
with a triangular contour and an early peak velocity
(blunt). This indicates elevated right atrial pressure or
a prominent regurgitant pressure wave in the RA due to
severe TR (Fig. 7.48).
Marked respiratory variation (decreased TR velocity
with inspiration) suggests an elevated RA pressure and
indirectly severe TR (Fig. 7.49).
Massive TR is often associated with a low jet velocity
(< 2 m/s) as there is near equalization of RV and RA
pressures (Figs 7.48 and 7.49).
The CW Doppler TR signal alternans is usually
associated with severe TR (Fig. 7.50).
Fig. 7.49: Respiratory variation of TR signal with decrease in velocity
during expiration (white arrow) compared to inspiration (red arrow).
SUMMARY
Tricuspid valve regurgitation is likely to be mild when:
No RA/RV dilatation and no malcoaptation are seen
on 2DE
There is small or narrow central color Doppler jet
There is no annular dilatation
Width of VC is < 7 mm
PISA radius is < 5 mm at a Nyquist limit of 28 cm/sec
There is normal hepatic vein flow during systole
Tricuspid early diastolic velocity is < 100 cm/s
There is a faint or incomplete CW Doppler envelope
Tricuspid valve regurgitation is likely to be severe if,
in absence of other right-sided pathology, following signs
are present:
Dilated right heart structures with paradoxically
moving interventricular septum
Large color Doppler jet area occupying > 50% of the
right atrium with swirling of the jet and entry into the
coronary sinus/superior vena cava and so forth
Dense CW Doppler spectral envelope with triangular
shape
The CW velocity is < 200 cm/s with augmented
respiratory variation
Tricuspid flow E wave velocity is > 100 cm/s without
evidence of obstruction
Width of vena contracta is > 7 mm
PISA radius is > 9 mm at Nyquist limit of 28 cm/s
Regurgitant volume by PISA is > 45 mL
Hepatic vein systolic wave flow reversal

Obviously large patent orifice in systole with no
coaptation.
The more of the above criteria are met, the more is
the likelihood of accuracy. However, criteria 68 should
be considered specific and others as supportive. From a
therapeutic viewpoint, morphology of the tricuspid valve
and geometry of the annulus are equally important.
References
1. Silver MD, Lam JH, Ranganathan N, et al. Morphology of
the human tricuspid valve. Circulation. 1971;43:33348.
2. Ho SY, Nihoyannopoulos P. Anatomy, echocardiography,
and normal right ventricular dimensions. Heart. 2006;92
(Suppl. 1):i2i13.
3. Rogers JH, Bolling SF. The tricuspid valve: current perspec
tive and evolving management of tricuspid regurgitation.
Circulation. 2009;119:2718-25.
4. Fukuda S, Saracino G, Matsumura Y, et al. Three-dimen
sional geometry of the tricuspid annulus in healthy subjects
and in patients with functional tricuspid regurgitation: a
real-time, 3-dimensional echocardiographic study. Circu
lation. 2006;114 (Suppl):I-492I-8.
5. Carpentier A, Deloche A, Hanania G, et al. Surgical
management of acquired tricuspid valve disease. J Thorac
Cardiovasc Surg. 1974;67:5365.
6. Dreyfus GD, Corbi PJ, Chan KM, et al. Secondary
tricuspid regurgitation or dilatation: which should be
the criteria for surgical repair? Ann Thorac Surg. 2005;79:
127-32.
7. Ton-Nu TT, Levine RA, Handschumacher MD, et al.
Geometric eterminants of functional tricuspid regurgi
tation: insights from 3-dimensional echocardiography.
Circulation. 2006;114:143-9.
8. Manoharan S, Mohan JC, Sethi KK, Organic tricuspid
involvement in rheumatic heart diseasea prospective
study by two-dimensional echocardiography. Ind Heart
J. 1986;38:60-3.
Tricuspid Valve 125
9. Deloche A, Guerinon J, Fabiani JN, et al. Anatomical study
of rheumatic tricuspid valve diseases: application to the
various valvuloplasties [in French]. Ann Chir Thorac
Cardiovasc. 1973;12:3439.
10. Badano LP, Agricola E, Perez de Isla L, et al. Evaluation of
the tricuspid valve morphology and function by transtho
racic real-time three-dimensional echocardiography. Eur
J Echocardiogr. 2009;10:477-84.
11. Fox DJ, Khattar RS: Carcinoid heart disease: Presentation,
diagnosis and management. Heart. 2004;90:1224-8
12. Morokuma H, Minato N, Kamohara K, et al. Three surgical
cases of isolated tricuspid valve infective endocarditis. Ann
Thorac Cardiovasc Surg. 2010;16:134-8.
13. Paranon S, Acar P. Ebsteins anomaly of the tricuspid
valve: from fetus to adult: congenital heart disease. Heart.
2008;94:237-43.
14. Mohan JC, Passey R, Arora R. Echocardiographic spectrum
of congenitally unguarded tricuspid valve orifice and patent
right ventricular outflow tract. Int J Cardiol. 2000;74:153-7.
15. Mohan JC, Tandon R. Congenital mitral and tricuspid
stenosis presenting with cyanosis. Ind Heart J. 1986;38:
481-2.
16. Gonzalez-Vilchez F, Zarauza J, Vazquez de Prada JA, et al.
Assessment of tricuspid regurgitation by Doppler color
flow imaging: angiographic correlation. Int J Cardiol.
1994;44:275-83.
17. Lancellotti P, Moura L, Pierard LA, et al. European
association of echocardiography recommendations for the
assessment of valvular regurgitation. Eur J Echocardiogr.
2010;11:307-32.
18. Tribouilloy CM, Enriquez-Sarano M, Bailey KR, et al.
Quanti fication of tricuspid regurgitation by measuring
the width of the vena contracta with Doppler color flow
imaging: a clinical study. J Am Coll Cardiol. 2000;36:472-8.
19. Velayudhan DE, Brown TM, Nanda NC, et al. Quantifi
cation of tricuspid regurgitation by live three-dimensional
transthoracic echocardiographic measurements of vena
contracta area. Echocardiography. 2006;23:793-800.
 Chapter

8 Pulmonary Valve

Introduction
Pulmonary valve is quite often overlooked while perfor
ming echocardiography in adults because of poor acoustic
window and rare organic involvement. However, study
of pulmonary valve and its hemodynamics provide
useful information. Pulmonary valve can get affected
by rheumatic process, carcinoid heart disease, trauma,
infective endocarditis, myxomatous degeneration and
congenital dysplasia. Functional pulmonary regurgitation
is frequent and provides information about pulmonary
pressures. Severe pulmonary regurgitation may result
in the right ventricular (RV) volume overload and heart
failure. Echocardiographic examination of the pulmonary
valve is critical before the Ross procedure. Fig. 8.1: Schematic short-axis view showing relationship of pulmonary
valve leaflets. Left lower panel shows transesophageal echocardio-
graphic image.
ANATOMY OF THE PULMONARY VALVE
The pulmonary valve divides the right ventricular outflow The cusps of the pulmonary valve are supported by free-
tract (RVOT) from the pulmonary artery. In normal standing musculature with no direct relationship with
conditions, the pulmonary valve prevents regurgitation the muscular septum.1 The normal pulmonary valve
of blood from the pulmonary artery back to the right is enclosed in a proximal sleeve of free-standing right
ventricle. It is a semilunar valve with three cusps, and it ventricular infundibulum supporting the fibroelastic
is located anterior, superior and slightly to the left of the walls of the pulmonary sinuses at the anatomical
aortic valve (Fig. 8.1). ventriculoarterial junction. The valvular leaflets are
The pulmonary valve is formed by three cusps, each attached in semilunar fashion across this junction,
with a fibrous node at the midpoint of the free edges as well delimiting the extent of the valvular sinuses.
as lunulae, which are the thin, crescent-shaped portions of The cusps are much thinner and lack a fibrous
the cusps that serve as the coaptive surfaces of the valve continuity with the anterior leaflet of the right atrio
(Figs 8.2 and 8.3). ventricular valve.

Fig. 8.2: Schematic diagram showing three cusps or leaflets of the
pulmonary valve without any definite fibrous annulus.
Fig. 8.4: Transthoracic echocardiographic subcostal coronal view.
Red arrows point to ventriculoarterial junction and the white arrow
shows the extent of pulmonary sinuses of Valsalva.
The cusps are defined by their relationship to the aortic
valve and are thus termed anterior or nonseptal, right
and left cusps.2,3 They can also be defined by their
relationship to a commissure found in the pulmonary
and aortic valves and hence termed right adjacent
(right facing), left adjacent (left facing) and opposite
(non-facing).
Anatomical studies have failed to demonstrate any
well-defined fibrous annulus that could be of clinical
relevance.
Pulmonary root is that part of the RVOT that supports
the leaflets of the pulmonary valve.4 It is limited distally by
the sinotubular junction (Fig. 8.4). Its components are:
Sinuses of Valsalva
Valvular leaflets
Pulmonary Valve 127
Fig. 8.3: Three-dimensional echocardiographic en face view of the
pulmonary valve in late diastole showing all the three leaflets and lack
of any definite annulus. (AV: Aortic valve; A: Anterior pulmonary leaflet;
L: Left; R: Right leaflets).
Interleaflet triangles
Right ventricular muscular infundibulum
The sinutubular junction separates the pulmonary
sinuses from the tubular component of the pulmonary
trunk. It also is the level of insertion of the peripheral ends
of the zones of apposition between the leaflets.
The sinuses of Valsalva are the three parts of the
pulmonary root confined proximally by attachments of the
valvular leaflets and distally by the sinotubular junction.
According to their relation to the aorta, these are labeled
as left-facing, right-facing and non-facing sinuses.
Commissures are the areas on the coapting surface of
the arterial valvular leaflets.
The interleaflet triangles are the areas of arterial
wall proximal to the attachments of the leaflets that are
incorporated within the ventricular cavity.
The ventriculoarterial junction is the zone of union
between the muscular right ventricular infundibulum and
the fibroelastic pulmonary arterial wall. It has no fibrous
continuity with the tricuspid annulus (Fig. 8.5).
PULMONARY VALVE DISORDERS
Pulmonary valve disorder can either present as right
ventricular outflow obstruction [pulmonary stenosis (PS)]
or valvular regurgitation (PR) or combination of the two.
Pulmonary stenosis is described as lesions that are
collectively associated with obstruction to the RVOT.
Stenosis may be valvular, subvalvular or supravalvular
128 Section 2: Valvular Heart Disease
(Figs 8.6 to 8.10). It is the most common cause of congenital
outflow tract obstruction, resulting in decreased flow from
the right ventricle to the pulmonary arteries.5 Isolated
RVOT obstruction is pulmonary valvular stenosis in 80%
of the cases.
Stenosis proximal to the pulmonary valve may result
from a number of causes, both congenital and acquired.
Congenital ventricular septal defect may also be associated
with RVOT obstruction secondary to development of
obstructive midcavitary or infundibular muscle (Figs 8.6
and 8.7).
Stenosis of the pulmonary artery above the valve (distal
to the valve) may occur in the main pulmonary trunk at the
bifurcation, or more distally in the branch vessels. In rare
instances, a membrane just above the valve may cause
stenosis (Figs 8.9 and 8.10).
Types of Valvular PS
Valvular PS is of four types:
1. Classic PS with fusion of commissures with no or mild
leaflet thickening and doming of the leaflets (Figs 8.8
and 8.11)
Most cases of pulmonary valvular stenosis are
congenital. Often times, the valvular abnormality is
associated with syndromes such as Noonan syndrome
and Leopard syndrome. The trileaflet pulmonary valve
ranges from thickened or partially fused commissures
to an imperforate valve.5 The pulmonary valve in
valvular PS can be unileaflet, bileaflet or trileaflet
(Figs 8.12 and 8.13).
2. Dysplastic PS with no commissural fusion6 but
obstruction due to bulky and voluminous leaflets
(Figs 8.14 and 8.15)
Fig. 8.5: Anatomical position of the four cardiac valves.
3. Annular stenosis with rudimentary or absent leaflets79
4. Any combination of the above (Figs 8.16 to 8.20)
Supravalvular lesion may occur in the setting of
tetralogy of Fallot, Williams syndrome, Alagille syndrome,
as well as Noonan syndrome.10
The dysplastic valves show cauliflower-like changes
that severely thicken the leaflets and obstruct the right
ventricular outflow merely by their size.9 The zones of
apposition between the dysplastic leaflets are not fused,
the sinuses are deep and the lines of attachment are
semilunar, all as seen in normal hearts. Only the distal
parts of the leaflets are affected by the myxomatous degen
eration (Fig. 8.21); the most proximal part, originating from
the right ventricular musculature, is smooth and delicate.
Acquired stenosis of the pulmonary valve is very
uncommon. Rheumatic PS is rare even when the valve
is affected by the rheumatic process.11 Carcinoid disease
is the commonest cause of acquired pulmonary valve
disease.12 Various tumors may compress the RVOT.
Pulmonary valve stenosis may also occur as part of
more complex congenital lesions such as tetralogy of
Fallot,13 complete atrioventricular canal, double outlet RV
and univentricular heart (Figs 8.22 and 8.23).
Peripheral pulmonary artery stenosis may coexist with
valvular PS such as in Noonan syndrome and Williams
syndrome (Fig. 8.24).
Pulmonary Stenosis Severity
Quantitative assessment of PS severity is based mainly
on the transpulmonary pressure gradient.14 Calculation
of pulmonary valve area by planimetry is not possible
Fig. 8.6: Parasternal long-axis view showing discrete stenosis in the
right ventricular cavity (arrow) at the level of aortic valve.
 Pulmonary Valve 129

Fig. 8.7: Short-axis view showing narrow turbulent color Doppler jet through the subvalvular stenosis just proximal to the pulmonary valve (arrow).

A B
Figs 8.8A and B: Two-dimensional echocardiographic image of valvular pulmonary stenosis. Doming of the pulmonary valve with narrowed
orifice (arrows); (B) Three-dimensional echocardiographic image of valvular pulmonary stenosis. Doming of the pulmonary valve with narrowed
orifice (arrows).

Fig. 8.9: Transthoracic echocardiographic short-axis view of the right Fig. 8.10: Color Doppler image of the right ventricular outflow tract.
ventricular outflow tract. Red arrows point to the pulmonary valve, while Note turbulent flow across the pulmonary valve due to valvular pulmo-
the yellow arrows show discrete supravalvular membranous stenosis. nary stenosis (red arrows) and very narrow jet across supravalvular
obstruction (yellow arrows).
130 Section 2: Valvular Heart Disease

Fig. 8.11: Valvular pulmonary stenosis with continuous wave Doppler Fig. 8.12: Two-dimensional echocardiographic appearance of a uni-
interrogation in the right panel. cuspid pulmonary valve (left panel) with no doming in systole. The
right panel shows eccentric and narrow orifice due to stenosis.

Fig. 8.13: Unicuspid pulmonary valve with single leaflet and single Fig. 8.14: Dysplastic pulmonary valve filling the right ventricular
commissure. outflow tract and causing obstruction. Right panel shows continuous
wave interrogation with peak velocity of 500 cm/s.

Fig. 8.15: Three-dimensional echocardiographic short-axis image Fig. 8.16: Transthoracic echocardiographic modified apical short-
showing dysplastic pulmonary valve (arrows) with evidence of stenosis axis image showing ventricular septal defect (VSD) and rudimentary
as well as regurgitation (right panel). pulmonary valve (red arrow), supravalvular pulmonary stenosis
(yellow arrows) and main pulmonary artery hypoplasia.
 Pulmonary Valve 131

Fig. 8.17: Subpulmonic stenosis (small arrow) with vestigial pulmo- Fig. 8.18: Absent pulmonary valve with dilated pulmonary artery and
nary valve and annular stenosis. hour-glass right ventricular outflow tract.

Fig. 8.19: Three-dimensional echocardiographic image. Absent pul- Fig. 8.20: Massive pulmonary artery dilatation with vestigial pulmo-
monary valve with so-called annular stenosis. Nodular constriction at nary valve tissue.
the ventriculoarterial junction.

Fig. 8.21: Dysplastic pulmonary valve with redundant distal parts. Fig. 8.22: Tetralogy of Fallot with narrow right ventricular outflow tract
and pulmonary valve stenosis (arrow).
132 Section 2: Valvular Heart Disease
Fig. 8.23: Double-outlet right ventricle with pulmonary stenosis and
aneurysmal dilatation of pulmonary artery.
Fig. 8.25: Hemispheric proximal isovelocity surface area in a patient
with severe pulmonary stenosis. Narrow vena contracta is seen.
since the required image plane is in general not available.
Continuity equation or proximal isovelocity surface area
method, although feasible in principle, has not been
validated in PS and is rarely performed (Fig. 8.25).
Pressure Gradient
The estimation of the systolic pressure gradient is
derived from the transpulmonary velocity flow curve
using the simplified Bernoullis equation P = 4v2
(Fig. 8.26).
This estimation is reliable, as shown by the good
correlation with invasive measurement using cardiac
catheterization.15,16
Fig. 8.24: Right pulmonary artery stenosis with a peak gradient of
40 mm Hg in Williams syndrome. Diastolic spilling maintains the flow
in the affected lung (right panel).
Fig. 8.26: Color-flow map-adjusted continuous wave Doppler to obtain
transpulmonary gradients. A peak velocity of 4.88 m/s indicates severe
pulmonary stenosis.
Continuous wave (CW) Doppler is used to assess
the severity when even mild stenosis is present. It
is important to line up the Doppler sample volume
parallel to the flow with the aid of color flow mapping
where appropriate.
In adults, this is usually most readily performed from a
parasternal short-axis view but in children and in some
adults, the highest gradients may be found from the
subcostal window.
A modified apical five-chamber view may also be used
where the transducer is angled clockwise to bring
in the RVOT. Ideally, the highest velocity in multiple
views should be used for the determination.15,16

Fig. 8.27: Severe pulmonary regurgitation causing over-estimation of
the forward flow velocities.
Fig. 8.29: Continuous wave Doppler envelope of valvular PS (left
panel) versus fixed infundibular PS (right panel). The latter begins late
and is triangular in shape. (PS: Pulmonary stenosis).
In most instances of valvular PS, the modified
Bernoullis equation is applicable and there is no need
to account for the proximal velocity as this is usually
< 1 m/s.
In the setting of subvalvular or infundibular stenosis
and PS as part of a congenital syndrome or as a result
of RV hypertrophy, the presence of two stenoses in
series may make it impossible to ascertain precisely
the individual contribution of each.
In addition, such stenoses in series may cause
significant PR resulting in a higher Doppler gradient
compared with the net pressure drop across both
stenoses (Fig. 8.27).
Pulmonary Valve 133
Fig. 8.28: Continuous wave Doppler pattern of dynamic infundibular
obstruction.
Pulsed wave Doppler may be useful to detect the sites
of varying levels of obstruction in the outflow tract and
in lesser degrees of obstruction.
Muscular infundibular obstruction is frequently chara
cterized by a late peaking systolic jet that appears
dagger-shaped, reflecting the dynamic nature of the
obstruction; this pattern can be useful is separating
dynamic muscular obstruction from fixed valvular
obstruction, where the peak velocity is generated early
in systole (Figs 8.28 and 8.29).
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
IN PULMONARY STENOSIS
Transesophageal echocardiography (TEE) may allow
a more accurate assessment of the pulmonary valve
and RVOT in patients with poor transthoracic echocar
diography (TTE) window. The pulmonary valve may
be identified from a midesophageal window at varying
transducer positions from 50 to 90, anterior to the aortic
valve. The RVOT is often well seen in this view.
It is difficult to correctly align CW Doppler cursor
to accurately ascertain maximal flow velocity. Other
windows in which the pulmonary outflow tract may be
interrogated include the deep transgastric view in which,
by appropriate torquing of the transducer, the RV inflow
and outflow may be appreciated in a single image. This
view can allow accurate alignment of the Doppler beam
with the area of subvalvular/valvular stenosis through the
RVOT.
The following definitions of severity have been
proposed in the 2006 American College of Cardiology/
American Heart Association (ACC/AHA) guidelines on the
management of valvular heart disease:14
134 Section 2: Valvular Heart Disease
Severe PS: Peak jet velocity > 4 m/s (peak gradient
> 64 mm Hg)
Moderate PS: Peak jet velocity of 34 m/s (peak
gradient 3664 mm Hg)
Mild stenosis: Peak jet velocity is < 3 m/s (peak gradient
< 36 mm Hg).
A useful index of severity is to determine the RV systolic
pressure in patients with PS from the tricuspid regurgitant
velocity and the addition of an estimate of right atrial
pressure. The pulmonary artery systolic pressure should
be RV systolic pressurepulmonary valve pressure
gradient. Severe PS is characterized by near-systemic RV
systolic pressures in subjects with no hypertension.
CONSEQUENCES AND ASSOCIATIONS OF
PULMONARY STENOSIS
Severe PS may be associated with right ventricular
hypertrophy, eventually right ventricular enlargement
and right atrial enlargement. Given the unusual shape
of the RV and its proximity to the chest wall, accurate
estimation of RV hypertrophy and enlargement may be
difficult. The parasternal long-axis and subcostal long-
axis views are often best in assessing RV hypertrophy. The
normal thickness of the RV is approximately 23 mm, but
given the difficulties in estimating thickness, a thickness of
> 5 mm is usually considered abnormal. RV enlargement is
typically assessed in the apical or subcostal four-chamber
view.
PS may be a part of other syndromes or may be
associated with other congenital lesions. Dilatation of the
pulmonary artery beyond the valve is common and is due
to weakness in the arterial wall in a manner analogous to
bicuspid aortic valve and is not necessarily commensurate
with the degree of obstruction.
Detection of other lesions such as infundibular
stenosis, ventricular septal defect or tetralogy of Fallot is
all important in the assessment of these patients.
ASSESSMENT OF PULMONARY
REGURGITATION
Pulmonary regurgitation is quite frequent although mostly
functional. Causes of organic tricuspid regurgitation
(TR) are:
Congenital: Bicuspid or quadricuspid valve, absent
pulmonary valve
Infective endocarditis
Carcinoid heart disease
Rheumatic heart disease
Myxomatous degeneration
Pulmonary valve prolapse
Postoperative17
Hypoplastic right heart syndrome
Assessment of PR requires detailed understanding of
morphology by TTE, TEE and real-time three-dimensional
(3D) echocardiography.
Color Flow Imaging
PR is diagnosed by documenting a diastolic jet in the
RVOT originating from the pulmonary valve. It is normally
present in > 50% of the echocardiographic examinations.
Pathological PR is distinguished from physiological PR
by a longer duration of flow (pan-diastolic) and a wider
jet as the regurgitant jet crosses the pulmonary valve
(Fig. 8.30).
Functional PR jets are usually very small, central and
spindle-shaped (Fig. 8.31).
In severe PR, where equalization of diastolic pulmo
nary artery and RV pressures occurs early in diastole,
the color jet area can be brief and inaccurate (Fig. 8.32).
The assessment of PR severity is usually estimated
by the diameter of the jet at its origin. The maximum
color jet diameter (width) is measured in diastole
immediately below the pulmonary valve.18,19
A jet width that occupies > 65% of the RVOT width
measured in the same frame is in favor of severe PR
(Fig. 8.33).
Pulmonary Regurgitation Vena Contracta
Vena contracta (VC) width is probably a more accurate
method than the jet width to evaluate PR severity by color
Doppler. A VC width of 6 mm is indicative of severe
PR.20 Advantages and limitations of the VC are same as
applicable to other regurgitant lesions (Fig. 8.34).
The shape of the VC is complex in organic PR. Hence,
simple jet width in short-axis plane may not be valid.
The 3D VC is correlated with the two-dimensional (2D)
VC but provides more quantitative assessment of PR.
The effective regurgitant orifice area values of < 20,
21 to 115 and > 115 mm2 have been proposed to serve
as cut-offs for PR grade mild, moderate and severe.21
By multiplying the 3D VC with the PR velocitytime
integral of the PR jet, the regurgitant volume can be
obtained.

Fig. 8.30: Wide bifurcated PR jet (arrows) across the pulmonary valve
in an operated tetralogy of Fallot.
Fig. 8.32: Non-holodiastolic severe PR as judged by rapid deceler-
ation; regurgitation confined to first half of diastole. In late diastole,
because of the RV diastolic pressure exceeding PA diastolic pressure,
there is forward flow in diastole (arrows).
The regurgitant volume values of < 15, 15 to 115 and
> 115 mL have also been proposed to serve as cut-offs
for PR grade mild, moderate and severe, respectively.21
However, these data require validation.
Proximal Isovelocity Surface Area Method
In some patients, the flow convergence zone can be
assessed. However, no studies have examined the clinical
accuracy of this method in quantifying the severity of
Pulmonary Valve 135
Fig. 8.31: Functional PR with structurally normal pulmonary valve.
Note small, central jet with a length of 10 mm.
Fig. 8.33: Measuring jet width of PR and comparison with right
ventricular outflow tract width in the same frame. A ratio > 65% is
suggestive of severe PR.
PR. There are practical difficulties in assessing proximal
isovelocity surface area (PISA) in many cases as shown in
Figure 8.35.
Pulsed Doppler
Pulsed wave Doppler assessment of the forward and
the reverse flows at the pulmonary annulus and in the
pulmonary artery can been used to calculate regurgitant
volume and regurgitant fraction.
136 Section 2: Valvular Heart Disease
Fig. 8.34: Measuring vena contracta of PR in transthoracic echocar-
diographic short-axis view.
Fig. 8.36: Comparing continuous wave Doppler spectrum of mild
versus severe PR. Note rapid deceleration of severe PR in the right
panel with increased forward flow (forward flow velocity of 1.6 m/s
versus 0.8 m/s).
The pulmonary annulus should be measured carefully
during early systole just below the valve. This technique is
subject to errors in geometric assumptions.
Continuous Wave Doppler and Pulmonary
Regurgitation Severity22
The density of the CW signal provides a qualitative specific for severe PR. Its absence suggests milder degree
measure of regurgitation.
In mild PR, there is a slow deceleration of the jet
velocity.
A rapid deceleration rate with termination of flow in
mid to late diastole is not specific but compatible with
severe regurgitation (Fig. 8.36).
Fig. 8.35: Two examples of severe PR. Proximal isovelocity surface
areas is not well-visualized in the left panel, while in the right panel, it
is bifid.
Fig. 8.37: Early diastolic PR with late diastolic antegrade flow across
the right ventricular outflow tract. Such PR is usually mild unless
associated with rapid deceleration.
CONSEQUENCES OF PULMONARY
REGURGITATION
Evaluation of the size and function of the RV in the absence
of pulmonary hypertension provides indirect clues to the
severity of PR. Evidence of RV dilatation is, however, not
of PR. Antegrade diastolic flow across the pulmonary valve
without prolonged PR interval is suggestive of markedly
elevated RV diastolic pressure and indirectly suggests
milder PR if deceleration time is not short (Fig. 8.37).
In summary, echocardiographic assessment of PR
includes integration of morphological data from 2D/3D

imaging of the pulmonary valve and RV as well as Doppler
measures of regurgitant severity. Validation studies of PR
severity are still few.
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J Cardiol. 1985;56(1):1315.
20. Williams RV, Minich LL, Shaddy RE, et al. Comparison of
Doppler echocardiography with angiography for determin
ing the severity of pulmonary regurgitation. Am J Cardiol.
2002;89(12):143841.
21. Pothineni KR, Wells BJ, Hsiung MC, et al. Live/real time
three-dimensional transthoracic echocardiographic
assessment of pulmonary regurgitation. Echocardiography.
2008;25(8):9117.
22. Lei MH, Chen JJ, Ko YL, et al. Reappraisal of quantitative
evaluation of pulmonary regurgitation and estimation of
pulmonary artery pressure by continuous wave Doppler
echocardiography. Cardiology. 1995;86(3):24956.
 Chapter

9
Evaluation of Prosthetic
Heart Valves

Introduction Table 9.1: Types of prosthetic heart valves

Mechanical Prosthesis Bio-prosthesis
Number of prosthetic heart valves implantation is
Ball-in-cage Stented porcine
increasing steadily, because of greater recognition of
Mono-disk Stentless porcine xenograft
degenerative valvular heart disease in the Western
world with increasing age and the persistent problem of Bileaflet Cadaveric homograft

rheumatic heart disease in the low and middle income Composite (sewed in a graft) Autograft

countries. New designs with greater durability and better

hemodynamics have been introduced in the recent past.
All prosthetic valves need lifelong surveillance as these
are prone to mechanical failure, wear and tear, host tissue
reaction, infection and thrombosis. Echocardiography
remains the cornerstone of evaluation and is being
increasingly used in fixing prosthetic valve complications,
besides its use during percutaneous valve implants. Some
prosthetic valves present with unique hemodynamic
features either because of design or prosthetic orientation
in situ. These pseudomalfunctions can be detected easily
by high resolution multidimensional echocardiography.
Transoesophageal three-dimensional echocardiography
has revolutionized the evaluation of the prosthetic heart
valves.
Cardiac valves have an important physiological
function. These direct intracardiac blood flow in one
direction. Atrioventricular valves open in diastole to aid
filling of the ventricles and close in systole. Semilunar
valves open in systole for blood ejection in great vessels
and close in diastole. The phasic rhythmicity and unidire
ctionality maintain desired function of the closed loop
of the cardiovascular system. Native valves have large
effective orifice area for forward flow with least amount
of pressure drop, show minimal regurgitation, if any and
are capable of self-repairing. Native heart valves become
dysfunctional because of a variety of pathologies leading
to either stenosis or regurgitation or the combination of
both. When valves become significantly dysfunctional and
cannot be repaired, these need replacement either with a
mechanical prosthesis or with a tissue valve. Implanted
valves, howsoever sophisticated, cannot perform as well
as natural valves.
Ideal heart valve, besides durability and low thrombo
genecity should produce minimal pressure drops, have
small regurgitation volumes, minimize turbulence,
reduce prevalence of high stresses and not create flow
separations in the vicinity of the valve.13 Challenge lies
in creating prosthetic valves that have no component of
nonphysiological flow pattern (Table 9.1)
BalL-in-Cage valve
Although discontinued since 2007, there are still a large
number of patients implanted with these valves and
hence an understanding of functioning of ball-in-cage

Fig. 9.1: Ball-in-cage mechanical prosthesis. Silicone ball is enclosed
in a metallic high-arched cage. Ball valves operate on the simple
principle that the ball will be forced to one side of the valve or the
other depending on which way blood is flowing. There is no central
flow with a ball. Manufacturing of this type of valve was discontinued
in 2007.
Fig. 9.3: Transesophageal echocardiographic four-chamber view
depicting ball-in-cage valve in systole. The ball is resting at the sewing
ring (arrow). Shadows of metallic arches are visible on the sides.
(LV: Left ventricle; LA: Left atrium)
valve is essential (Figs 9.1 to 9.4). Ball-in-cage valve has a
silicone ball housed in metallic cage (three metallic
arches) that is attached to the base ring.
During the forward flow phase, flow emerging from the
valve forms a circumferential jet that separates from
ball, hits wall of the flow chamber and then flows along.
A region of high-velocity gradient, and thus of high
shear stress, exists at the edge of forward flow jet and
recirculation region.2,3
During end flow phase, the ball moves back on the
valve seat, but a small gap may form, thus permitting a
mild regurgitation.
Evaluation of Prosthetic Heart Valves 139
Fig. 9.2: Diagram of flow across ball-in-cage mechanical prosthesis
in aortic position. Flow is from sides of ball when latter is displaced
in the cage due to pressure development in the left ventricle. The ball
occludes valve orifice and thus passively prevents backflow. During
forward flow phase, high blood pressure pushes ball downstream, thus
opening the orifice, with metal cage holding ball distal to orifice.
(LVOT: Left ventricular outflow tract).
Fig. 9.4: Circumferential flow around the ball in Starr-Edwards
ball-in-cage prosthesis in mitral position. Transthoracic echocardio-
graphic four-chamber view.
(LV: Left ventricle; LA: Left atrium)
TILTING OR MONO-Disk VALVE
Mono-disk or tilting-disk prostheses have a single disk of
pyrolite carbon housed in a titanium casing with the help
of struts or hinges (Figs 9.5 to 9.11).
In open position, the disk tilts to form a major orifice
and another minor orifice for the blood to flow.46
A large forward flow jet emanates from the major
orifice, whereas a smaller jet of lesser velocity emanates
from the minor orifice.
These two jets of different velocity induce a recirculation
in the wake of disk. A recirculating flow pattern forms
in the sinus region.
140 Section 2: Valvular Heart Disease
Fig. 9.5: Mono-disk mechanical prosthesis. Mono-disk prosthesis
has a single disk secured by lateral or central metal struts. The
opening angle of the disk relative to the plane of valve annulus ranges
from 60 to 80, resulting in two distinct orifices of different sizes.
Fig. 9.7: Graphic representation of the mono-disk valve. Performance
index is dependent upon the opening angle, which can be gauged by
cine-fluoroscopy as well as by echocardiography.
During the closed phase, the tilting disk moves back
and seats on the valve housing to occlude the valve
orifice; however, a small gap may be present at the
periphery of disk, thus permitting a small amount of
flow regurgitation
BILEAFLET PROSTHETIC VALVES
Bileaflet design consists of two semicircular disks which
pivot on hinges. Bileaflet valves have the best central
flowthe leaflets open completely, allowing very little
resistance to blood flow (Figs 9.12 to 9.18).4,5
Fig. 9.6: Tilting mono-disk prosthesis in aortic position. There are two
eccentric orifices for forward flow. Angle of disk opening depends upon
the design. The disk totally occludes valve orifice in closed position
and tilts to an angle in open position. The disk can rotate during normal
function, thus preventing excessive contact wear from the retaining
strut components on a particular region.
Fig. 9.8: Transesophageal long-axis view. Tilting-disk prosthesis in
aortic position in diastole (arrow).
(AO: Aorta)
Open leaflets divide the area available for flow into
three regions: two lateral orifices and a central orifice.7
The major part of forward flow emerges from two
lateral orifices.7
High turbulent shear stress is present at locations of
high velocity gradients and at locations immediately
distal to the valve leaflets.
The design of bileaflet mechanical heart valves includes
some degree of leakage flow.
During the leakage flow phase, the leaflets rotate to
occlude the valve orifice.

Fig. 9.9: Transesophageal echocardiographic four-chamber view
showing an open tilting disk in mitral position. Note the angle of opening.
(RA: Right atrium; RV: Right ventricle).
Fig. 9.11: Medtronic-Hall valve #23 ( mono-disk prosthesis ) in mitral
position in an apical view. Forward flow through major orifice (longer
arrow) and minor orifice (shorter arrow). Recirculation zone is seen
lateral to the major orifice.
BIOPROSTHESIS
The leaflet components of the bioprosthetic valves are
composed of animal pericardium or animal valvar tissue.
There is a substantial use of these valves in the elderly
population and in females of childbearing age (Figs 9.19
to 9.24).
Bioprosthetic heart valves are composed of three
leaflets that open to form a central orifice for the
blood to flow through, thus closely resembling a native
semilunar valve.8
Evaluation of Prosthetic Heart Valves 141
Fig. 9.10: Three-dimensional transesophageal view from the top in a
patient with mono-disk Medtronic-Hall valve in mitral position. Arrows
point to the sewing ring. Note single disk with two orifices.
A jet-like flow emerges from open leaflets during the
forward flow phase. The jet is characterized by vena
contracta immediately downstream of the valve,
followed by an expansion region.8,9
The forward flow jet is surrounded by counter-rotating
recirculation regions.
During closed phase, the leaflets coapt to prevent
regurgitation; however, leakage flow may emanate
from centre of the valve if leaflets do not close properly.
General flow characteristics of all bioprosthetic
valves are the same, differences do exist on valve-to-
valve basis because of subtle changes in valve design,
such as the height of the valve, the material (porcine,
pericardial etc.) and stent characteristics (stented vs
stentless valves).
Stentless valves have superior performance with the
largest effective orifice area.10
Pericardial stented valves are known to have larger
effective orifice area than porcine bioprostheses.11
HEMODYNAMIC ASSESSMENT OF
PROSTHETIC VALVES
All prosthetic valves are inherently stenotic as well as
regurgitant. A baseline postdischarge echocardiographic
evaluation is a prerequisite for detecting any change
during serial studies. The echocardiographic evaluation
of a prosthetic valve requires knowledge of valve details,
concommitant procedures performed, anticoagulation
status, and so on. It is essential to study the prosthetic valve
142 Section 2: Valvular Heart Disease
Fig. 9.12: Bileaflet mechanical prosthesis. Bileaflet valves are made
of two semilunar disks attached to a rigid valve ring by small hinges.
The opening angle of the leaflets relative to the annulus plane ranges
from 75 to 90, and the open valve has three orifices: a small, slit-like
central orifice between the open leaflets and two larger semicircular
orifices laterally.
Fig. 9.14: Transesophageal echocardiographic four-chamber view
showing bileaflet mitral prosthesis in diastole. Arrows point to two
open disks with three orifices.
structural details with its hemodynamic performance
along with the functioning of the receiving chambers.
Normal transprosthetic regurgitation is seen as
small two to three jets originating from the prosthesis
and extending 11.5 cm into the receiving chamber
(Figs 9.25 and 9.26). Regurgitation is of significance if
color flow mapping shows transprosthetic jets of sufficient
vena contracta (3 mm or more) or if the jet(s) originate
from the side of the prosthetic ring.
Fig. 9.13: Note a central small orifice and two lateral orifices. Within
the annular housing, each leaflet has an extension region, known as
leaflet ear, which pivots about a recessed or protruding hinge.
(LVOT: Left ventricular outflow tract)
Fig. 9.15: Same as in Figure 9.14 except that bileaflet valve is seen
in closed position.
Hemodynamic evaluation includes measurement
of transprosthetic pressure gradients, flow and effective
orifice area. Effective orifice area (EOA) of a prosthesis is of
critical significance. The EOA is a physiological parameter
that represents the minimal cross-sectional area of the
transprosthetic blood flow jet, and is easily measured
by Doppler echocardiography. Pressure gradient and
effective orifice area are correlated with total energy loss
and can be estimated noninvasively.
 Evaluation of Prosthetic Heart Valves 143

A B
Figs 9.16A and B: Doppler color flow map showing three forward flow jets across the bileaflet mitral prosthesis in diastole. Left panel is a
transesophageal image while the right panel shows transthoracic image.

Fig. 9.17: Three-dimensional transesophageal image of bileaflet Fig. 9.18: Three-dimensional transesophageal echocardiographic
St Jude #27 mitral prosthesis in open position. Line in the upper part of en-face view from the top of the bileaflet mitral prosthesis in closed
the image represents stitch artifact. position.

Internal geometric area of a prosthesis is another
anatomical parameter calculated from the static measure
ment of the internal diameter of the prosthesis. Geometric
area measurement varies from one type of prosthesis
to the other, while the ratio between the EOA and the
geometric area also varies widely from one type and/or
size of prosthesis to another.
As blood flows through the prosthetic heart valve,
a sudden pressure drop occurs across the valve due to
reduction in cross-sectional area within the valve housing.
This can be quantified through the continuity equation
and Bernoullis equation (Fig. 9.27).
There is a variable pressure drop across prosthetic
valve depending upon the size, design and orientation
of the prosthesis and the body size of the patient.
A good performance is assured if the indexed aortic
prosthetic valve area exceeds 0.85 cm2/m2 and the
mitral prosthetic valve area is 1.3 cm2/m2 (Fig. 9.28).
Estimated prosthetic valve areas below this threshold
can either be due to prosthetic valve stenosis or patient-
prosthesis mismatch.
Higher pressure drop causes higher shear stress and
flow separation adjacent to the valve and pre-disposes
to thrombus formation.
144 Section 2: Valvular Heart Disease

Fig. 9.19: Diagram of bioprosthesis with three leaflets like a natural Fig. 9.20: Diagram depicts flow pattern (single central flow jet) across
semilunar valve supported by three flexible pillars. a trileaflet tissue valve in aortic position.

Fig. 9.21: Parasternal long-axis view. #27 Carpentier-Edwards Fig. 9.22: Transthoracic short-axis view showing mitral Carpentier-
bioprosthesis in diastole at mitral position. Arrows point to flexible Edwards bioprosthesis in closed position. Note three pillars (P) and
pillars. Leaflets are thin and hardly visible. three leaflets (L).

Fig. 9.23: Single central jet of forward flow in diastole. #27 Carpentier- Fig. 9.24: Transesophageal echocardiographic four-chamber view
Edwards bioprosthesis (Fig. 9.16). showing leaflets of a mitral bioprosthesis in open position. Note the
leaflets are thin.
 Evaluation of Prosthetic Heart Valves 145

A B

Figs 9.25A and B: #23 Medtronic-Hall valve in aortic position imaged in apical three-chamber view. There are two small jets of transprosthetic
regurgitation in early diastole (closure backflow) and holodiastolic (leakage backflow).

Fig. 9.26: Transesophageal image of a bileaflet mitral prosthesis in Fig. 9.27: Diagram illustrating pressure drop across a prosthesis.
systole showing three physiological regurgitant jets. Beyond the prosthesis, pressure drop decreases (pressure recovery).
Pressure recovery varies depending upon the design of the valve.

Effective orifice area is a metric of impedance to flow
through the valve. A higher orifice area means less
energy loss.
Performance index is the effective orifice area
divided by the size of the valve. It is reciprocal of flow
impedance. Bileaflet valves typically have higher
performance index than tilted-disk valves, which in
turn have higher index than caged-ball valves.1215
Doppler gradients should be calculated based on side
orifice velocity measurements or the Doppler gradient
estimation should include the pressure loss coefficient
when based on central orifice velocities (Fig. 9.29).
Application of the simplified Bernoullis equation to
Doppler velocity measurements across the central
orifices of St Jude valves will yield significantly higher
calculated pressure gradients across the valve than
the pressure gradient measured during cardiac
catheterization ( Fig. 9.30).
Pressure recovery is the variable increase in lateral
pressure downstream from a stenotic orifice.
An early peaking Doppler velocity profile of the aortic
prosthesis would suggest either a pressure recovery
phenomenon or increased flow across an unobstructed
valve. Increased E velocity across mitral prosthesis
146 Section 2: Valvular Heart Disease

Fig. 9.28: Relationship of mean transprosthetic valve gradients with
indexed effective orifice area at rest. There is an exponential increase
in pressure gradients beyond a certain threshold of valve area.
Fig. 9.29: Graph illustrating pressure drop across a bileaflet prosthetic
valve. Through the central small orifice, there is a greater pressure drop
and greater pressure recovery downstream. Continuous wave Doppler
interrogation of the central orifice will result in higher transprosthetic
pressure gradients and smaller calculated effective orifice area.

A B
Figs 9.30A and B: Continuous wave (CW) interrogation of a normally functioning bileaflet valve in mitral position. (A) Figure shows velocity
profile across a central orifice (peak velocity 185 cm/sec with a peak gradient of 14 mm Hg). (B) Figure shows velocity profile across lateral
orifice (peak velocity 149 cm/sec with a peak gradient of 9 mm Hg).

can occur in tachycardia, high output states, small
prosthetic size, stenosis or regurgitation and caged-ball
valves or central orifice of a bileaflet valve (Fig. 9.31).
Pressure recovery is responsible for 50% or more of the
Doppler gradients for almost all conditions (Fig. 9.31).
Incorporation of the experimentally determined
pressure loss coefficient for a bileaflet valve in the
simplified Bernoullis equation is necessary for a
comparison of noninvasive Doppler gradients with
the invasive gradients measured during cardiac
catheterization.
Pressure loss coefficient is similar for all valve sizes.
When the Doppler gradient (1/2v2) across the central
orifice is multiplied by the pressure loss coefficient
K = 0.64, an excellent agreement is observed between
the noninvasive and invasive transvalvular pressure
gradients in patients with St Jude prosthesis.14
Occasionally, high transprosthetic pressure gradients
are observed in patients who have eccentric orifice
resulting into jet convergence on adjacent walls of
the receiving chamber or vessel. This is because the
jet converges twice before finally diverging (Figs 9.32
and 9.33).
 Evaluation of Prosthetic Heart Valves 147

A B

Figs 9.31A to C: (A) Transprosthetic flow velocity profile across a

normally functioning Starr-Edwards mitral prosthesis showing a peak
velocity of 2.7 m/s (peak gradient of 28 mm Hg). Rapid deceleration sug-
gests unobstructed valve. (B and C) A normally functioning tilting-disk
aortic prosthesis with a transprosthetic peak gradient of 100 mm
Hg due to phenomenon of double convergence (one at the site of
prosthetic orifice and second at the posterior aortic wall as the jet takes
C a turn away from the wall after hugging it.

A B
Figs 9.32A and B: Normally functioning Medtronic-Hall tilting-disk prosthesis at aortic position in a 25-year old young man. Eccentric orifice
results in high transprosthetic pressure gradients (peak pressure gradient 77 mm Hg, mean 41 mm Hg). Triangular shape of the Doppler
spectrum suggests nonobstructed valve.
148 Section 2: Valvular Heart Disease
Fig. 9.33: Graphic illustration of greater pressure drop in a prosthesis
with eccentric opening. Convergence-1 occurs at the prosthetic valve
while convergence-2 at the level of posterior aortic wall as the jet redi-
rects itself into the central lumen of the aorta.
Fig. 9.35: Intermittent transprosthetic mitral regurgitation. There is no
regurgitation in first two cardiac cycles while the last three show it.
If prosthetic valve dysfunction is suspected, careful
examination of leaflet excursion by transthoracic or
transesophageal imaging is necessary. When abnormal
leaflet excursion is present (or suspected):
the Doppler gradients across the central orifice
should be calculated without incorporating
the pressure loss coefficient into the simplified
Bernoulli equation and/or
the Doppler gradients should be measured across
the side orifices, where pressure recovery is
minimal and the simplified Bernoullis equation is
adequate.
Fig. 9.34: Continuous wave Doppler spectrum of a normally
functioning aortic prosthesis. Despite a high peak velocity (4.39 m/s),
There is a rapid acceleration, triangular shape of the spectrum with early
systolic peak. Note the second Doppler flow velocity spectrum
between opening and closure artefacts.
A transesophageal examination (2D or 3D) is mandatory
whenever abnormally high transprosthetic pressure
gradients are observed. High transprosthetic pressure
gradients can occur with or without prosthetic valve
dysfunction.
The contour of the flow velocity through the prosthesis
is a valuable index of prosthetic valve function in
aortic position that is used in conjunction with the
other quantitative indices.16 In a normally functioning
prosthetic valve, even during high flow, there is a
triangular shape of the continuous wave (CW) Doppler
spectrum, with early peaking of the velocity and a short
acceleration time (Fig. 9.34).16 Ratio of acceleration
time to ejection time has been used in aortic prosthetic
valves to decipher the significance of high gradients.
A ratio of > 0.4 indicates prosthetic aortic valve
obstruction.4
With prosthetic aortic valve obstruction, the flow
velocity contour is rounded with midsystolic peaking
and slow acceleration.
There may be intermittent obstruction occasionally
and hence prolonged and careful examination may be
necessary (Fig. 9.35).
TECHNICAL CONSIDERATIONS
A prior knowledge of the type and size of prosthesis is
essential. Size of the prosthesis denotes outer diameter
of the suture ring in mm. Body surface area should be

Fig. 9.36: Transthoracic echocardiographic off-axis view of the ventri-
cles showing a bileaflet valve in mitral position. Angulating the probe
to the right while imaging in short axis provides details of the mitral
prosthesis.
recorded to detect patient-prosthesis mismatch. Heart rate
variation will cause change in transprosthetic gradients
and hence should always be recorded and mentioned
along with the pressure gradients.
Transthoracic echocardiographic (TTE) examination is
often tedious because of acoustic shadowing produced
by the prosthesis and surgically altered rib cage.
Transthoracic echocardiography requires multiple
angulations and use of off-axis views (Fig. 9.36).
Transesophageal echocardiographic (TEE) exami
nation is more often needed for evaluation of prosthetic
valves. 3D TEE is a valuable tool to detect cause of
prosthetic valve obstruction.
A complete examination of the chambers, other valves
and functional quantification is required in every case.
In case of aortic prosthesis, measurement of aorta at
different locations is vital. Aortic root tends to dilate
and there is propensity for dissection after replacement
of a bicuspid aortic valve.
Prosthetic valve components need to be imaged and
examined carefully.
The opening and closing motion of the moving parts
of the prosthesis (leaflets for bioprosthesis and disks/
ball for mechanical prostheses should be recorded and
semiquantified.
Presence or absence of leaflet calcifications or
abnormal echo density attached to the sewing ring,
occluder, leaflets, stents or cage and so on should be
recorded.
Evaluation of Prosthetic Heart Valves 149
Fig. 9.37: Transthoracic echocardiographic parasternal long-axis view
shows native chords (c) preserved and tucked behind the sewing ring
of a mitral bileaflet valve. Papillary muscle (PM) is shown.
Appearance and motion of the sewing ring should be
studied. Any separation from the native annulus and
abnormal rocking motion should be carefully excluded.
Increased mobility of the mitral prosthesis may be
observed in those with preserved native leaflets and
chordae. These should be differentiated from any
abnormality (Fig. 9.37).
Presence or absence and number of microbubbles
upstream of transprosthetic flow should be docum
ented.17,18
Aortic root may be thickened after insertion of a
stentless valve due to edema and hematoma.19 This
may take 36 months to resolve (Fig. 9.38).
In patients with or without suspicion of infective
endocarditis, a search for the presence of abscess
formation in the region of the prosthetic valve annulus
or sewing ring should be undertaken (Fig. 9.39).
Prosthetic dehiscence should be looked for diligently.
Prosthesis dehiscence can cause paraprosthetic
regurgitation (Fig. 9.40) or occasionally subannular
pseudoaneurysms (Fig. 9.41).
For hemodynamic evaluation of prosthetic valves,
proximal and distal velocities should be recorded as in
native valves. Effective orifice area should be estimated
by the continuity equation using measured outflow tract
diameter and not that provided by the manufacturer.
A peak velocity 2 m/s across a mitral prosthesis
should be considered abnormal and a transaortic
peak velocity 4 m/s should be viewed with suspicion.
150 Section 2: Valvular Heart Disease

A B
Figs 9.38A and B: Immediate postoperative stentless prosthesis in aortic position in diastole. Note the thickening of the aortic root (arrows) due
to edema and hematoma. This tends to disappear over time.

Fig. 9.39: Transthoracic echocardiographic parasternal long-axis view Fig. 9.40: Transesophageal echocardiographic image showing
in a patient with aortic mechanical prosthesis and clinical diagnosis of paraprosthetic hole marked by an arrow ( dehiscence) in a patient with
infective endocarditis. Abscess (A) surrounded by arrows is depicted. tilting disk prosthesis in mitral position.

Fig. 9.41: Transthoracic echocardiographic parasternal long-axis view in a patient with aortic mechanical prosthesis. Arrow points to the sub-
annular pseudoaneurysm extending anterior to the aortic root.
 Evaluation of Prosthetic Heart Valves 151

A B
Figs 9.42A and B: Measurement of dimensionless index (DI) for a tilting-disc aortic prosthesis. A DI of 0.19 indicates prosthetic valve obstruction.

A B
Figs 9.43A and B: Continuous wave (CW) Doppler interrogation of a mechanical mitral prosthesis. (A) Pressure-half time is 154 msec with
pressure half-time derived mitral valve area of 1.43 cm2 (Left panel). (B) Figure shows valve area of 0.64 cm2 by continuity equation as stroke
volume was 36 mL and mitral VTI 56.7 cm.

In these situations, further examination including TEE
and cinefluoroscopy become essential. Similarly, a
mean gradient of 10 mm Hg across a mitral prosthesis
should be considered abnormal.
Dimensionless velocity index (DI) is an easily obtainable
parameter of aortic prosthetic valve function. It is
the ratio of left ventricular outflow tract velocity
to peak transprosthetic velocity. DI of > 0.300.35
indicates normal function, especially if associated
with a short acceleration time of < 100 msec. DI of
0.25 should be viewed with suspicion (Fig. 9.42).
Dimensionless velocity index has also been suggested
for mitral prosthesis (normal 0.45) but is rarely used
clinically.
Pressure half-time measurement is frequently used in
evaluating mitral and tricuspid valve prostheses. There
is no validation for its use and mostly, valve area is
overestimated unless there is moderate to severe valve
stenosis. However, a pressure-half time exceeding
150 msec should be viewed with suspicion
(Figs 9.43A and B) and prosthetic valve stenosis is
likely if it exceeds > 200 msec.20
In presence of atrial fibrillation, Doppler data from
5 to 15 cardiac cycles should be averaged. A sweep speed
of 100 mm/sec is essential for Doppler measurements.
Stentless valves are more likely to have minor regurgi
tation than stented biological valves (Fig. 9.44). Some
times, these leaks are more than minor.
152 Section 2: Valvular Heart Disease
Fig. 9.44: Transthoracic echocardiographic parasternal long-axis
view showing aortic regurgitation (arrow) in a stentless prosthesis.
(LV: Left ventricle; AO: Aorta; LA: Left atrium).
Fig. 9.46: Transesophageal echocardiographic four-chamber view
showing flail leaflet (arZrow) of a mitral bioprosthesis.
(LA: Left atrium; LV: Left ventricle).
MICROBUBBLE FORMATION (CAVITATION)
It is not uncommon to see microbubbles upstream of the
prosthetic valves. Microbubbles form due to shear stress
in the vena contracta and implode in divergence cone
where pressure recovery occurs (Fig. 9.45).
Cavitation is suspected as a contributing factor in blood
cell damage and increased risk of thromboembloic
complications.
Collapse of the microbubbles can cause pressure or
thermal shockwaves and blood microjets that can
damage a surface.
Fig. 9.45: Parasternal long-axis view in a patient with bileaflet valve in
mitral position. Arrow points toward the microbubbles upstream of the
valve in diastole.
Table 9.2: Dysfunctions of the prosthetic heart valves
Mechanical failure
Infection
Thrombosis
Degeneration of tissue valves
Dehiscence and paraprosthetic leaks
Part embolization
Patient-prosthesis mismatch
Hemolysis
Cavitation
More microbubbles are seen in conditions that
increase contractility.
A few microbubbles may not be of much conseq
uence.17,18
PROSTHETIC VALVE DYSFUNCTION
Prosthetic valve are prone to wear and tear, mechanical
failure, thrombosis, infection and host tissue reaction.
Table 9.2 lists the prosthetic valve dysfunctions.
BIOPROSTHETIC DEGENERATION
In bioprosthetic degeneration, the leaflets get thickened,
flail, torn or calcified with or without fusion of the
commissures (Figs 9.46 and 9.47).2124 Degenerative
calcification results in stenosis and regurgitation of the
valve. Not all bioprostheses showing structural valve

Fig. 9.47: Transthoracic echocardiographic four-chamber view
showing structural degeneration of the mitral bioprosthesis (arrow).
Fig. 9.49: Transthoracic echocardiographic (TTE) four-chamber view
showing torn leaflet of a mitral bioprosthesis.
degeneration suffer from stenosis and calcification
(Fig. 9.48). Some valves show only rupture of the cusps
(Fig. 9.49) whereas others show the combination of leaflet
calcification and rupture.
Tears in the leaflets are associated with microscopic
or macroscopic calcification of the tissue.2124 For stentless
porcine aortic valves, the mode of failure leading to
reoperation is predominantly cusp rupture, inducing
sudden regurgitation. Flail and torn leaflets tend to
segment the orifice (Fig. 9.50).
Following points are worth mentioning in regard to
structural degeneration:
Evaluation of Prosthetic Heart Valves 153
Fig. 9.48: 3D Transesophageal echocardiographic view from the top in
a patient with Carpentier-Edwards (CE) Bioprosthesis in mitral position
showing stenosis (arrows) of the orifice in diastole.
Fig. 9.50: 3D Transesophageal echocardiographic view from the top
of a mitral bioprosthesis in diastole. There is segmentation of the ori-
fice due to torn leaflets (arrows).
(P: Pillar; STL: Septal tricuspid leaflet; ATL: Interior tricuspid leaflet;
PTL: Posterior tricuspid leaflet).
It usually occurs 78 years after implantation.
More common with porcine than bovine pericardium.
More often in mitral position.
More often in younger patients.
More often in older generation of bioprostheses.
PROSTHETIC AND PARAPROSTHETIC
REGURGITATION
Mechanical prostheses have a normal regurgitant volume
known as leakage backflow. This physiological regurgitation
prevents blood stasis and thrombus formation using a
154 Section 2: Valvular Heart Disease
Fig. 9.51: 3D Transesophageal echocardiographic view from the top
of a mitral prosthesis in diastole. Disk on the left side is completely
open and the one on the right side is stuck in partially open position.
Partially opened fixed disk causes transprosthetic mitral regurgitation.
A B
Figs 9.53A and B: Transesophageal echocardiographic images of a mitral bioprosthesis in a young female. The leaflets are thin but there is a
tear (arrow) with severe mitral regurgitation (right panel).
washing effect.25 As opposed to the pathological regurgitant
jets, the physiological regurgitation jets are characterized
by being short in duration, narrow and symmetrical.
Abnormal prosthetic regurgitation can occur due to:
Mechanical failure of the prosthesis (Fig. 9.51).
Degeneration of a bioprosthesis (Fig. 9.52).
Interference by an abnormal structure like thrombus,
vegetation or remnants of the native valve.
Leaflet tear (Fig. 9.53).26
Severity of transprosthetic mitral regurgitation is
judged by parameters similar to those applied to the
native valves although not well validated. Prominent
Fig. 9.52: 2D Transesophageal echocardiographic view showing se-
vere transprosthetic regurgitation across a mitral bioprosthesis. Note
large proximal flow acceleration.
proximal flow acceleration (Fig. 9.52) and a peak E mitral
velocity > 2.5 m/s (Fig. 9.54) strongly suggests severe
mitral regurgitation. Other indirect clues are enlarged left
ventricle and significant pulmonary hypertension.
PARAPROSTHETIC REGURGITATION
Paraprosthetic regurgitation occurs due to dehiscence of
the sewing ring either because of degenerative structural
changes of the surrounding tissue, suture giving away,
calcification of the native annulus or due to infective
endocarditis. Large paraprosthetic leaks tend to cause

Fig. 9.54: Degenerated Carpentier-Edwards mitral bioprosthesis
showing severe transprosthetic mitral regurgitation by continuous
wave (CW) Doppler interrogation. Note Peak E velocity exceeding
3 m/s (pressure half-time is 150 msec) with dense systolic regurgitant
jet signals.
A B
Figs 9.56A and B: Small paraprosthetic mitral regurgitation with clear delineation of the dehiscence (arrow).
(LV: Left ventricle; AO: Aorta; LA: Left atrium).
rocking of the prosthesis. The assessment of severity is
similar to that of native valves with minor differences.
A regurgitant orifice area 0.5 cm2 is considered to
represent severe mitral regurgitation. Similar values
are not reported for paraprosthetic aortic regurgitation.
However, acoustic shadowing during TTE may create
difficulty in assessing presence and severity of regurgitation
and multiple off-axis views may be needed to discover
regurgitation jet. Transesophageal echocardiography
is of immense value and should be routinely used
when paraprosthetic regurgitation is suspected (Figs 9.55
to 9.59).
Evaluation of Prosthetic Heart Valves 155
Fig. 9.55: Transthoracic echocardiographic (TTE) parasternal
long-axis view showing eccentric paraprosthetic mitral regurgitation
(arrows). Marked proximal flow acceleration is seen.
(AO: Aorta; LV: Left ventricle; LA: Left atrium)
PROSTHETIC VALVE STENOSIS
The presence of increased transprosthetic gradient
(mean gradient > 1520 mm Hg for aortic prostheses and
> 5-7 mm Hg for mitral prostheses) at rest with normal
range of heart rates is not uncommon in normally
functioning prostheses and may not be equated with
intrinsic prosthesis dysfunction. A high gradient can be due
to an associated subvalvular obstruction or a hyperkinetic
circulatory state or valvular regurgitation. Such occurr
ences can be suspected when the dimensionless index is
normal. Distinction must be made between obstruction
156 Section 2: Valvular Heart Disease
A B
Figs 9.57A and B: Transesophageal echocardiographic examination of ball-in-cage valve in mitral position. Note two jets of paraprosthetic
regurgitation with bigger jet on the lateral side (arrow).
Fig. 9.58: Transesophageal echocardiographic long-axis view
showing eccentric paraprosthetic aortic regurgitation (arrow) in a
patient with tilting-disk implantation. Vena contracta width of 9 mm
suggests severe regurgitation.
resulting from patient-prosthesis mismatch, which is by
far the most frequent cause of high pressure gradients
(present right from the immediate postoperative
phase), and intrinsic prosthesis dysfunction, which is a
pathological condition requiring immediate attention.27
If the calculated EOA is below the reference value
and if the prosthesis is not a bileaflet mechanical valve,
prosthesis valve dysfunction should be considered,
and confirmation should be sought with TEE, and
cinefluoroscopy. Incidence of prosthetic valve obstruction
can be as high as 4% per year.4
Main causes of prosthetic valve stenosis are:
Pannus formation (Figs 9.60 to 9.65).
Fig. 9.59: Dehiscence of a Starr-Edwards mitral prosthesis (arrow)
Thrombosis (Figs 9.66 to 9.68).
Pannus + Thrombosis (Fig. 9.69).
Structural degeneration of the bioprosthesis
(Figs 9.70 and 9.71).
Ball variance due to lipid absorption (Figs 9.72
and 9.73).
Mechanical failure (Fig. 9.74).
Pannus is a membrane of granulation tissue in
response to healing. Pannus grows in the tissue valve
interface usually. It tracks and creeps along the suture
lines. This does not encroach the valve orifice or chamber
space generally, but the hanging edges can hit upon a
leaflet occasionally. This is more common with tilting disk

Fig. 9.60: Transesophageal echocardiographic four-chamber view in
a 29-year old female with #27 Omniscence tilting disk valve. Arrow
points to the pannus.
Fig. 9.62: 2D Transesophageal echocardiographic view of a Starr-
Edwards mitral prosthesis. Arrows point to the circumferential pannus
reducing the internal diameter of the sewing ring.
on the side of minor orifice. When excessive it can make a
valve leaflet almost standstill. Pannus overgrowth narrows
circumferentially the inflow and outflow aspects of the
prosthesis by extending into both atrial and ventricular
sides. The incidence of pannus formation in prosthetic
heart valves in the aortic position is described as between
0.1% and 0.6% per patient per year.4,27
There is a significant overlap between echocardio
graphic appearance of a pannus and a thrombus.
Thrombus tends to have echogenic texture similar to
myocardium and is not as echo-dense as a pannus is.
It is usually more localized, more mobile and tends to
Evaluation of Prosthetic Heart Valves 157
Fig. 9.61: 2D Transesophageal echocardiographic view shows
arrested lateral disk of a bileaflet valve. Red arrows point to the
pannus.
Fig. 9.63: 3D Transesophageal echocardiographic view from the top
of a bileaflet mitral valve showing circumferential nodular pannus
(arrows).
obstruct orifice. Compared to pannus formation, thrombi
are usually larger and, in the case of mitral prostheses,
extended more often into the left atrium. There is a clinical
need to define a thrombus and its location. The different
therapeutic modalities available for valve thrombosis
(heparin treatment, fibrinolysis, surgery) are influenced
by the presence of valvular obstruction, by valve location
(left- or right-sided), and by clinical status. Biological
valves rarely get thrombosed. Thrombus formation on
a mechanical valve is more common than is clinically
recognized. Routine TEE in postoperative period shows
about 10% patients with some degree of thrombus
158 Section 2: Valvular Heart Disease

Fig. 9.64: 3D Transesophageal echocardiographic view from the top Fig. 9.65: 3D Transesophageal echocardiographic view from the
of a tilting-disk mitral prosthesis. Arrows point to pannus formation with top showing pannus (arrows) in a patient with tilting disk aortic valve
impingement upon the orifice. Note that no suture loops are visible due prosthesis.
to tissue growth.

A B
Figs 9.66A and B: (A) Transthoracic echocardiographic parasternal long-axis view showing thrombus (arrow) between the two leaflets of a
bileaflet valve.(B) Figure shows transprosthetic gradients.

Fig. 9.67: Transesophageal echocardiographic view of a bileaflet Fig. 9.68: Transesophageal echocardiographic four-chamber view
mitral valve showing a large thrombus (arrow T). Thrombus is showing a tilting- disk mitral valve with a thrombus (yellow arrow) and
obstructing the affected disk. pannus ( white arrow).

Fig. 9.69: 2D Transesophageal echocardiographic view of a bileaflet
mitral prosthesis. Arrows point to thrombi. Note a thrombus in left atrial
appendage (right arrow).
Fig. 9.71: 3D Transesophageal echocardiographic view of mitral
bioprosthesis of the same patient as in Figure 9.70. Note the orifice
narrowing and thickening and fusion of the three leaflets.
formation. In a study by Deviri et al.27 evaluating the
surgical findings of 112 obstructed mechanical valves,
pannus formation was the underlying cause in 10.7% of
valves, pannus in combination with thrombus was present
in 11.6%, whereas thrombus alone or with little pannus
formation was found in 77.7%.
Inadequate anticoagulation not only can predispose to
valve thrombosis but also thrombus formation elsewhere
like in left atrial appendage (Fig. 9.69).
Ball variances observed in ball-in-cage prosthesis
include increase or decrease in size, deformation or
Evaluation of Prosthetic Heart Valves 159
Fig. 9.70: Transesophageal echocardiographic four-chamber view
showing a very narrow flow jet across a mitral bioprosthesis due to
structural degeneration.
Fig. 9.72: Starr-Edwards ball-in-cage valve showing ball variance due
to lipid absorption.
lobulation, changes in color and considerable softness
(Fig. 9.65). The loss of random motion of the ball due to
pathway impingement leads to more injury to the cage.
Increased velocity of blood flow across the ball due to
leakage or obstruction drives lipids into the ball making it
more swollen up and still greater obstruction.28
The intermittent or permanent mechanical dysfunc
tion causing jamming of the leaflet(s) may be a result of
dynamic or fixed distortion of the pivot guards during the
cardiac cycle (Fig. 9.74).29 Disk fracture and embolization
have been reported rarely.30 Patients with hypertrophy of
160 Section 2: Valvular Heart Disease
Fig. 9.73: 2D Transesophageal echocardiographic four-chamber
view in a patient with Starr-Edwards mitral prosthesis. Note the
pannus (white arrows) causing severe narrowing of the annulus along
with ball variance (multiple horizontal lines, yellow arrow).
Fig. 9.75: Trileaflet bioprosthesis in pulmonary valve position in a case
of operated tetralogy of Fallot.
the basal septum may be more susceptible to intermittent
jamming of the aortic bileaflet valve and leaflet pivots due
to distortion of the pivot guards.
TRICUSPID AND PULMONARY
PROSTHETIC VALVES
There is limited data with regard to tricuspid and
pulmonary valve prostheses. Usual indications are in some
patients with congenital heart disease, carcinoid valvular
disease and rheumatic heart disease. In tricuspid valve
disease, usually repair with annuloplasty is recommended
Fig. 9.74: Transesophageal echocardiographic four-chamber view
showing an arrested disk (arrow) causing high transprosthetic
gradients (inset). There is no evidence of a thrombus or pannus on
the valve.
Fig. 9.76: Continuous wave (CW) Doppler interrogation through a
pulmonary valve bioprosthesis. Forward flow velocity is 2 m/s. Some
regurgitation is noted.
due to high chance of valve thrombosis or degeneration.
However, mechanical or biological valves are also used.
Normally functioning tricuspid prosthetic valves have
a mean gradient < 5 mm Hg and pressure half-time
< 150 msec. Transprosthetic regurgitation is assessed in a
manner similar to that of mitral prosthesis.
In pulmonary valve position, usually bioprostheses
(homografts or xenografts) are used when there is
severe pulmonary regurgitation (Figs 9.75 and 9.76).
Peak forward flow velocities 3 m/s are considered
abnormal. Pulmonary regurgitation can be assessed with
similar parameters as used for aortic prosthetic valve

regurgitation although with limited validation. Some
degree of regurgitation is invariably recorded in pulmo
nary bioprostheses.
SUMMARY AND KEY POINTS
Evaluation of prosthetic heart valves requires an
integrated approach using history, intra- and posto
perative data, clinical examination, echocardiography
and cinefluoroscopy.
A baseline echocardiogram with detailed evaluation
is required to follow-up these patients. Serial studies
are of use when an asymptomatic abnormality is sus
pected.
Reliance on pressure gradients or EOA alone may be
fallacious because prosthetic valves have peculiar
hemodynamics.
Structural details are best seen by TEE. 3D TEE has
emerged a powerful tool for structural evaluation.
Patient-prosthesis mismatch needs to be noted
immediately after the operation.
Chamber reverse remodeling or lack of it is to be noted
besides prosthetic valve evaluation in each patient.
Catheter-based procedures to treat paraprosthetic
regurgitation, degenerative aortic valve stenosis and
biological valve stenosis are multiplying. This requires
a greater integration of several imaging modalities with
echocardiography.
Although stress echocardiography has been used for
evaluation of prosthetic valves, validation studies are
lacking.
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2. Yoganathan AP, He Z, Casey Jones S. Fluid mechanics of
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4. Zoghbi WA, Chambers JB, Dumesnil JG, et al. Recom-
mendations for evaluation of prosthetic valves with
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Society of Echocardiography and the Canadian Society
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5. Zoghbi WA. New recommendations for evaluation of
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7. Jones M, Eidbo EE. Doppler color flow evaluation of pros-
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Coll Cardiol. 1989;13(1):234-40.
8. Weintraub WS, Clements SD, Dorney ER, et al. Clinical,
echocardiographic, continuous wave and color Doppler
evaluation of bioprosthetic cardiac valves in place for more
than ten years. Am J Cardiol. 1990;65(13):935-6.
9. Alam M, Rosman HS, Hautamaki K, et al. Color flow
Doppler evaluation of cardiac bioprosthetic valves. Am J
Cardiol. 1989;64(19):1389-92.
10. Mohammadi S, Tchana-Sato V, Kalavrouziotis D, et al.
Long-term clinical and echocardiographic follow-up of
the Freestyle stentless aortic bioprosthesis. Circulation.
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11. McCarthy FH, Bavaria JE, Pochettino A, et al. Comparing
aortic root replacements: porcine bioroots versus pericar-
dial versus mechanical composite roots: hemodynamic
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12. Baumgartner H, Khan S, DeRobertis M, et al. Discrepan-
cies between Doppler and catheter gradients in aortic pro
sthetic valves in vitro. A manifestation of localized gradients
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13. Khan SS. Assessment of prosthetic valve hemodynamics
by Doppler: lessons from in vitro studies of the St. Jude
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14. Vandervoort PM, Greenberg NL, Powell KA, et al. Pressure
recovery in bileaflet heart valve prostheses. Localized high
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tic and mitral position. Circulation. 1995;92(12):3464-72.
15. Fisher J. Comparative study of the hydrodynamic function
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17. Glen SK, Wilson ES, Grosset DG. Transesophageal echocar-
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20. Mohan JC, Agrawal R, Arora R, et al. Improved Doppler
assessment of the Bjork-Shiley mitral prosthesis using the
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25. Nellessen U, Schnittger I, Appleton CP, et al. Transesopha-
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27. Deviri E, Sareli P, Wisenbaugh T, et al. Obstruction of me-
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e280-1.
 SEction 3
Systolic and Diastolic Function

Chapters

Left Ventricular Systolic Function Diastolic Function

Echocardiographic Assessment of Right Ventricular
Function: Methods and Clinical Applications
 Chapter
10
Introduction
The left ventricular (LV) systolic function is the most
commonly ordered and sought after information by
a cardiovascular physician because of the diagnostic,
therapeutic and prognostic decisions that are made with
its help. The LV is a pressurized chamber with a definite
architecture. It is a bidirectional asynchronous pump that
actively and passively receives blood from the pulmonary
circulation and ejects it further into the systemic
circulation. Ejection is the part of systole, which has been
used to estimate systolic performance most often.
Quantitative and qualitative measures of systolic
performance are both determined. The LV contracts
and then deforms in systole. However, contraction and
Fig. 10.1: Three arbitrary parts of the left ventricle.
(LVOT: Left ventricular outflow tract).
Left Ventricular
Systolic Function
deformation need to be studied separately and together
to understand the LV systolic function. Conventional
quantitative indexes include the assessment of ejection
fraction, ventricular volumes, ventricular mass and wall
stress. However, newer and simpler parameters have been
explored, which provide useful clinical information and
complement the conventional parameters.
MORPHOLOGY OF THE LEFT VENTRICLE
Normal LV comprises of an inlet, apical trabecular, and
an outlet portion1 although these portions do not have
discrete anatomical borders (Fig. 10.1).
The ventricular wall is thickest near the cardiac
base and thins to 12 mm at the apex (Fig. 10.2). This is
Fig. 10.2: Myocardial wall thickness and curvature at the apex.
166 Section 3: Systolic and Diastolic Function
Fig. 10.3: Helical orientation of the myocardial fibers with a figure of
8 near the apex.
Fig. 10.5: Three-layered structure of the interventicular septum (IVS).
The right-sided layer is the inner layer of the right ventricular oblique
fibers.
responsible for greater wall stress at the apex and more
often aneurysm formation.
Transmurally, through the ventricular wall, the
myoarchitecture has a typical arrangement of myocardial
fibers that change orientation from being oblique in the
subepicardium to circumferential in the middle and
to longitudinal in the subendocardium (Figs 10.3 and
10.4). This helical structure has functional significance.2
Interventricular septum (IVS) is three-layered and
hence more echogenic than the rest of the walls. It also
thickens less than the rest of myocardium due to its
anatomy (Figs 10.5 and 10.6).
Fig. 10.4: Graphic cross-sectional image of the LV. Blue color
represents subendocardial descending fibers and the red color depicts
outer subepicardial ascending fibers.
Fig. 10.6: Para-sternal short axis view showing three-layered interven-
ticular septum (IVS) with increased echogenic texture.
The normal LV comprises of an inlet portion containing
the mitral valve apparatus, an outlet portion leading to
the aortic valve, and an apical portion containing fine
trabeculations (Fig. 10.7).
The shape of the left ventricle approximates to a cone
or prolate ellipse with the right ventricle hugging it.1
This shape is an evolutionary process to make it most
energy efficient (Fig. 10.8).
Fine muscular strands or so-called false tendons that
extend between the septum and the papillary muscles
or the parietal wall are seen in nearly 50% of all subjects
(Fig. 10.9).

Fig. 10.7: 3D echocardiographic image of the left ventricle (LV) show-
ing fine trabeculations at the apex.
Fig. 10.9: Fibromuscular strand extending between anterior interven-
tricular septum and the posterior wall of the left ventricle (LV).
In many disease states, there are prominent trabe
culations that may make endocardial border delineation
difficult. The pathological entity of noncompaction, or
spongy myocardium, is characterized by prominent
and excessive trabeculations with correspondingly deep
recesses in between walls (Fig. 10.10). Herein, automatic
endocardial border detection may be a challenge.
The ventricular septum in the normal heart is curved,
convexing into the right ventricular cavity. It is muscular
except for a small portion immediately beneath the aortic
valve, which is a thin fibrous structure, the ventricular
component of the membranous septum (Fig. 10.11).
The papillary muscles supporting the mitral valve
are an integral component of the left ventricular wall
Left Ventricular Systolic Function 167
Fig. 10.8: Conical shape of the left ventricle (LV) cavity by 3D echo.
Fig. 10.10: 3D cross-sectional image of the mid-LV. Arrows point to
trabeculations and deep recesses.
and participate in the longitudinal function of the LV
(Fig. 10.12). These extend from apical third of the ventri
cular walls to the mitral annulus via tendinous chords.1
Physiology of the Left Ventricle
The LV systole is defined as that part of cardiac cycle
wherein active contraction occurs. Typically, it occurs
with the closure of the mitral valve and when the LV
developed pressure exceeds that of the left atrium.3
Contractile performance is the basis of the LV systolic
function. Due to this contraction, when the developed
systolic LV pressure exceeds that of aorta, blood is ejected
into the latter (Fig. 10.13).
168 Section 3: Systolic and Diastolic Function
Fig. 10.11: Arrow points to membranous (MS) part of the interventricular
septum (IVS).
Fig. 10.13: Phases of cardiac cycle of the LV.
(IVCT: Isovolumic contraction time; ITC: Isotonic contraction, ITR:
Isotonic relaxation).
The total blood ejected into aorta in one cardiac cycle
is stroke volume (SV) and the work done to achieve this
SV is called stroke work. At the end of systole, the volume
left in the LV (end-systolic volume) and the end-systolic
pressure are indicative of intrinsic LV contractility, and
the SV and stroke work represent systolic function and
more accurately when normalized for the end-diastolic
volume.4 These functions can be accurately depicted by
the LV pressurevolume loop (Fig. 10.14).
Pressurevolume loop cannot be studied nonin
vasively. However echocardiography helps to estimate
SV, end-systolic volume and ejection fraction (SV/end-
Fig. 10.12: Graphic apical three-chamber view showing anterolateral
(ALPM) and posteromedial (PPM) papillary muscles. The thin chords
extending to the mitral valve are the tendinous chords.
Fig. 10.14: The left ventricular pressure-volume loop. Width of the
loop represents stroke volume (SV) and area of the loop is stroke
work. (IVC: Isovolumic contraction; (IVR: Isovolumic relaxation).
diastolic volume), the commonly used parameters of the
LV systolic function.
The LV systole has two parts:
1. Isovolumic contraction (IVC)
2. Ejection
Ejection is further divided into rapid ejection (isotonic
contraction) and slow ejection (isotonic relaxation)
The LV function can be studied in all these four
phases of tensiontime sequence (Fig. 10.15). Combined
myocardial performance index is a ratio of isovolumic
time/isotonic time and provides information about
systolic and diastolic function. This can be obtained by

Fig. 10.15: The left ventricular tension-time sequence.
Fig. 10.17: Common indices of systolic function like fractional short-
ening, ejection fraction and mitral annular systolic excursion are
measured at end-systole.
Doppler echocardiography.5 Rate of maximum pressure
development (dP/dT) is measured during IVC phase
and is afterload independent. This can be obtained from
the continuous wave (CW) Doppler signal of mitral
regurgitation.6
Tension development peaks in early systole while the
maximal deformation of the LV occurs at end-systole or
slightly beyond it (Figs 10.16 and 10.17). Hence, there are
two types of LV systolic function indices commonly studied7:
1. Peak systolic indices
2. End-systolic Indices
Peak systolic velocity indices [mitral annulus tissue
velocities, ejection velocities, and strain rate (SR)] exhibit
Left Ventricular Systolic Function 169
Fig. 10.16: Myocardial tissue velocity spectrum in a single cardiac
cycle. Rate of tissue motion or deformation (systolic velocity) peaks in
early systole coinciding with peak of isotonic contraction.
Fig. 10.18: Graphic depiction of the LV showing three major vectors
of deformation.
(L: Longitudinal; R: Radial and circumferential).
greater variation than end-systolic indices during inotropic
alterations from which it is assumed that they better reflect
LV contraction (Figs 10. 16 and 10.17).
End-systolic indices are less sensitive to heart rate
manipulation compared to peak systolic indices. However,
it is not clear if there are significant differences between
the two types of indices.
Myocardial Muscle Mechanics
Development of tension results in deformation. Systolic
function is a manifestation of deformation. There are
four recognizable vectors of deformation (Fig. 10.18)
170 Section 3: Systolic and Diastolic Function
Fig. 10.19: Relationship of left ventricle ejection fraction (LVEF) with
shape of the left ventricle for a fixed 15% long-axis shortening.
Fig. 10.21: Relationship of velocity of shortening and afterload. With
increasing preload, the curve shifts upward.
1. Longitudinal shortening
2. Radial thickening
3. Circumferential shortening
4. Rotation
Complex interplay of these vectors of deformation
results in energy-efficient systolic function. These
deformation indices also provide useful information about
the systolic function. Longitudinal deformation indexes
are getting accepted for clinical use although other types
of deformation are under active validation.8
There is a relationship between longitudinal defor
mation and the left ventricular shape. Longitudinal
shortening is a good surrogate for global systolic function
(Fig. 10.19).
Fig. 10.20: Determinants of left ventricle systolic function.
Determinants of LV Systolic Function
For a certain degree of contractility (the intrinsic contractile
strength of the myocardium), the SV of the ventricle,
which is the most obvious systolic function parameter, is
determined by the preload (the end diastolic ventricular
volume, pressure or stretch), afterload (the force opposing
ejection) and the heart rate, which has biphasic effect
of increasing contractility and reducing diastolic filling
period (Fig. 10.20).
Contractility can be altered by adrenergic stimulation,
heart rate and calcium.
To some extent, preload-adjusted parameters can be
estimated by using end-diastolic length or volume as the
denominator, the most prominent example of which is
ejection fraction wherein SV is indexed for end-diastolic
volume.
Physiological Principles
Governing LV Systolic Function3
Starlings law: Ability of the heart to change its force of
contraction and therefore SV in response to changes in
venous return is called the Frank-Starling mechanism
(or Starlings Law of the heart). Increasing the sarcomere
length increases troponin C calcium sensitivity, which
increases the rate of cross-bridge attachment and
detachment, and the amount of tension developed by
the muscle fiber (Figs 10.21 and 10.22)
Bowditch effect: It is an autoregulation method by
which myocardial contractility increases with an

Fig. 10.22: Relationship between the preload [end-diastolic volume or
end-diastolic pressure (EDV and EDP)] and the SV.
Fig. 10.24: The method of measuring wall stress.
increase in heart rate. Also known as the Treppe
phenomenon, Treppe effect or staircase effect
(Fig. 10.23). Mechanism is that the Na+-Ca+ membrane
exchanger, which operates continually, has less time
to remove the Ca++ that arrives in the cell because of
the decreased length of diastole with positive
chronotropy. With an increased intracellular Ca++
concentration, there follows a positive inotropy.3
Laplaces law: The Laplaces law governs the
relationship of wall stress to radius and wall thickness
in presence of a given amount of force generated by the
LV. Wall thickening increases to maintain normal wall
stress whenever the LV dilates. Increased wall stress is
the initial manifestation of the declining systolic
function (Fig. 10.24). End-systolic volume normalized
Left Ventricular Systolic Function 171
Fig. 10.23: Relationship between force developed and the heart rate.
for end-systolic wall stress is a fairly good index of
systolic elastance or contractility.
Long Axis LV Function
Base of the heart, referred to as the atrioventricular (AV)
plane or ring, moves toward the apex during systole, and
the apex makes very slight movements.9 Long axis motion
of the mitral annulus reflects the function of longitudinally
oriented left ventricular myocardial fibers (Fig. 10.25)
This rapid motion of the mitral annulus is dependent
on stored energy from the previous systole and contributes
significantly to LV (suction and early) filling in normal
hearts.
The normal mean mitral annular total amplitude of
motion in healthy adults ranges from 10 mm to 15 mm.
These values may be higher in younger subjects and have
been reported to decline from 15 mm at 2040 years to about
10 mm at 6180 years.10
Characteristically, when the overall long-axis ampli
tude is low, peak shortening and lengthening rates are
reduced and global ejection fraction is reduced.11
Methods to study long axis function are:
Mitral annulus plane peak systolic excursion (MAPSE)
by two-dimensional (2D)-directed M-mode (Fig. 10.26)
Tissue tracking or displacement by color Doppler
myocardial imaging
Peak systolic velocity of the mitral annulus by tissue
Doppler imaging
Use of 2D or three-dimensional echocardiographic
(3DE) methods to study long-axis shortening from
172 Section 3: Systolic and Diastolic Function
Fig. 10.25: Graphic depiction of descent of the LV base during systole
and longitudinal expansion during diastole.
apical endocardial peak to midpoint of mitral annulus
in apical views.
Method for MAPSE Estimation
The 2D-targeted M-mode beam is directed from
the apex along the hinge points of the mitral valve
apparatus and lateral, septal, inferior, anterior and
posterior LV walls in four-, two- and three-chamber
views.
The regional displacement is calculated after 60 ms
from the beginning of the QRS complex to the first peak
of the mitral annular waveform.
To normalize MAPSE measurements, the longitudinal
LV inner distance is measured from the apical
endocardial border to the AV plane at the end of
diastole.
Anatomical M-mode is used to overcome limitations
with regards to parallel alignment of the M-mode beam
to the plane of mitral annulus.
Color tissue Doppler M-mode can be used as an
additional method to assess the amplitude of MAPSE,
as this technique ensures high spatial and temporal
resolutions.
Tissue tracking algorithm of the color Doppler
myocardial imaging can provide this information
off-line.
LV Volumetry
A comprehensive quantitative assessment of end-systolic
and end-diastolic volumes of the entire left ventricle is
most sought after information to obtain ejection fraction
Fig. 10.26: Mitral annulus plane systolic excursion (MAPSE) by
2D-guided M-mode from apical view.
and to monitor the LV remodeling. It is best provided
by the 3DE with semiautomated or automated edge-
detection algorithms. However, in clinical practice, 1
or 2D echocardiographic techniques are commonly
used with geometric assumptions to obtain LV volumes.
Typical simplifications, which require only a limited
number of measurements, are currently made based upon
geometric assumptions of the left ventricular geometry.12
All assumptions more closely approximate true left
ventricular chamber sizes when the heart is normal,
resulting in greater errors when there is global enlargement
or dysfunction. The greatest errors occur in settings of
regional anatomic distortion or systolic dysfunction. A
summary of these is given below:
Cube Formula and its Modification
M-mode calculations of LV volumes assume that the LV is
a prolate ellipse and that by measuring a single minor axis
dimension and cubing it, volume can be calculated.
The volume of a cube is based upon a single left
ventricular measurement of midcavity diameter (LVID),
which is derived from M-mode data obtained from the
2D para-sternal long- or short-axis view. Volume is
derived from the following formula:
Volume [V] = D3
Teichholz modified this formula for better correlation
with other methods of volume estimation.13
The Teichholz equation
Volume = [7/(2.4 + LVID)] [LVID]3
Although commonly present in most echocardio
graphic calculation packages, it has been given up due to
inaccuracies (Fig. 10.27).

Fig. 10.27: Minor axis diameter obtained can cause marked variations
in volume calculation by cube formula.
Fig. 10.29: Biplane ellipsoid formula to estimate LV end-diastolic
volume. There is a difference of 10 mL volume between the two planes.
Single-Plane Ellipsoid
The volume of a single-plane ellipsoid uses left ventricular
length (L) and midcavitary area (A) measurements
obtained from the apical four-chamber view (Fig. 10.28).
The volume may be calculated as follows:
Volume = 0.85 A2/L
Biplane Ellipsoid Formula
(Biplane Area-length Method)
The volume formula using a biplane ellipsoid employs
left ventricular length (L) and area (A) measurements
obtained from the apical four-chamber view (A1) as well
as two-chamber view (A2). The smaller of the two lengths
is used as denominator (Fig. 10.29).
Volume = 0.85 A1 A2/ Lmin
Left Ventricular Systolic Function 173
Fig. 10.28: Single-plane ellipsoid formula to estimate volume.
Fig. 10.30: Bullet method to estimate left ventricle volume.
(LVOT: Left ventricle outflow time).
Bullet Formula
The volume of a bullet shape uses the left ventricular
length (L) from the apical four-chamber view with the left
ventricular chamber area (A) from the para-sternal short-
axis midcavity view (Fig. 10.30).
Volume = 0.83 A L
Modified Simpsons Rule
(Disk Summation Method)
The modified Simpsons rule determining left ventricular
volume consists of a summation of discs using a measure
ment of the left ventricular length (L) from the apical four-
chamber view and the two-chamber view. Height of each
disc is predetermined and discs are placed equidistant
174 Section 3: Systolic and Diastolic Function
Fig. 10.31: Modified Biplane Simpson or disk summation method to
estimate LV volumes. Disks are stacked from base to apex at equal
distance.
(Fig. 10.31). Biplane method of discs is recommended by
the American Society of Echocardiography.12
Modified Quinones Method
The modified Quinones method is commonly used and
employs linear measurements.14 It uses single measure
ments of the LV cavity in the midventricle in both
end-diastole and end-systole, and can be employed using
either M-mode or 2D imaging (Fig. 10.32).
Because only two linear measurements are needed, the
modified Quinones method often requires less time to
perform than other methods and only needs adequate
visualization of the endocardium in the midventricle.
However, because this method only measures circum
ferential contraction in a single plane, significant
assumptions about LV chamber geometry have to be
made so that a change in a linear measurement can act
as a surrogate for a change in volume.
The contribution from longitudinal contraction on
LVEF is not directly measured, but rather a correction
factor is used to adjust the measured LVEF based on a
visual grading of the apical contraction.
In situations where there is asymmetry of contraction,
such as in ischemic LV dysfunction, this method has
significant limitations.
With the modified Quinones method, the cavity size
can be overestimated if the ultrasound beam/image is not
perpendicular to the ventricular cavity, or underestimated
if the ultrasound beam/image is not in the center of the
cavity.
Fig. 10.32: Modified Quinones Method. Measurement of midcavity
diameters and qualitative assessment of the apex.
(LVEDD: Left ventricular end-diastolic diameter; LVESD: Left ventricular
end-systolic diameter).
LVEF = LVEDD2 LVESD2/LVEDD2 100 + K (constant)
K values are
Normal apex +10%
Hypokinetic apex +5%
Akinetic apex 0%
Dyskinetic apex 10%
Endocardial Border Delineation
For LV volumetry, accurate endocardial border delineation
is paramount. This can be performed using:
Harmonic imaging.
Use of contrast for chamber opacification (Fig. 10.33).
Automatic endocardial border detection.
Ejection Fraction
Left ventricular ejection fraction (LVEF) is the fraction
of blood pumped out of the LV with each heart beat.
It can be measured by the invasive methods and
noninvasive methods like gated blood pool heart
scan, computerized tomography, cardiac magnetic
resonance imaging and echocardiography.
In a clinical situation, LV volumes and EF measure
ments for a specific patient are classified as normal
or abnormal based on established normal limits.
Although LV ejection fraction is a continuous biological
variable, a value < 55% has been termed abnormal
by the recent guidelines of the American Society of
Echocardiography (ASE).

Fig. 10.33: Apical four-chamber (left) and two-chamber (right) views
with chamber opacification with Sonovue. Contrast use makes endo-
cardial border stand out. But plane of mitral annulus may be difficult
to identify.
Prognosis and therapeutic decisions are often based on
left ventricular ejection fraction (LVEF), which means
the LVEF needs to be accurately measured.
Reference values for normal people:12
LV end-diastolic volume index 3575 mL/m2
LV end-systolic volume index 1230 mL/M2
LVEF >55%.
A temporal variability in ejection fraction (EF) of 5%
might occur with 3DE due to physiological differences
and measurement variability, whereas this might be
>10% with 2D methods. Overall, 3DE has the best intra-
and interobserver as well as test-retest variability.15
M-Mode Echocardiography
M-mode echocardiography has fallen in disrepute as
a technique to assess LV systolic function because of
significant limitations. However, some people still continue
to use it under 2D-echocardiographic guidance. It is the
simplest way to obtain LV dimensions and wall thickness
and if obtained with anatomical M-mode (a technique to
steer the cursor so that it remains perpendicular to the LV
walls), is reasonably accurate.16
Left ventricular chamber size reduction during systole
is the consequence of the simultaneous contraction of
myocardial layers in the different directions, yielding the
three basic left ventricular geometric changes: reduction
of minor axis, shortening of long axis and twisting of the
Left Ventricular Systolic Function 175
Fig. 10.34: M-mode measurements can be obtained using 2D echo-
cardiographic guidance from parasternal long-axis or short-axis views.
apex. M-mode echocardiography can be used to estimate
the first two changes.
However, minor axis shortening is a valid surrogate
of global systolic function only if the ventricle contracts
symmetrically and without any geometric alteration
(Fig. 10.34).
M-mode echocardiography has been used to estimate:
LV dimensions.
LV wall thickness.
Fractional shortening of the LV.
Circumferential fiber shortening.
Velocity of circumferential fiber shortening.
Ejection fraction by modified cube formula.
Midwall shortening fraction.
Meridional wall stress (using LaPlace law).
Mitral E point-Septal separation distance.
Relative wall thickness.
Segmental wall motion abnormality confined to ante
rior interventricular septum (IVS) or posterior wall.
Endocardial fractional shortening is usually preserved
while midwall fiber shortening is reduced with onset of
systolic dysfunction. In fact, there is an epicardium-to-
endocardium thickening gradient in systole, which is a
better index of systolic function than one-dimensional
endocardial shortening alone.
The magnitude of systolic shortening measured at
the endocardium does not directly reflect the intramural
shortening.
176 Section 3: Systolic and Diastolic Function
Fig. 10.35: M-mode cross-sectional view at the level of mitral leaflets
with various measurements shown on the right side of the image.
Fig. 10.37: M-mode of the basal part of the LV showing mitral E point
very close to IVS indicating normal systolic function.
Method
M-mode tracing is obtained by placing the cursor
just beyond the tips of the mitral valve leaflets in
2D-echocardiographic para-sternal long-axis view
(Fig. 10.35).
Ultrasound beam is kept parallel to the IVS.
Measurements are made by leading-edge method,
using R wave on ECG as the end-diastole and the peak
of LV posterior wall thickening as the end-systole.
(Fig. 10.35).
LV dimensions and wall thickness are measured both
at end-diastole and end-systole.
Fig. 10.36: Measurement of LV ejection time (ET) from the box-like
opening of the aortic valve.
Fig. 10.38: Increased EPSS in a patient with LV systolic dysfunction.
Ejection time (ET) is measured from the M-mode
tracing of the aortic valve (Fig. 10.36).
Mitral valve E points to IVS distance (EPSS) in early
diastole is measured as an indirect index of LV systolic
dysfunction (Figs 10.37 and 10.38).
Measurements: Following measurements and calcula
tions are made:
LV end-diastolic dimension (normal 3.55.3 cm).
LV end-systolic dimension (2.53.9 cm).
LV fractional shortening (LV diastolic dimension
minus end-systolic dimension divided by end-diastolic
dimension 100, normal values 2745%).

Fig. 10.39: Estimation of velocity of circumferential fiber shortening.
Ejection time is obtained from the aortic valve (right panel).
LV ejection fraction, which is automatically calculated
by the system using Teichholz method.
Velocity of circumferential fiber shortening (Normal
> 1.0 circumference/s) (Fig. 10.39).
The 2D-guided mitral plane systolic excursion
(MAPSE). An average value of medial and lateral
edge is normally > 12 mm and corresponds well to 3D
ejection fraction.
Measurement of circumferential left ventricular
shortening in the middle of the diastolic wall thickness
(midwall shortening17).
Limitations of M-mode Echocardiography16
Limited ice pick view of the LV (accuracy will depend
upon the slice being examined).
Measurements not valid for asymmetric ventricles.
Errors due to nonparallel cursor.
Geometric assumption in measurement of ejection
fraction.
Paradoxical motion of IVS (LBBB, postoperative, RV
volume overload) leads to false and inaccurate functi
onal parameters.
Current Use of M-mode Echocardiography in
LV systolic Function Assessment
Measurement of MAPSE
Myocardial performance index can be measured by
sweeping the beam from mitral valve to aortic valve to
get opening and closing of both valve leaflets in a single
image
Left Ventricular Systolic Function 177
Fig. 10.40: M-mode image of the mitral valve (above) and aortic valve
(below) and M-mode of the color tissue velocity image of the poste-
rior wall. Note prolonged isovolumic contraction period (before aor-
tic valve opening) and also isovolumic relaxation period (aortic valve
mitral valve opening). There is continued thickening of the posterior
wall during IVRT indicative of systolic dysfunction.
(AVO: Aortic valve opening; MVO: Mitral valve opening; AVC: Aortic
valve closure).
M-mode color flow propagation velocity of the mitral
valve to get early diastolic suction effect and hence
indirect idea about systolic function
M-mode of the tissue color Doppler images to under
stand physiology better with high temporal resolution
(Fig. 10.40)
2D Echocardiography and LV Systolic Function
2D Echocardiographic Minor Axis Shortening
Minor axis endocardial shortening has been considered
a valid surrogate for regional ejection fraction (Fig. 10.41)
and could also be used for global function in case the LV
is contracting symmetrically and a constant is used for
apical myocardial behavior.
However, endocardial shortening becomes a poor
indicator of LV function in presence of increased wall
thickness, concentric remodeling and in presence of
segmental asynchrony.
Systolic shortening of longitudinally oriented sube
picardial and subendocardial fibers squeezes the
circumferentially oriented fibers at the midwall level,
thereby potentiating cross-fiber myocyte thickening
and cross-fiber left ventricular radius shortening.
Ventricular radius shortening at the endocardium is
the consequence of the interaction of contraction and
thickening of differently aligned myocardial muscular
layers located at a distance.
178 Section 3: Systolic and Diastolic Function
Fig. 10.41: Endocardial shortening fraction at the level of chordae
tendinae. Normal values are 2745%.
Fig. 10.43: Midwall fiber shortening, a technique that was in great
vogue before the advent of acoustic speckle tracking for cross-fiber
function.
Endocardial radius shortening provides much
less information about systolic function compared
to midwall shortening or circumferential shortening
(Figs 10.42 and 10.43).
2D Echocardiographic Ejection Fraction
Although eyeballing for estimation of ejection fraction
from 2D echocardiographic views is quite in vogue,18 most
laboratories still measure LV volumes. The most commonly
used and recommended method is biplane Simpson
method because it has least geometric assumptions.19 It is
also possible to create an automatic grid by marking two
points of the mitral annulus and the apex. The grid can then
be manually modified to correctly trace endocardium.
Fig. 10.42: 2D echocardiographic parasternal long axis view showing
method of assessing circumferential fiber shortening.
Technical Tips for LV Volume
Estimation by the Simpson Method
End-diastole and end-systole are identified from 2DE
cine-loops using frame-by-frame analysis of the apical
four- and two-chamber LV views as the largest and
smallest cavity during the cardiac cycle, respectively.
Tracing of endocardial border is manually done in
both frames, paying attention to include the papillary
muscles within the LV cavity.
Left ventricular ejection fraction is automatically
calculated by the software using the biplane disk-
summation algorithm (modified Simpsons rule).
Use of biplane imaging makes it easier to estimate
volumes of the two views in the same frame. It also
allows alignment of the cursor to define apex better.
Border detection can be improved by use of harmonic
imaging and with optimum sector width.
Volumetime curves can also be generated using
vendors software.
Fully automated measurements with no manual
correction of LV volumes produce an underestimation
of LV volumes in comparison with manually corrected
ones.
High image quality is a prerequisite for any border-
detection method and no less dependent on the
operators expertise in image acquisition. All efforts
should be made to obtain crisp endocardial delineation
in as many segments as possible.
If there are more than two segments showing
endocardial dropouts in any view, contrast should be
liberally used for chamber opacification20 (Fig. 10.44).

Fig. 10.44: LV opacification by a contrast agent. It is easy to
include papillary muscles and trabecular recesses in the cavity by this
technique to get larger volumes than by standard 2D gray-scale
imaging. Note quantitative analysis of the LV volumes by 2D echo-
cardiography is highly experience-dependent and uses only
partial information about cardiac anatomy and function contained in
predefined cross-sectional views. Therefore, it may be subject to
substantial measurement errors, particularly in patients with regional
wall-motion abnormalities and/or distorted LV geometry.21
Limitations of 2D Echocardiography
for LV Volume Estimation
Geometric assumptions for estimating volume, which
may not be valid.
Apical foreshortening (typically, long-axis diameter
in an adult should be > 8 cm: failure to achieve this,
indicates apical foreshortening).
Off-axis imaging (plane positioning error).
Translation and rotation from diastole to systole.
Suboptimal images and difficulties in tracing the entire
endocardium.
Challenge of endocardial delineation in situations of
hyper-trabeculation.
High intraobserver, interobserver and test-retest
variability.
Operator-dependent and requires experience.
Real-Time 3D Echocardiography for
Study of LV Systolic Function
Real-time 3D-echocardiography obviates the limitations
inherent in 2D echocardiographic volumes and ejection
fraction estimation.21,22 It is possible to obtain these
measurements within minutes using various algorithms
Left Ventricular Systolic Function 179
Fig. 10.45: Full-volume data set recorded from an apical view.
built in the systems. The key to 3D imaging is a matrix-
array transducer and an inbuilt software algorithm for 3D
calculation.
Method of 3D Volumetry and
Ejection Fraction Measurement
In a system capable of 3D imaging, a full-volume data
set is recorded in held respiration, using a matrix array
transducer in any apical view over 46 beats (Fig.
10.45). In this way, a pyramidal 3D data set of 90 90
is obtained at a frame rate of 2025 Hz.
The pyramidal volume data set is transferred to 3D
calculation package. The volume data set is usually
recorded in 46 beats and these volume slices
are stitched together to get a pyramidal set. It is
also possible to obtain full volume data set in one
cardiac cycle although temporal resolution is usually
suboptimal (Fig. 10.46).
In multiplane reconstruction mode, the system
displays two or more apical images, one or none
short-axis image and one pyramidal data set in a quad
screen format (Fig. 10.47).
Using longitudinal and horizontal cursors, longest
apical views with best endocardial delineation are
obtained.
The software guides to place points on the two edges
of the mitral annulus and at the peak of endocardium
at the true apex both in end-systole and end-diastole.
The endocardium is traced > 700 points. Manual
correction is frequently performed for optimization of
endocardial tracking.
180 Section 3: Systolic and Diastolic Function
Fig. 10.46: Pyramidal full volume data set acquired in 4 cardiac cycles.
Fig. 10.48: 3D reconstruction of the LV cavity from the tracked
endocardium. Graph below shows regional volumes with marked
end-systolic volumes.
Once endocardial delineation and tracking is
accepted by the operator, the system automatically
calculates regional and global volumes and ejection
fraction along with systolic dyssynchrony index
(Figs 10.48 and 10.49). The software creates a mathe
matical model or cast of the LV, which allows time
volume calculations to be performed for the entire
cardiac cycle.
If there are stitch artifacts, the data set needs to be
discarded.
Further parametric calculations for onset of contraction
and amount of shortening in various regions can also
be displayed in bulls eye map.
In a ventricle with synchronous contraction of all
segments, one expects each segment to achieve its
minimum volume at almost the same point in the cardiac
Fig. 10.47: Multiplane reconstruction of the 3D full volume data set.
Fig. 10.49: Display of 3D data set calculation. All 16-segments
contract to reach end-systolic volume nearly simultaneously in this
subject.
cycle, whereas in a dyssynchronous ventricle there will be
a dispersion in the timing of the point of minimum volume
for each of the 16 or 17 segments. The degree of dispersion
can be calculated by measuring the standard deviation of
the time to achieve minimum volume and then correcting
that for the R wave to R wave (R-R) interval. This allows
derivation of a systolic dyssynchrony index, which can be
used to quantify the degree of LV dyssynchrony from a
comparison of all segments (Fig. 10.50).
Advantages of 3D Echo
Low intraobserver and interobserver variability.
Automatic endocardial delineation with small manual
correction; 3D measures endocardial position at
> 700 points.

Fig. 10.50: Marked dyssynchrony shown by greater dispersion of
regional end-systolic points.
Fig. 10.52: Annular tissue velocities recorded from the lateral edge of
the mitral annulus. Arrows point to peak systolic velocity. First systolic
wave during ejection is due to contraction of longitudinal fibers.
High concordance with gold standards like cardiac
magnet resonance imaging.
No geometric assumptions.
Regional volumes and functions can be studied with
ease.
Better description of sphericity index (calculated by
dividing the LV end diastolic volume (calculated from
a 3D data set) by the volume of a sphere, the diameter
of which is the LV major end diastolic long axis).
Analysis of regional function in time domain and study
of intraventricular dyssynchrony.
Patients with a higher dyssynchrony index have a lower
ejection fraction (Fig. 10.51).
Parametric bulls eye displays of the timing of LV
contraction are also available.
Left Ventricular Systolic Function 181
Fig. 10.51: 3D volumes, ejection fraction and systolic dyssynchrony
index ( SDI) displayed simultaneously. An SDI of < 8% is considered
normal.
Limitations of 3D
The details of how the endocardium is traced are
important.
Spatial resolution of 3D echocardiography is still
limited.
The trabeculae may be attributed to the LV wall.
The reliability of automated correction methods that
can be used to track the compacted myocardium
seems encouraging but warrants further study.
The application of contrast during 3D imaging may
improve some of these problems but continues to pose
challenges that relate to the definition of the mitral
annular plane.
The optimal balance between multibeat imaging,
which offers better spatial resolution but has the risk of
stitching artifact, and single-beat acquisitions remain
to be elucidated.
Studies have demonstrated differences between online
and offline measurement of LV volumes, possibly
related to differences in the automated detection
algorithms.
Intervendor differences need to be sorted out.
All in all, 3DE estimation of ejection fraction and
dysynchrony index is likely to replace 2D parameters in
near future.
Systolic Velocities of the Mitral Annulus
During the ventricular ejection period, longitudinal
shortening of the LV can affect the movement of mitral
annulus and produce S wave (Fig. 10.52), which is peak
annular systolic velocity.23
182 Section 3: Systolic and Diastolic Function
Fig. 10.53: Marked difference in S velocity on medial versus lateral
edge due to wall motion abnormality.
The systolic motion of the mitral annulus is not entirely
due to myocardial longitudinal shortening or contraction
but rather is the summation of contraction and rotation.
Apical rotation itself can be regarded as a main driving
force of longitudinal shortening
These velocities are measured with ease, less influenced
by the loading condition of the LV and have low inter- and
intraobserver variability.
Tips to Record Mitral Annular Velocities
Mitral annular longitudinal velocities are recorded
using pulsed-wave mode by positioning the Doppler
cursor with a 5 mm sample volume at the lateral, septal,
inferior, anterior and posterior AV margins in LV tissue
Doppler apical images.
Care is taken to ensure that the ultrasound beam is
kept parallel to the mitral annular motion.
The filters and gains are set low in accordance with
the recommendations for quantification of Doppler
echocardiography.
Peak systolic velocity is measured avoiding the initial
peak that is observed during IVC time. However,
during ejection also, there can be two peaks, usually
at the lateral edge. The first systolic wave represents
contraction of longitudinal fibers.
The advantage of mitral annular velocities is that these
are not dependent upon quality of images.
A good association between S and apical rotation
under a variety of LV inotropic conditions has been
shown.
Fig. 10.54: A peaks velocity of 5 cm/s (medial edge of the mitral
annulus) in a subject with dilated cardiomyopathy and ejection
fraction of 30%.
The location of tissue Doppler sample volume is another
issue in the assessment of global LV contractility. The
major advantage of the medial (septal) mitral annulus
is that the ultrasound beam is most parallel to the LV
longitudinal movement.24
Global left ventricular function can be estimated
by recording mitral annular systolic velocity. The
implementation of a cutoff limit of 8 cm/s gives a simple
guide for differentiating between normal and abnormal left
ventricular systolic function that might be useful clinically
in patients without regional wall-motion abnormalities.
However, in patients with important segmental
wall-motion abnormalities during systole, left ventricular
longitudinal shortening may be an imperfect surrogate
for ejection fraction (Fig. 10.53).
The best differentiation of normal (> or = 50%)
from abnormal (< 50%) ejection fraction is provided
by peak systolic velocity > or = 8 cm/s for the medial
(sensitivity 80%, specificity 89%) or lateral (sensitivity 80%,
specificity 92%) mitral annulus.25
Vinereanu et al.25 showed that 90% of the patients with
systolic heart failure (LVEF < 50%) had impaired mitral
annular systolic velocity less than 7.05 cm/s. Park et al.26
compared their data of mitral annular systolic velocity
(medial edge) of less than 6.8 cm/s with 3DE ejection
fraction, which showed best sensitivity, specificity of
94% and 87%, respectively, for systolic dysfunction
(LVEF < 50%) (Figs 10.54 and 10.55).
A rest-stress difference of > 2.0 cm/s in S velocity
indicates myocardial reserve that can be of help in
detecting myocardial viability.27

Fig. 10.55: Same patient as in Fig. 10.54. Note about 1cm/s S velocity
difference between two sites.
Fig. 10.57: dP/dt of 572 mm Hg/sec in a patient with dilated cardio
myopathy and ejection fraction of 28%.
The dP/dt of the LV as a
Doppler Measure of Contractility
The LV contractility dP/dt can be estimated by using
time interval between 1- and 3m/s on MR velocity CW
spectrum during isovolumetric contraction, that is, before
aortic valve opens when there is no significant change in
LA pressure (Figs 10.56 and 10.57).28
32
dP/dt =
T
Left Ventricular Outflow Tract Velocity
Time Integral
Left ventricular outflow tract velocity-time integral
(LVOTvti) is an effective and noninvasive method when
Left Ventricular Systolic Function 183
Fig. 10.56: Graphic display of estimation of the LV dP/dt from CW
mitral regurgitation signal.
assessing LV systolic function under conditions of varying
preload, heart rate, and inotropic state (Fig. 10.58)
LVOTvti is thought to be a better indicator of LV systolic
function than is SV, without the confounding factor of
LVOT-area measurements.
The Doppler VTI method in estimating SV and
cardiac output correlates well with results of concurrent
thermodilution cardiac output determinations in patients
without significant left-sided valvular regurgitation.
Normal values range from 17 cm to 24 cm. Its best use
lies in emergency care where serial measurements may be
important to assess SV.
This is also the parameter most often used for
optimizing resynchronization therapy.29
Global Longitudinal Strain and
Strain Rate
With tissue Doppler imaging and speckle tracking, quanti
fication of the LV function has moved beyond the simple
ejection fraction measurements and wall-motion score.
Systolic dysfunction might be initially apparent in the
longitudinal direction because subendocardial fibers,
which are the ones more vulnerable to myocardial isch
emia and fibrosis, are longitudinally oriented (Fig. 10.59).
Systolic longitudinal strain is defined as the percent
shortening of the myocardium during the systole
and its rate of shortening is called SR. Typically,
global longitudinal strain of the LV exceeds -15% and SR
exceeds 1/s-1.
Strain parameters can be estimated using tissue
Doppler technique (unidimensional) or acoustic speckle
184 Section 3: Systolic and Diastolic Function
Fig. 10.58: Estimation of LVOTvti in a normal subject.
Fig. 10.60: Longitudinal strain (left panel) and strain rate (right panel) by myocardial Doppler technique. Peak longitudinal strain of basal
interventricular septum (IVS) is -12% and peak strain rate is 0.8 s-1.
tracking (2D or 3D). Tissue Doppler-based strain is
slightly higher due to greater temporal resolution
(Figs 10.60 and 10.61).
Non-Doppler 2D strain by acoustic speckle tracking is
angle-independent, easy to use and provides both regional
and global strain from gray-scale images. It has lower
temporal resolution than the Doppler-based method but
is more reproducible (Fig. 10.62).
Strain and SR measurements are well documented
and validated tools for the quantification of myocardial
Fig. 10.59: Graphic description of longitudinal shortening of the LV
during systole.
function.30 While strain correlates with SV and ejection
fraction, SR has strong correlation with dP/dt. The
potential for detecting subclinical LV systolic dysfunction
by the alteration of longitudinal strain is the premise for its
use in clinical conditions.31
Through longitudinal strain analyses in four-chamber,
two-chamber and apical long-axis views, both regional
(relative to each of the 16 or 17 LV segments) and global
strain values (global longitudinal strain) can be obtained
(Fig. 10.63).

Fig. 10.61: Acoustic speckle tracking of the IVS showing spectrum of longitudinal strain in right upper panel (-11%).
Global longitudinal strain is a superior outcome
predictor compared to the EF and wall-motion score
index.32 Further, significant correlation between global LS
and e confirms the link between systole and diastole.
Method of Assessing Longitudinal Strain
Using commercially available 2D strain software,
the endocardial border in the end-systolic frame is
manually traced.
Three apical views are used to estimate global LS.
A region of interest is drawn to include the entire
myocardium. The software algorithm automatically
segments the LV into six equidistant segments and
selects suitable speckles in the myocardium for
tracking.
The software algorithm then tracks the speckle patterns
on a frame-by-frame basis using the sum of absolute
difference algorithm.
Finally, the software automatically generates time-
domain LV strain profiles for each of the six segments
of each view from which end-systolic strain was
measured (Fig. 10.60).
Left Ventricular Systolic Function 185
The average value of strain at each level (basal, middle
and apical) and global strain obtained from averaging
the strain values of 16 or 17 LV segments is calculated
(Fig. 10.63).
Advantages of Longitudinal strain and
Strain Rate Analysis
Good correlation between longitudinal strain and the
left ventricular ejection fraction.
Longitudinal strain provides a quantitative myocardial
deformation analysis of each LV segment, also allowing
for early systolic dysfunction detection in patients with
a preserved LVEF.
Subclinical systolic dysfunction assessment when
ejection fraction and other parameters are normal.
Incremental prognostic value in a variety of diseases
like heart failure, postmyocardial infarction, valvular
heart disease, and so forth.
Limits of agreement between various speckle-tracking
software are narrower for global longitudinal strain,
making it a more robust parameter than the radial or
circumferential strain.
186 Section 3: Systolic and Diastolic Function
Fig. 10.62: Unifrom 2D longitudinal strain extracted from all the six segments in the four-chamber view in a normal person. Average longitudinal
strain is -22% and there is very little temporal dispersion.
LIMITATIONS
Strain analysis is contingent on the presence of
adequate echocardiographic views.
It is not possible to conduct strain measurements in
patients with nonsinus rhythms.
Results depend critically on the machine with which
the analyses are performed, and these are not inter
changeable among different manufacturers at least as
of now.
SUMMARY
There are many ways in which LV function can be
determined, but every measure that is commonly used
is only a surrogate marker of LV function due to the fact
that it is impossible to characterize the complex geometric
and volumetric function of the ventricle in a single
number. There is no one perfect measure of LV function.
The ejection fraction has emerged as the pre-eminent
method to express LV performance. Although ejection
fraction is universally accepted, there are a number of other
techniques that can assess LV function and, when taken
together, provide a more comprehensive picture both of
global and regional LV function. Each of these measures
(including ejection fraction) has variable dependence
on loading conditions, heart rate and geometric position
that limits its accuracy. Understanding the limitations of
each measure will allow the physician to more intelligently
understand the true status of the myocardium.

Fig. 10.63: Global longitudinal strain from three apical views in a patient with aortic stenosis. Global longitudinal strain is -10.5% and shows
marked heterogeneity.
In short, LV systolic function should be assessed by
a multiparametric approach that includes LV geometry,
ejection fraction, long axis function, global longitudinal
strain and time-domain function like ratio of isovolumic
to ejection periods and so forth.
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1. Ho Sy. Anatomy and myoarchitecture of the left ventricular
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2. Greenbaum RA, Ho SY, Gibson DG, et al. Left ventricular
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4. Sagawa K. The end-systolic pressure-volume relation of the
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5. Tei C. New non-invasive index for combined systolic and
diastolic ventricular function. J Cardiol. 1995;26:1356.
6. Bargiggia GS, Bertucci C, Recusani F, et al. A new method
for estimating left ventricular dP/dt by continuous-wave
Doppler echocardiography. Validation studies at cardiac
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8. Sengupta PP, Korinek J, Belohlavek M, et al. Left ventricular
structure and function: basic science for cardiac imaging. J
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9. Pai RG, Bodenheimer MM, Pai SM, et al. Usefulness of
systolic excursion of the mitral anulus as an index of left
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10. Jones CJ, Raposo L, Gibson DG. Functional importance of
the long axis dynamics of the human left ventricle. Br Heart
J. 1990;63:21520.
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11. Ballo P, Bocelli A, Motto A, et al. Concordance between
M-mode, pulsed tissue Doppler, and colour tissue Doppler
in the assessment of mitral annulus systolic excursion in
normal subjects. Eur J Echocardiogr. 2008;9:74853.
12. Lang RM, Bierig M, Devereux RB, et al. Recommendations
for chamber quantification. Eur J Echocardiogr. 2006;7:
79108.
13. Teichholz LE, Kreulen T, Herman MV, et al. Problems in
echocardiographic volume determinations: echocardi-
ographic-angiographic correlations in the presence of
absence of asynergy. Am J Cardiol. 1976;37(1):711.
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simplified and accurate method for determining ejection
fraction with two-dimensional echocardiography. Circula-
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15. Thavendiranathan P, Grant AD, Negishi T, et al. Repro-
ducibility of echocardiographic techniques for sequential
assessment of left ventricular ejection fraction and
volumes: application to patients undergoing cancer chem-
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16. Sahn DJ, DeMaria A, Kisslo J, et al. Recommendations
regarding quantitation in M-mode echocardiography: re-
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17. Devereux RB, de Simone G, Pickering TG, et al. Relation
of left ventricular midwall function to cardiovascular risk
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18. Gudmundsson P, Rydberg E, Winter R, et al. Visually
estimated left ventricular ejection fraction by echocardiog-
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ods. Int J Cardiol. 2005;101:20912.
19. Schiller NB, Shah PM, Crawford M, et al. Recommendations
for quantitation of the left ventricle by two-dimensional
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two-dimensional echocardiograms. J Am Soc Echocardi-
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20. Lang RM, Mor-Avi V, Zoghbi WA, et al. Pearlman AS: The role
of contrast enhancement in echocardiographic assessment
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21. Nahar T, Croft L, Shapiro R, et al. Comparison of four
echocardiographic techniques for measuring left ventri
cular ejection fraction. Am J Cardiol. 2000;86:135862.
22. Shimada YJ, Shiota T. A meta-analysis and investiga-
tion for the source of bias of left ventricular volumes and
function by three-dimensional echocardiography in com-
parison with magnetic resonance imaging. Am J Cardiol.
2011;107:12638.
23. Nikitin NP, Witte KKA. Application of tissue Doppler imag-
ing in Cardiology. Cardiology. 2004; 101:17084.
24. Nikitin NP, Witte KK,Thackray SD, et al. Longitudinal ven-
tricular function: normal values of atrioventricular annu-
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two-dimensional color Doppler tissue imaging. J Am Soc
Echocardiogr. 2003;16:906-21.
25. Vinereanu D, Khokhar A, Tweddel AC, et al. Estimation of
global left ventricular function from the velocity of longitu-
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26. Park JS, Park JH, Ahn KT, et al: Usefulness of mitral annular
systolic velocity in the detection of left ventricular systolic
dysfunction: comparison with three dimensional echocar-
diographic data. J Cardiovasc Ultrasound. 2010;18:15.
27. Ha JW, Lee HC, Kang ES, et al. Abnormal left ventricular
longitudinal functional reserve in patients with diabetes
mellitus: implication for detecting subclinical myocar-
dial dysfunction using exercise tissue Doppler echocar
diography. Heart. 2007;93:15716.
28. Chung N, Nishimura RA, Molmes DR, et al. Measurement
of left ventricular dp/dt by simultaneous Doppler echocar-
diography and cardiac catheterization. J Am Soc Echocardi-
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nal strain: a novel index of left ventricular systolic function.
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31. Marwick TH. Measurement of strain and strain rate by
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 Echocardiographic Assessment
Chapter of Right Ventricular Function:

11
Methods and Clinical
Applications

INTRODUCTION
Importance of the right ventricle (RV) in health and
disease has seen a sea-change from being just a
conduit to an important contractile chamber, which
significantly impacts cardiac physiology, hemodynamics
and development of symptoms.1 It is the final barrier
between compensated versus decompensated heart.
Right ventricular musculature when stressed expresses
several important enzymes and activates several signal
transduction pathways involved in hypertrophy, fibrosis
and pulmonary vasoconstriction.2 These changes bring
new meaning to pharmacotherapy of heart failure and the
role of the RV. Under normal conditions, the RV is coupled
with a low-impedance, highly distensible pulmonary
Fig. 11.1: Schematic diagram of low impedance right heart circulation.
vascular system (Figs 11.1 to 11.3). Short-axis view.
Compared with the systemic circulation, pulmonary
circulation has a much lower vascular resistance and
greater pulmonary artery distensibility.3 Under normal
Unlike the LV, there is no torsion of any significance
conditions, right-sided pressures are significantly lower
and hence hardly any circumferential shortening
than comparable left-sided pressures. Despite this, the RV
(Fig. 11.6).
ejects similar or somewhat greater volume during systole
Radial shortening is unimpressive unlike the LV, partly
compared to the left ventricle (LV) 46 (Figs 11.4 and 11.5).
because myofiber orientation and muscle volume is
different (Fig. 11.7).
PECULIARITIES OF THE RIGHT VENTRICLE
Highly trabeculated and spongy appearance of the
The right ventricular systolic function is predominantly cavity allows it to work as an efficient volume pump
afterload-dependent and minimally affected by the but poses challenges with regard to geometric volume
preload. estimations7 (Fig. 11.8).
190 Section 3: Systolic and Diastolic Function
Fig. 11.2: Distribution of pulmonary artery systolic pressure in normal
subjects.
Fig. 11.4: Right ventricular pressure-volume loop.
Presence of a transverse moderator band prevents
undue chamber dilatation and hence despite signi
ficant combined pressure and volume overload in
heart failure, it is not uncommon to see minimum
geometric alterations.8 This makes eye-balling highly
deceptive in assessing right ventricular function
(Fig. 11.9).
In advanced diseased states, outflow may become
a dominant contractile chamber by virtue of its
circumferential muscle orientation. Little attention
has been given to the importance of this phenomenon
(Figs 11.10 and 11.11).
Fig. 11.3: Distribution of pulmonary artery mean pressure in normal
subjects. A mean pressure 25 mm Hg indicates presence of pulmo-
nary hypertension.
Fig. 11.5: Comparison of pressure-volume loop of the right ventricle
(yellow) with that of the left ventricle (white).
FUNCTION PARAMETERS
Function of the RV is to transmit blood from the venous
system to the LV through pulmonary arteries.
As normal adult circulation is in series, right ventricular
stroke volume is nearly similar to that of the LV.
If we assume the RV as a mechanical pump, function is
its behavior in developing pressure at varying volumes
during cardiac cycle.9
There are phases in cardiac cycle, which have variable
functional importance and temporal dimension needs
to be coupled with a mechanical event for complete
 Echocardiographic Assessment of Right Ventricular Function: Methods and Clinical Applications
Fig. 11.6: Right ventricular basal circumferential strain of only -4% in
a normal subject. Paradoxically, many segments show circumferential
lengthening.
Fig. 11.8: Transthoracic echocardiography short-axis view showing
spongy right ventricle.
Fig. 11.10: Conceptual diagram. The two contractile chambers of the
right ventricle with distinct morphologies.
191
Fig. 11.7: Comparison of basal right ventricular radial strain (10%)
with the left ventricular basal radial strain (55%) in a normal subject.
Fig. 11.9: The right ventricle is a tripartite structure with an inflow part
including the tricuspid valve apparatus; a trabecular part that includes
pronounced trabeculations that function as an absorptive sponge, fill-
ing during diastole and releasing blood in systole; and an outflow tract
that consists of a muscular infundibulum, separating the tricuspid from
the pulmonary valve.
assessment. Thus, a pressurevolume loop during a
single beat in temporal domain is possibly the best
way of assessing function.10 However, it is clinically
impractical to obtain this information by a convenient
and reproducible method. So, we look for surrogates
and correlates.
In spatial domain, fractional area change or ejection
fraction or volume leftover at end-ejection are
parameters of function (Figs 11.12A and B).
In temporal domain, ejection period or filling period
or a ratio of time spent during isovolumic phase to
ejection phase provide functional information of
clinical value.
192 Section 3: Systolic and Diastolic Function

Fig. 11.11: Transthoracic echocardiography short-axis view. Complex geometry of the right ventricular chamber; inflow on the left side, trabecu-
lar portion in the middle and the conus on right side. The right ventricular outflow tract (RVOT) becomes an important contractile chamber in
diseased states.

A B
Figs 11.12A and B: Estimation of the right ventricle function by optimizing a transthoracic echocardiography four-chamber view. Fractional area
change and end-systolic volume can be estimated.

Typically, the RV spends less time during isovolumic
phase compared to the LV and hence it is more energy-
efficient (Fig. 11.13). Increase in this period is the early
indication of the failing RV.
The right ventricular ejection time is about
3050 milliseconds longer because of the outflow
chamber, which contracts near the end of systole.
The right ventricular ejection period shows phasic
variation with increase during inspiration.
Lack of phasic variation may suggest onset of
dysfunction if there is no abnormal interchamber
communication (Fig. 11.14).
Indirect assessment of the right ventricular function
includes integrity of inflow valve and the outflow
valve. Fortuitously, there are ubiquitous tricuspid and
pulmonary valve leaks, which can provide information
on preload, afterload and forward vascular resistance
(Figs 11.14 and 11.15).
Slopes of tissue velocity propagation during isovo
lumic phase do correlate with intrinsic contractility
(Fig. 11.16).
Geometric alterations are not an indicator of
dysfunction but suggest that the latter may be present
or will occur in future.
Quantum and speed of longitudinal motion of this
complex chamber has also found clinical utility,
because most deep fibers of the RV are longitudinally
arranged. Longitudinal motion has fair correlation
with ejection performance.
Patterns of flow and tissue movements also help in
detecting abnormalities in pressurevolume loops and
provide some meaningful information.
 Echocardiographic Assessment of Right Ventricular Function: Methods and Clinical Applications
Fig. 11.13: Right ventricle free wall tissue velocity image. Note that
isovolumic contraction (IVC) and isovolumic relaxation (IVR) periods
are very brief.
Fig. 11.15: Physiological tricuspid regurgitation jet with a peak veloc-
ity of 2.68 m/s. Note the respiratory variation. A peak transtricuspid
velocity 3.5 m/s is suggestive of elevated right ventricular systolic
pressure and velocities between 2.8 and 3.4 m/s are of borderline
significance.
RIGHT VENTRICLE DIASTOLIC FUNCTION
AND PRESSURES
Preload is an important determinant of the right
ventricular function. A crude measure of the preload
is right atrial pressure or right ventricular end-diastolic
pressure.
It is difficult to measure right atrial volume or the right
ventricular diastolic volume by echocardiography.
193
Fig. 11.14: Continuous wave Doppler interrogation of the right ven-
tricular outflow tract. Physiological pulmonary regurgitation with a peak
diastolic velocity of 2 m/s is observed. Note the duration of regurgi-
tation increasing during expiration and decreasing during inspiration.
Lack of phasic variation is a sign of dysfunction.
Fig. 11.16: Right ventricle (RV) free wall tissue velocity profile. Note
the difference between acceleration slopes in left (normal subject)
and right panel [inferior myocardial infarction (INF MI) with possible
RV infarction).
Respiratory variations in filling may be better markers
of preload11 (Figs 11.14 and 11.15).
Right atrial pressure or RV end-diastolic pressure can
be measured directly during right-heart catheterization
or estimated noninvasively by assessing inferior vena
cava diameter and collapse index.12 Dilated ( 20 mm)
and noncollapsing inferior vena cava is suggestive of
mean right atrial pressure 15 mm Hg (Fig. 11.17).
A dilated inferior vena cava with inspiratory or
194 Section 3: Systolic and Diastolic Function
Fig. 11.17: Dilated inferior vena cava indicates elevated right atrial
pressure. Reduced inspiratory collapse is specific. A collapse index <
50% is highly suggestive of right atrial pressure > 10 mm.
Fig. 11.19: Transthoracic echocardiography four-chamber view at
end-diastole showing bulge of the interatrial septum to the left, indi-
cating right atrial pressure higher than left atrial pressure in diastole.
sniff-related collapse of < 50% indicates elevated mean
right atrial pressure ( 10 mm Hg).
The annular tricuspid E/e ratio and annular tissue
Doppler relaxation time have also shown moderate
correlation with right atrial pressure.13
Raised right atrial pressure can also be judged from
movement of the interatrial septum or the hepatic vein
flow spectrum14 (Figs 11.19 and 11.20). A decrease in
systolic wave and a marked increased in atrial reversal
wave in hepatic veins indicate raised right atrial
pressure.
Estimation of the right ventricular end-diastolic
pressure from the Doppler pulmonary regurgitation
Fig. 11.18: M-mode section of the inferior vena cava with reduced
inspiratory collapse.
Fig. 11.20: Prominent diastolic tricuspid regurgitation indicating
elevated right ventricle diastolic pressures in a patient with dilated
cardiomyopathy.
signal can be a good surrogate when jugular venous
pressure is added to the pulmonary end-diastolic
pressure gradient.
Elevated right ventricular diastolic pressures can also
be judged from the presence of diastolic tricuspid
regurgitation, diastolic antegrade flow across the
pulmonary valve or from the patterns of pulmonary
regurgitation (Figs 11.20 to 11.25).
It is also possible to estimate dP/dt from tricuspid
regurgitation signal (Fig. 11.26).
Pulsed wave Doppler tricuspid flow velocities can
also be used for assessing RV diastolic function. An E/A <
0.8 indicates abnormal relaxation. A combined flow and
 Echocardiographic Assessment of Right Ventricular Function: Methods and Clinical Applications
Fig. 11.21: Flow Doppler alternans of the tricuspid regurgitation with
normal right ventricular systolic pressure. Doppler alternans is sugg
estive of global right ventricle dysfunction.
Fig. 11.23: Rapidly decelerating pulmonary regurgitation jet with
end-diastolic antegrade flow across pulmonary valve (arrows) sugg
estive of raised right ventricle end-diastolic pressure.
Fig. 11.25: Restrictive transtricuspid pulsed wave Doppler flow
velocities. A deceleration time varies with respiration, from 100 to
130 milliseconds. Averaging five beats in quiet respiration is required
to obtain mean values.
195
Fig. 11.22: Operated tetralogy of Fallot in an adult showing antegrade
diastolic flow across pulmonary valve (arrows), indicating elevated
right ventricular diastolic pressure.
Fig. 11.24: Continuous wave Doppler interrogation of the pulmonary
regurgitation jet. The pattern is classic of normal right ventricular
diastolic pressure as estimated by end-diastolic gradient and
mid-diastolic dip.
tissue early diastolic velocity ratio E/e > 6 is also abnormal.
A E/A ratio of > 2 with deceleration time < 120 milliseconds
is suggestive of restrictive RV diastolic function.
Right Ventricular Volumetric Function
In clinical practice, the right ventricular ejection fraction
(RVEF) is the most commonly used index of RV contra
ctility. Although widely accepted, RVEF is highly depen
dent on loading conditions and may not adequately reflect
contractility.15 Because the RV chamber is larger than the
LV chamber, RVEF is, under normal conditions, lower
than LV ejection fraction. The normal range of RVEF varies
between 40% and 76% depending on the methodology
used.16 Magnetic resonance imaging (MRI) is the most
accurate method for measuring RVEF. According to
Lorenz et al.4 the normal value of RVEF is 61 7%, ranging
196 Section 3: Systolic and Diastolic Function
Fig. 11.26: Estimation of dP/dt from tricuspid regurgitation (make it
yellow) signal. Pressure drop from 1 m/s velocity to 2 m/s is multiplied
by the time taken to attain 2 m/s velocity.
from 47% to 76%. RV images can be acquired in the short-
axis or long axial direction. Alfakih et al.15 demonstrated
that the axial orientation resulted. in a better intraobserver
and interobserver reproducibility than the short-axis
orientation. The lower limit of radionuclide-derived
normal RVEF ranges from 40% to 45%.17 To be accurate,
volume assessment should always take into account the
complex shape of the RV. Furthermore, the infundibulum
should be included in the volume measurement because
it can account for as much as 25% to 30% of RV volume.18
The simplest and most routinely used method for
assessing RV volume includes linear dimensions and
areas obtained from single tomographic echocar
diographic planes. The best correlations between
single-plane measurements and RV volumes have
been obtained with the maximal short-axis dimension
and the planimetered RV area (in the four-chamber
view; Fig. 11.27).
Significant overlap has been noted, however, between
normal and volume-overloaded conditions, especially
for mild to moderate enlargement.18
In an effort to be more accurate, different approaches
have been sought to directly measure RV volume.
These include the arealength method and Simpsons
approach. In two-dimensional (2D) echocardiography,
numerous studies showed that the arealength method
that uses an ellipsoid or pyramidal model correlates
better with RV volume than Simpsons rule.18 The
main difficulty seen with the application of Simpsons
rule to 2D echocardiographic images is obtaining two
appropriate orthogonal views with a common long axis.
Fig. 11.27: Right ventricle short-axis dimension and area in
four-chamber view are the two best correlates of the volumes.
Three-dimensional (3D) echocardiography is a promi
sing technique that could lead to more accurate
assessment of RV volume.19,20 Echocardiography is less
accurate than the nuclear methods. Two-dimensional
assessment of RVEF with Simpsons rule and the
arealength method show moderate correlation with
radionuclide- or MRI-derived RVEF.18 In the clinical
setting, 3D echocardiography has also shown variable
correlations with RVEF,19,20 although there have been
some studies that have not supported the strong
relationship. Diffi
culties include delineation of the
anterior wall and identification of the infundibular
plane.
Right ventricle fractional area change represents the
ratio of systolic area change to diastolic RV area. It
is measured in the four-chamber view and can be
incorporated systematically into the basic echocardio
graphic study. A fractional area change of 35%
indicates RV systolic dysfunction. In diverse conditions,
a good correlation has been reported between RV
fractional area change and RVEF21 (Fig. 11.28).
Assessing Longitudinal Function
The RV contracts by three separate mechanisms:
1. Inward movement of the free wall, which produces a
bellows effect
2. Contraction of the longitudinal fibers, which shortens
the long axis and draws the tricuspid annulus toward
the apex (Fig. 11.29)
 Echocardiographic Assessment of Right Ventricular Function: Methods and Clinical Applications 197

A B
Figs 11.28A and B: Fractional area change (44%) in a normal person estimated in four-chamber view.

Fig. 11.29: Longitudinal shortening of the right ventricle free wall (-38%), which is nearly twice that of the interventricular septum.
198 Section 3: Systolic and Diastolic Function
Fig. 11.30: Right ventricle (RV) apical circumferential strain compared to the left ventricle apical one in a normal subject. There is hardly any
circumferential strain in the RV apex.
Fig. 11.31: Tricuspid annular plane systolic excursion (TAPSE)
displayed in M-mode in a normal adult patient.
3. Traction on the free wall at the points of attachment to
the LV. There is no twisting or rotation (Fig. 11.30).
Longitudinal motion is the predominant way of
ejection.22 Large surface area due to trabeculations pro
duces effective stroke volume at low pressure.23 However,
it is difficult to assess area change accurately in any view.
Tricuspid annular plane systolic excursion is
another useful quantitative measurement of RV systolic
performance24 (Fig. 11.31). This method reflects the longi
tudinal systolic excursion of the lateral tricuspid valve
annulus toward the apex. It is usually measured with
2D-directed M-mode imaging in the four-chamber view.
Normal values are usually > 15 mm25 (Fig. 11.31). Studies
showed moderate correlation between tricuspid annular
plane systolic excursion (TAPSE) and RVEF measured
by radionuclide angiography.26,27 However, some studies
show better correlation between RVEF by MRI and TAPSE
than with real-time 3D echocardiography.27 Measure
ments of tricuspid annular motion are easy to obtain,
correlate with RV systolic function and have a high
specificity and negative predictive value for detecting
abnormal RV systolic function25 (Fig. 11.32).
TRICUSPID ANNULAR PEAK
SYSTOLIC VELOCITY
Longitudinal motion of the RV can also be assessed by
studying the tricuspid annular velocities. Tissue Doppler
imaging, which measures myocardial velocities, also
allows quantitative assessment of RV systolic function 28,29
 Echocardiographic Assessment of Right Ventricular Function: Methods and Clinical Applications
Fig. 11.32: Tricuspid annular plane systolic excursion (TAPSE)
displayed in M-mode in an adult patient with hypoplastic right heart
syndrome. Reduced TAPSE and post-systolic excursion are both
indicative of systolic dysfunction.
Fig. 11.34: TAPSV of 6 cm/s indicative of right ventricle systolic
dysfunction. Markedly prolonged isovolumic relaxation time (IVRT)
suggests abnormal myocardial performance index.
(Fig. 11.33). Systolic tissue Doppler signal of the tricuspid
annulus (TAPSV) has been studied as an index of RV
function in patients with heart failure (Fig. 11.34).
Various cut-off limits have been proposed. In one
study, peak systolic values < 11.5 cm/s identified the
presence of ventricular systolic dysfunction (RVEF
< 50%) with a sensitivity and specificity of 90% and
85%, respectively.28 A recent study has found good
discriminating power when compared to real-time 3D
echocardiographic ejection fraction when a threshold of
< 9.5 cm/s is used for predicting RVEF < 40%.30 A proposed
199
Fig. 11.33: Tricuspid annular peak systolic velocity (TAPSV) of
12 cm/s (normal) in a 74-year-old male. TAPSV does not decrease
linearly with advancing age. Reduced early diastolic velocity is
indicative of diastolic dysfunction.
Fig. 11.35: Assessment of myocardial performance index (MPI) from
combined right ventricle inflow and outflow Doppler spectra.
threshold value of < 10 cm/s is a good way to remember.25
This cut-off value predicts cardiac index < 2 L/min/m2 with
a sensitivity of 89% and specificity of 87%.31
Myocardial Performance Index
Right ventricular myocardial performance index (MPI),
which is the ratio of isovolumic time intervals to ventri
cular ejection time, has been described as a nongeometric
index of global ventricular function32 (Fig. 11.35). It can be
obtained either by superimposing tricuspid inflow and the
200 Section 3: Systolic and Diastolic Function
Fig. 11.36: Isovolumic acceleration (IVA). Time velocity integral
(TVI)-based right ventricle contractility index: isovolumic velocity from
first sharp peak during systole at onset of QRS/time to peak velocity. In
the Figure shown, this value is 12/0.025 = 4.8 m/s2. Normal values are
> 1.5 m/s2.
right ventricular outflow Doppler flow, provided there are
no differences in heart rate. Alternately, tissue Doppler
spectrum of the tricuspid annulus can be used to measure
isovolumic periods and ejection time.
Right ventricular MPI appears to be relatively
independent of preload, afterload and heart rate, and
has been useful in assessing patients with congenital
heart disease, valvular heart disease and pulmonary
hypertension.3335
The normal value of this index is 0.28 0.04, and it
usually increases in the presence of RV systolic or diastolic
dysfunction. A threshold value of > 0.50 is a good clinical
parameter.35 Its correlation with RVEF is modest, but
specificity is very high.
Pseudonormalized MPI can occur in acute RV
myocardial infarction, which can probably be explained
by a decrease in isovolumic contraction time associated
with an acute increase in RV diastolic pressure.36
Other Parameters of Right Ventricle
Doppler Myocardial Imaging
Isovolumic acceleration (IVA) represents a new tissue
Dopplerderived parameter of systolic performance.37 It is
calculated by dividing the maximal isovolumic myocardial
velocity by the time to peak velocity: IVA = maximum
velocity/time to peak (Fig. 11.36).
Vogel et al.37 studied the value of myocardial IVA in a
closed-chest animal model during modulation of preload,
afterload, contractility and heart rate. Their study showed
Fig. 11.37: Markedly reduced tricuspid annular systolic and early
diastolic velocities (34 cm/s) in a 64-year-old male patient with
stable coronary artery disease. The patient needed prolonged
inotropic support following coronary artery bypass grafting (CABG).
that IVA reflects RV myocardial contractile function and
is less affected by preload and afterload within a physio
logical range than either the maximum first derivative
of RV pressure development (dP/dtmax) or ventricular
elastance. Clinical studies have confirmed its value in
congenital heart disease, that is, after repair of tetralogy
of Fallot and in transposition.38 IVA positively correlates
with global longitudinal strain and strain rate (SR) and
negatively with MPI.38
There have been a few studies on the utility of early
diastolic myocardial velocities of the tricuspid annulus
and the RV free wall as a marker or global or diastolic
dysfunction23 (Fig. 11.37).
RIGHT VENTRICLE STRAIN AND
STRAIN RATE ANALYSIS
Strain is defined as the degree of deformation of an
object, whereas SR represents the speed at which strain
occurs. Ultrasound-based Strain SR/strain imaging is a
practical, reproducible clinical technique, which allows
the calculation of regional longitudinal and radial defor
mation from RV segments. Indices such as SR and strain
are free of geometric assumptions and, thus, may provide
new insights into right ventricular function.39 Both
these indices correlate with multiple parameters of RV
systolic function. In echocardiography, RV longitudinal
strain can be assessed reliably from apical views, whereas
radial strain is difficult and is hampered by near-field
artifacts and extremely small computational distance.
 Echocardiographic Assessment of Right Ventricular Function: Methods and Clinical Applications
Fig. 11.38: TVI-based strain of right ventricle free wall in a normal
subject. Longitudinal Doppler strain is -27% (normal > -20%).
In mathematical models and in experimental studies,
longitudinal strain appears to correlate best with changes
in stroke volume, whereas longitudinal SR is more related
to local contractile function and appears to be more
independent of loading 40 (Figs 11.38 and 11.39).
Strain and SR can be estimated either by Doppler
myocardial imaging or by non-Doppler 2D-strain using
acoustic speckle tracking or velocity vector imaging.38,40
The latter is gaining more ground because it is angle-
independent and more reproducible. In a recent study,38
good correlations were found between RVEF and free wall
SR and strain.
Right ventricle, septal systolic strain and SR may
allow the recognition of early RV dysfunction even when
conventional RV systolic parameters are normal.41
SUMMARY
The RV, an underestimated chamber, is affected by
primary disorders of the right heart diseases, which affect
both ventricles concomitantly as a result of ventricular
interdependence when the LV alone is involved and
secondary to back-pressure effects. Knowledge about the
role of the right ventricular function in health and disease
has lagged behind that of the LV. However, seminal
work has been published in the past two decades. It is
a thin-walled chamber with complex geometry, heavy
trabeculations, three distinct parts and three distinct
muscle bundles. There is now increasing information
about the importance of the RV in patients with stable
coronary artery disease, heart failure, acute myocardial
201
Fig. 11.39: Two-dimensional longitudinal strain in an adult patient with
hypoplastic right heart syndrome. Global systolic strain is markedly
reduced (-7.7%) and there is evidence of post-systolic strain in right
ventricle free wall along with paradoxical strain in the interventricular
septum.
infarction, pulmonary hypertension, Eisenmenger
syndrome, adult congenital heart disease, response to
drug therapy, exercise capacity in various disorders and
valvular heart disease. Right ventricular volumetry and
ejection fraction estimation unlike that of the LV is a
tedious, less robust and less validated parameter of the
right ventricular function despite use of real-time 3D
echocardiography. In clinical practice, assessment of
right ventricular function is a combination of several
parameters that include estimation of its size and mass,
movement of tricuspid annulus plane, peak systolic
velocity of the tricuspid annulus motion, global myocardial
performance index, estimation of the Doppler and non-
Dopplerderived strain and SR of the RV in general and
its free wall in particular, and estimation of the right
ventricular systolic and diastolic pressures by flow Doppler
spectrum of tricuspid and pulmonary regurgitations.
Global longitudinal strain of the RV by acoustic speckle
tracking appears to be a very robust technique that needs
further cross-sectional and longitudinal studies and its
impact on prognosis in diverse disorders. Impetus to this
field has been given by competing techniques like MRI
and computed tomography CT.
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 Chapter
12
Introduction
Both ventricles of the heart are bidirectional hemodynamic
pumps and engage in functions of suction (relaxation)
and ejection (contraction). Relaxation aids in filling
during diastole, and therefore, filling parameters denote
diastolic function. The phenomena of relaxation and
contraction are interlinked and energy-dependent.
Diastole precedes systole, because no ejection is possible
unless there is filling first. The processes of relaxation and
filling constitute diastolic function. Increased resistance to
filling is the simplest way of defining diastolic dysfunction.
Diastolic dysfunction is the first manifestation of a
disease process and explains the symptoms better.
Abnormalities of diastolic function are common to
virtually all forms of cardiac disease. Noninvasive
evaluation of diastolic ventricular function is based
on Doppler echocardiographic visualization of inflow
and/or ventricular tissue re-extension, although many
more parameters are described.
The study of pressurevolume loop during diastole is
the ideal way to understand and assess diastolic function.
However, there are several surrogate methods and
parameters in echo-Doppler techniques, which provide
reasonable, reliable and actionable information about
diastolic function. In general, diastolic dysfunction may
be characterized by enlargement of upstream chamber
(atrium), alteration in various phases of diastole and
raised filling pressures. However, diastolic dysfunction
is dynamic and in early phases, filling pressures are
Diastolic Function
not increased. Assessment of diastolic function in
simulated physiological situation, like exercise, may
provide enhanced information. Diastolic compensatory
mechanisms that maintain filling volume are the earliest
evidence of dysfunction. There is also evidence of regional
diastolic wall motion nonuniformity. Noninvasive
surrogates often reported in clinical studies reflect
integrative properties that lack specificity.
PHYSIOLOGY OF DIASTOLE
Diastolic dysfunction is the physiological expression
of morphological cardiovascular disease. The healthy
myocardium is an active, nonlinear, nonhomogeneous
and anisotropic viscoelastic material. During diastolic
lengthening, normal cardiac muscle behaves like a spring.
When the spring is more forcefully compressed during
systole, diastolic lengthening is higher and vice versa
(Fig. 12.1).
There is a certain degree of systolic elastance and also
a definite degree of diastolic elastance.1 In several disease
states like hypertension, diabetes and left ventricular
hypertrophy as also with aging, systolic elastance remains
unaffected or may actually increase, and diastolic
elastance decreases, which can be studied and assessed by
echo-Doppler parameters of diastolic function (Fig. 12.2).
On the other hand, when systolic elastance is reduced,
diastolic elastance initially increases due to remodeling
and diastolic dysfunction denoted by filling pressures,
therein, is a manifestation of fluid overload. Most systemic

Fig. 12.1: Left ventricular pressure-volume loop. Note that the diastole
is a mirror image of systole.
(IVR: Isovolumic relaxation; IVC: Isovolumic contraction; RF: Rapid
filling; AS: Atrial systole).
Fig. 12.3: Diastolic dysfunction in clinical sense is raised diastolic
pressures, which means reduced compliance or increased diastolic
stiffness.
diseases affect the left ventricle (LV) primarily, and
therefore, it is pertinent to discuss largely about the left
ventricular diastolic function/dysfunction.
FACTORS CONTRIBUTING TO DIASTOLE
Decline of the myocardial active state following systole
Passive effects of connective tissue
Rapid changes in atrial and ventricular pressures
Transmitral flow
Interactions with the right ventricle and pericardium
Atrial systole
Diastolic Function 205
Fig. 12.2: Pressure-volume loop of a normal subject (green color) and
that of a subject with diastolic dysfunction (red color). Note the same
end-systolic elastance but with reduced end-diastolic elastance.
SIGNIFICANCE OF DIASTOLIC FUNCTION
Identification of preclinical diseases in probands
Diagnosis of clinical syndrome of heart failure
Marker of incremental prognosis in diverse cardiac
disorders
Monitoring therapy and follow-up
Understanding exercise physiology
Cardiac versus noncardiac dyspnea
Physiological versus pathological remodeling
Optimizing devices and drugs response
Evaluation of intraventricular dyssynchrony
Study of pericardial diseases
There is no single definition for diastolic dysfunction;
many features can get altered, and any one change
or their combination is typically called diastolic
dysfunction, although the pathophysiology and functional
significance varies greatly.24 Clinically, the most common
manifestation is an elevated end-diastolic pressure and
altered filling patterns, but neither of these identifies
specific features of diastolic dysfunction (Fig. 12.3).
When diastolic dysfunction is detected, it has some
morphological, cellular and proteomic connotations.
These are:
A change in the extracellular matrix of the myocardium,
with the formation of excess collagen tissue5
At the cellular level, there is reduced phosphorylation
of sarcomeric proteins
At the proteomic level, an isoform change in important
structural macromolecular proteins such as titin.6
206 Section 3: Systolic and Diastolic Function
Fig. 12.4: Graphical representation of various phases of the cardiac
cycle of the left heart.
(DFP: Diastolic filling period).
Fig. 12.6: Doppler signal from left ventricular inflow close to outflow
tract showing all phases of cardiac cycle.
(ET: Ejection time; IVC: Isovolumic contraction).
Diastole starts with closure of the aortic valve and ends
with onset of ventricular contraction (Fig. 12.4). It has
an initial period of ventricular relaxation without filling
(isovolumic relaxation time [IVRT]) and then three phases
of ventricular filling (DFP). The four phases of diastole are:7
1. Isovolumic relaxation phase
2. Rapid filling phase
3. Diastasis
4. Late diastolic filling due to atrial contraction.
Diastolic LV function can be assessed in each of the four
phases of diastoleisovolumic relaxation, rapid filling,
slow filling and atrial contraction (Fig. 12.5). These four
phases uniquely reflect cardiomyocyte, myocardial or LV
Fig. 12.5: Continuous wave Doppler interrogation with sample volume
placed between the left ventricular outflow and the inflow showing all
four phases of diastole.
(IVR: Isovolumic relaxation; RF: Rapid filling; diastasisslow filling
and AClate filling due to atrial contribution).
physiology, and are invariably accessible to noninvasive
evaluation. Diastolic dysfunction is an abnormality that
causes impaired relaxation (and decreased ventricular
suction), poor filling or loss of atrial contraction.7
There are two phases in systole (Fig. 12.6). These are:
1. Isovolumic contraction phase (IVC)
2. Ejection phase.
Combined systolic and diastolic function can be
assessed by the ratio of IVRT + IVC time/ejection time.
This ratio has been called myocardial performance index.8
Although used for prognosis in various diseased states,
it has not found practical utility for daily use in most
echocardiography labs.
ISOVOLUMIC RELAXATION TIME
Isovolumic relaxation time, which corresponds to the time
interval from aortic valve closure to mitral valve opening,
is difficult to appreciate from simultaneous LV pressure,
aortic pressure and wedge pressure recordings but is
easily measured by continuous wave Doppler from the
simultaneous display of the end of aortic ejection and the
onset of mitral inflow (Fig. 12.7).
IVRT has a predictable quantitative relationship to
constant of isovolumic relaxation and to left atrial (LA)
and aortic pressures.8
Prolonged IVRT indicates poor myocardial relaxation.
A normal IVRT is about 70 12 milliseconds, and
approximately 10 milliseconds longer in people above
40 years of age.

Fig. 12.7: Doppler interrogation between left ventricle outflow and
inflow showing measurement of isovolumic relaxation time (IVRT).
At heart rate of 66 beats/min, IVRT is 76 milliseconds in this normal
subject.
In abnormal relaxation, IVRT is usually in excess of
110 milliseconds.
With restrictive filling, it is usually under
60 milliseconds.
If IVRT is prolonged (> 110 milliseconds), LA pressure is
not elevated because the delay in mitral valve opening
is related to lower pressure crossover between LV and
LA in the setting of delayed relaxation.
It is safe to conclude that LA pressure is elevated if the
IVRT is short (< 60 milliseconds) in the presence of
cardiac disease.
Its clinical value as an index of diastolic LV function
is limited, because it depends on mitral valve opening
pressures and, therefore, is not uniquely related to
LV dysfunction.
RAPID FILLING PHASE
In early diastole, chamber wall relaxation unmasks stored
elastic strain, allowing the LV to recoil and act as a suction
pump by aspirating blood into the ventricle. Normal left
ventricular (LV) filling occurs rapidly early in diastole
caused by a progressive pressure gradient within the
ventricle and with a low LA pressure.
Rapid filling phase accounts for 70% of left ventricular
filling. It gets shorter in duration with raised filling
pressures and is prolonged in subjects with impaired
relaxation alone.9 When both impaired relaxation and
raised LA pressure coexist, it has variable duration like in
Diastolic Function 207
Fig. 12.8: Variables affecting rapid filling phase in diastole.
(PR: P wave to ORS wave interval).
normal subjects. Rapid filling phase is denoted by early
diastolic (E) mitral flow wave and antegrade diastolic (D)
flow wave of the pulmonary veins. Variables affecting
rapid filling phase are shown in Figure 12.8.
DECELERATION TIME OF EARLY FILLING
WAVE (MITRAL E- AND PULMONARY
D-WAVES)
Deceleration time (DT) is the duration between the peak
of early filling wave and where its linear descending slope
reaches zero (Fig. 12.9). Nonlinear slopes are not measured.
Conditions associated with increased LV stiffness are
associated with a more rapid rate of deceleration of early
filling and a shorter time for this deceleration.10
It is an index of resistance to early filling with normal
values in range of 150250 milliseconds.
DT denotes chamber stiffness regardless of heart rate,
afterload and contractility.
DT of < 150 milliseconds indicates restrictive filling
and relatively noncompliant LV (Fig. 12.10).
DT > 250 milliseconds indicates compensatory mecha
nism is in place to overcome impaired relaxation.
Prolonging of DT during therapy is a positive sign
of recovery.
There is a close inverse relationship between DT and
pulmonary wedge pressure.
DT is affected by age as well as pericardial restraint.
As myocardial relaxation becomes less active with
208 Section 3: Systolic and Diastolic Function
Fig. 12.9: Graphical display of deceleration time (DT) of mitral early
filling wave.
Fig. 12.11: Right upper pulmonary vein flow in a patient with atrial
fibrillation. Measuring deceleration time of D-wave.
aging or abnormally delayed due to a disease process,
the rate of LV pressure decline during the early diastole
is reduced, and it takes a longer time to reach the
minimal LV diastolic pressure.
Longer DT indicates impaired diastolic reserve.
In this situation with abnormal myocardial relaxation,
a reduced diastolic filling period and a lack of atrial
contraction compromise LV filling.
During the time of early flow deceleration, there is
rapid flow into the LA from the pulmonary veins. DT of
pulmonary vein diastolic wave has same significance as
that of mitral DT (Fig. 12.11). A pulmonary vein DT of < 150
milliseconds has much greater specificity for predicting
elevated filling pressures.11
Fig. 12.10: Restrictive filling pattern with deceleration time of
85 milliseconds in a patient with dilated cardiomyopathy.
Fig. 12.12: Pulsed wave Doppler mitral flow showing positive wave
(L-wave) during diastasis.
DIASTASIS
During the slow LV filling phase or diastasis, residual
effects of LV relaxation and dynamic effects of fast LV
inflow have dissipated. This phase is used to construct
diastolic LV pressurevolume relations from a single
cardiac cycle and allows LV stiffness, the slope of the
diastolic LV pressurevolume relation, to be derived
under so-called static conditions. In subjects with
impaired relaxation and longer cardiac cycle, residual
effects of LV relaxation may persist and positive filling
wave during diastasis (L-wave) may be observed
(Fig. 12.12). Mitral valve L-waves may be evident in
healthy patients with relatively low heart rates.12

Fig. 12.13: Mid-diastolic negative L-wave in a patient with left ventricular
diastolic dysfunction.
Fig. 12.15: Graphical display of longitudinal and radial expansion of
the left ventricle during diastole (arrows).
Importance of L-Wave
The L-wave may be seen in relatively bradycardic
patients with normal hearts. It is usually < 20 cm/s in
velocity.
A pathological L-wave typically is found in patients with
delayed active relaxation with increased LV stiffness.
In the echo laboratory, patients will often have clinical
heart failure, left ventricular hypertrophy with normal
systolic function or LV systolic dysfunction.
A pathological L-wave is suggestive of elevated
LV preload (pseudonormalization).
A pathological L-wave has prognostic value, in that it is
predictive of future hospitalizations with heart failure.
Diastolic Function 209
Fig. 12.14: Monophasic mitral flow with normal PR interval and heart
rate of 69 beats/min in a 90-year-old subject.
Occasionally, there can be negative L-wave or
mid-diastolic mitral regurgitation due to rapid rise in
LV diastolic pressure as a consequence of early filling
(Fig. 12.13). Its exact significance is not clear.
ATRIAL KICK OR CONTRIBUTION
Late diastolic filling wave is of short duration and occurs
due to atrial contraction just before systole starts. This
accounts for 2040% of ventricular filling and is absent in
atrial fibrillation. This gets partly or completely obliterated
in first degree heart block and markedly raised ventricular
stiffness. Atrial kick is reflected by late diastolic (A) mitral
flow wave and atrial flow reversal (Ar) in pulmonary veins.
In markedly elevated left ventricular diastolic pressure,
atrial contraction may not produce any antegrade flow
wave and may be seen to send flow retrogradely in
pulmonary veins (Fig. 12.14).
TISSUE MOTION AND
DIASTOLIC FUNCTION
As transmitral flow commences in diastole, the mitral
annulus moves longitudinally upward toward the
atrium. Due to tissue and blood incompressibility, as the
annulus rises, the wall thins, and the endocardium is
simultaneously displaced radially outward toward the
epicardium. During filling, the short and long axes change
simultaneously (Fig. 12.15). Therefore, rate of longitudinal
displacement and radial endocardial displacement are
good indicators of diastolic function.13 Early diastolic
longitudinal excursion rate can be easily obtained from
tissue Doppler studies (Fig. 12.16).
210 Section 3: Systolic and Diastolic Function
Fig. 12.16: Biphasic longitudinal expansion of the left ventricle
during diastole. E, early diastolic and A, late diastolic longitudinal tis-
sue velocity waves.
Fig. 12.18: Estimation of biplane end-systolic left atrial volume by
arealength method.
The LV wall motion generates the atrioventricular
pressure gradient resulting in the early transmitral flow
(Doppler E-wave) and associated vortex formation.
Substantial residual LV relaxation pressures in
mid-diastole present in some patients with stiff LV can
result in a positive wave called tissue L-wave14 (Fig. 12.17).
LEFT ATRIAL VOLUME AND DIASTOLIC
FUNCTION/DYSFUNCTION
The measurement of maximum LA volume is an essential
component of the comprehensive assessment of LV
diastolic function.15,16 More recently, LA volumes have
been obtained by 3D echocardiography.
Fig. 12.17: Tissue L-wave in diastasis (arrow).
The LA volume is usually measured by biplane
arealength method (Fig. 12.18). In current guidelines,
assessment of diastolic function mandates measurement
of LA volume index in every subject. Although it has
limited role in assessing diastolic function or dysfunction
in acute situations, it has great relevance in chronic stable
cardiovascular conditions.
The LA volume can be viewed as a morphological
expression of LV diastolic dysfunction.
Left atrial volume is regarded as a barometer of the
chronicity of diastolic dysfunction.
This simple measure of LA volume provides significant
insight into an individuals risk for the development of
adverse cardiovascular events, including myocardial
infarction, stroke, atrial fibrillation and heart failure.
Normal values for LA volume are 22 6 mL/M2.
Left atrial volume is graded relative to risk, 2833 mL/
M2 = mild; 3439 mL/M2 = moderate; and 40 mL/M2
= high or severe.
Normal subjects 22 6 mL/M2
Mild LA enlargement 28 33 mL/M2
Moderate LA enlargement 3439 mL/M2
Severe LA enlargement 40 mL/M2
Diastolic dysfunction is more likely if the LA volume
index exceeds 34 mL/M2.
However, LA volume can increase in mitral regur
gitation, athletes and in the presence of sinus brady
cardia without concomitant diastolic dysfunction.

Fig. 12.19: Left atrial (LA) longitudinal lengthening in a normal
subject compared to that of the left ventricle shortening. Typically, LA
lengthening is twice or more than that of the LV shortening.
Fig. 12.21: Sites for assessing diastolic function in an apical four-
chamber view.
There is a fairly good positive correlation between
LA volume index and grade of diastolic dysfunction.
Maximum LA systolic lengthening and its rate have
also been found to correlate with diastolic dysfunction
(Figs 12.19 and 12.20).
It is possible to use LA strain during ventricular
systole along with LA pressure or its Doppler
echocardiographic surrogate (E/e) to calculate
LA chamber stiffness.17
LA stiffness has good accuracy in identifying patients
in diastolic heart failure.
Change in volumepressure relationships in left atrium
also indicates change in material properties (ischemia,
Diastolic Function 211
Fig. 12.20: Significantly reduced left atrial global strain in the presence
of diastolic dysfunction.
fibrosis, etc.) and physiological or pathological
remodeling in the LV.
Factors extrinsic to the left ventricular myocardium
may influence the end-diastolic pressurevolume
relationship. Changes in intrathoracic pressure (as with
spontaneous or assisted ventilation), pericardial
constraints and interventricular interactions may each
influence ventricular diastolic pressure (when referenced
to atmospheric pressure), which therefore influences this
relationship. In the absence of these, intrinsic diastolic
function governs this relationship. Various equations have
been derived from mitral flow and tissue expansion rate to
predict end-diastolic pressure. E/e ratio has the strongest
relation to pulmonary capillary wedge pressure (PCWP)
[r = 0.86, PCWP = 1.55 + 1.47(E/Ea)], irrespective of the
pattern and ejection fraction.18
HOW TO PERFORM A STUDY FOCUSING
ON DIASTOLIC FUNCTION
After estimation of biplane LA volume, one proceeds
to interrogate by pulsed wave (PW) Doppler, four
different sites as shown in Figure 12.21.
With the patient supine, apical four-chamber views
using a 2.5-MHz transducer are obtained with the
sample volume gated at 1.55 mm directed between
the tips of the mitral valve leaflets and orthogonal to
the mitral valve plane.
Continuous wave Doppler is used to record aortic
outflow and mitral inflow from the apical view for
determination of the IVRT using a sweep speed of
100 mm/s.
212 Section 3: Systolic and Diastolic Function
Fig. 12.22: Biphasic mitral flow with sample volume at the tips of the
mitral leaflets.
In apical four-chamber view, ostium of the right upper
pulmonary vein is interrogated by PW Doppler.
M-mode of the color flow propagation velocity across
the mitral valve up to 4 cm into the cavity is obtained.
Doppler tissue imaging (DTI) of the medial and the
lateral mitral annulus and M-mode images are also
recorded. DTI is performed at a sample size gated at
2.5 mm.
Effect of Valsalva maneuver is also observed for the
mitral and pulmonary vein flow.
Sometimes, supine exercise is used to study diastolic
function parameters. Post exercise E/A ratio as an
independent determinant of severity of exercise
induced dyspnea and impaired exercise tolerance.
Longitudinal strain and untwisting rate of the LV are
also recorded by acoustic speckle tracking.
After obtaining all the measurements, the diastolic
dysfunction, if present, is graded and occasionally it
may be noted as indeterminate if multiparameters give
conflicting results.
MITRAL INFLOW VELOCITIES
The mitral inflow velocity profile is initially used to
characterize LV filling dynamics (Fig. 12.22).
E velocity (E) represents the early mitral inflow velocity
and is influenced by the relative pressures between the
LA and LV, which, in turn, are dependent on multiple
variables including LA pressure, LV compliance and
the rate of LV relaxation.19
Fig. 12.23: Grade I diastolic dysfunction in transmitral flow with
prolonged deceleration time.
A velocity (A) represents the atrial contractile
component of mitral filling and is primarily influenced
by LV compliance and LA contractility.
The DT of the E velocity is the interval from peak E to
a point of intersection of the deceleration of flow with
the baseline and it correlates with time of pressure
equalization between the LA and LV. Incomplete or
delayed relaxation causes a delay in the transfer of
blood from atria to ventricle.
As the early LA and LV filling pressures either evolve
toward or away from equivalence, so will the DT either
shorten or lengthen, respectively.
Diastolic dysfunction is directly related to the reduction
in early LV relaxation compromising the effective
transfer of the blood from the atrial reservoir into the
LV cavity.
Diastolic dysfunction can be categorized into
three stages based upon transmitral filling patterns.24
Grade I: Impaired relaxation denoted by DT > 250
milliseconds and E/A velocity ratio < 0.8 (Figs 12.23 and
12.24). The American Society of Echocardiography(ASE)
and European Association of Echocardiography (EAE)
guidelines suggest DT > 200 milliseconds in Grade I.
Early in the evolution of diastolic dysfunction,
the delay in emptying (DT > 250 milliseconds) is partially
compensated by a more vigorous end-diastolic atria
contraction, and, therefore, the E/A ratio is reduced
(< 0.8).
Grade II: Pseudonormal pattern with DT of 150250
milliseconds and E/A ratio between 0.8 and 1.5. ASEEAE
guidelines put DT in range of 160200 milliseconds.

Fig. 12.24: Grade I diastolic dysfunction denoted by deceleration time
of 278 milliseconds and E/A 0.7.
Pseudonormal pattern needs confirmation by
increased LA volume (> 34 mL/M2) or mitral E-wave
velocity/annular tissue early diastolic velocity > 15
(medial) or > 12 (lateral) or pulmonary vein flow increased
duration of atrial flow reversal wave or Valsalva maneuver
to unearth impaired relaxation in mitral flow.
Presence of L-wave or DT < 150 milliseconds could
also provide clue to pseudonormal pattern if E/A velocity
ratio is 0.81.5.
Grade III: Restrictive flow or reduced compliance
pattern with DT < 160 milliseconds and E/A ratio 2.0.
Others have used DT cut-off limits of < 150 milliseconds
and < 130 milliseconds as well.
Mitral Inflow Measurements
Following measurements should be made in each
examination:
Peak early filling (E-wave)
Late diastolic filling (A-wave) velocities
E/A ratio
DT of early filling velocity
IVRT
Mitral A-wave duration (obtained at the level of the
mitral annulus)
Diastolic filling time
A-wave velocitytime integral
Total mitral inflow velocitytime integral (and thus the
atrial filling fraction) with the sample volume at the
level of the mitral annulus
Diastolic Function 213
Fig. 12.25: Pseudonormal or Grade II diastolic dysfunction denoted by
presence of L-wave (arrow).
Mid-diastolic flow is an important signal to recognize.
Low velocities can occur in normal subjects, but when
increased ( 20 cm/s), they often represent markedly
delayed LV relaxation and elevated filling pressures.
Most confusions arise in so-called pseudonormal
pattern, wherein one or the other parameter can be
discordant (Fig. 12.25). Help can be obtained from using
multiple parameters and any of the other abnormality
could be construed as abnormal diastolic function
especially if the early diastolic annular tissue velocity is
significantly reduced.3,4
Restrictive flow is relatively easy to detect and is
unambiguous in adult patients with heart disease
(Fig. 12.26).20 These criteria can not be used in children
and young adults who normally have large E-waves and
short DT due to very active suction of the LV.
Although not supported by the ASE, others have used
Grade IV diastolic dysfunction as the one in which either
the restrictive pattern is irreversible21 or has monophasic
flow pattern with absent A-wave despite sinus rhythm,
normal PR interval and usual heart rates (Fig. 12.27).
Mitral Inflow: Acquisition and Feasibility
PW Doppler is performed in the apical four-chamber
view to obtain mitral inflow velocities to assess
LV filling.
Color flow imaging can be helpful for optimal
alignment of the Doppler beam, particularly when the
LV is dilated.
Performing continuous wave Doppler to assess peak E
214 Section 3: Systolic and Diastolic Function
Fig. 12.26: Restrictive (Grade III) flow pattern with short deceleration
time and E/A ratio 2.
Fig. 12.28: Valsalva maneuver changing restrictive flow pattern
(left panel) to pattern of impaired relaxation (right panel).
(early diastolic) and A (late diastolic) velocities should
be performed before applying the PW technique to
ensure that maximal velocities are obtained.
A 1- to 3-mm sample volume is then placed between
the mitral leaflet tips during diastole to record a crisp
velocity profile.
Optimizing spectral gain and wall filter settings is
important to clearly display the onset and cessation of
LV inflow.
Spectral mitral velocity recordings should be initially
obtained at sweep speeds of 2550 mm/s for the
Fig. 12.27: Monophasic transmitral flow pattern in a patient with
advanced diastolic dysfunction and heart failure due to previous
anterior wall myocardial infarction.
evaluation of respiratory variation of flow velocities, as
seen in patients with pulmonary or pericardial disease.
If variation is not present, the sweep speed is increased
to 100 mm/s, at end-expiration, and averaged over
three consecutive cardiac cycles.
The Valsalva maneuver is performed by forceful
expiration (approximately 40 mm Hg) against a closed
nose and mouth, producing a complex hemodynamic
process involving four phases. It helps to identify
pseudonormal mitral inflow and irreversible restrictive
flow. A decrease in E/A ratio 0.5 is the criterion
(Figs 12.28 and 12.29).
In cardiac patients, a decrease of 50% in the E/A
ratio during Valsalva maneuver is highly specific for
increased LV filling pressures, but a smaller magnitude of
change does not always indicate normal diastolic function.
No change in restrictive flow is an ominous sign.21
MITRAL ANNULAR VELOCITIES
Diastolic tissue velocities measured at the mitral annulus
show low-velocity deflections during early filling (e) and
with atrial contraction (a) with great clarity.22,23 These
indicate biphasic longitudinal expansion rate of the LV
(Fig. 12.30).
e is presumed to correlate closely with LV relaxation
indexes and to be relatively preload insensitive.
Similar to mitral E flow, e appears to be age-dependent.

Fig. 12.29: Effect of Valsalva. Upper panel shows restrictive flow
pattern, which changes to pseudonormal pattern with an L-wave at the
end of Valsalva maneuver.
Fig. 12.31: Upper panel shows mitral inflow pattern and the lower
panel depicts annular velocities from the lateral edge of the mitral
annulus. An E/e of 7 indicates normal diastolic function as the e is
10 cm/s.
E depends on LA pressure, residual LV relaxation
pressure and age and because e is presumed to
depend only on LV relaxation pressure, dividing E by e
eliminates LV relaxation pressure and age, so the E/e
ratio becomes a noninvasive estimate of LA pressure
(Fig. 12.31).
Septal and lateral mitral annular e velocities differ.
Recent guidelines for the detection of diastolic
dysfunction recommend use of an E/e value that is the
average of septal and lateral mitral annular e.
Diastolic Function 215
Fig. 12.30: Annular tissue velocities from lateral edge of the mitral
annulus. See text for description.
Fig. 12.32: Upper panel shows restrictive transmitral flow and the
lower panel shows annular velocities of septal edge of the mitral
annulus. An E/e ratio of 10 falls in indeterminate zone.
A value of medial E/e > 15 is usually proposed as
evidence for elevated LV filling pressure and a value of
E/e < 8 as evidence for normal LV filling pressure.
There is a wide range of E/e values912 for which
additional investigations are required to obtain a LV
filling pressure estimate (Fig. 12.32).
Technical limitations include angle dependency,
signal noise, signal drifting, spatial resolution, sample
volume and tethering artifacts.
216 Section 3: Systolic and Diastolic Function
Fig. 12.33: Lateral edge mitral annular velocities showing l (arrow).
Diastolic dysfunction is also suggested by e < a.
e can be decreased erroneously by mitral annular
calcification, surgical rings or prosthetic valves.
An average of septal and lateral E/e 13 is suggestive
of elevated filling pressures.
A reduced s velocity is an indirect index of diastolic
dysfunction, because there is a close correlation
between longitudinal systolic function and early
diastolic function.
In healthy young individuals, septal e is 10 cm/s
and lateral e 15 cm/s at rest. But there are vendor-
dependent variations.
e < 5 cm/s in cardiac disease is reflection of advanced
diastolic dysfunction.
E/e may not work well in patients with severe mitral
regurgitation, intraventricular conduction delay, or
pacemaker.
HOW TO OBTAIN ANNULAR
TISSUE VELOCITIES
PW Doppler tissue imaging is performed in the apical
views to acquire mitral annular velocities.
The sample volume should be positioned at or 1 cm
within the septal and lateral insertion sites of the mitral
leaflets.
It is recommended that spectral recordings be obtained
at a sweep speed of 50100 mm/s at end-expiration
and that measurements should reflect the average of
three or more consecutive cardiac cycles.
Primary measurements include the systolic (s), early
() and late () diastolic velocities.
Fig. 12.34: Upper panel shows mitral E of 130 cm/s and the
lower panel shows septal edge e of 7 cm/s. E/e ratio is 19, indicating
Grade II diastolic dysfunction.
For the assessment of global LV diastolic function, it is
recommended to acquire and measure tissue Doppler
signals at least at the septal and lateral sides of the
mitral annulus and their average.
In patients with cardiac disease, can be used to correct
for the effect of LV relaxation on mitral E velocity, and
the E/ ratio can be applied for the prediction of LV
filling pressures.
The E/ ratio is not accurate as an index of filling
pressures in normal subjects or in patients with
heavy annular calcification, mitral valve disease and
constrictive pericarditis.
Presence of tissue Doppler wave during diastasis (l) is
suggestive of diastolic dysfunction (Fig. 12.33).
Higher accuracy of a single-cycle E/e ratio in predicting
mean wedge pressure in patients with atrial fibrillation
using a dual Doppler echocardiographic probe has
been shown.
Strain rate during IVRT has good correlations with
the time constant of LV relaxation and dP/dt and is
not affected by changes in preload. Strain rate can be
obtained by tissue velocity imaging.24
Practical Tips
In the presence of normal or pseudonormal mitral
flow pattern, an E/e ratio 15 obtained from either
edge of the mitral annulus suggests Grade II diastolic
dysfunction (Fig. 12.34).
In long-standing disease, an E/e ratio may not
accurately reflect the magnitude of filling pressures but
may be indicative of stiff LV (Fig. 12.35).

Fig. 12.35: Upper panel shows transmitral flow, while the lower
panel shows annular velocities at the septal edge in a patient on
maintenance hemodialysis. An E/e ratio of 34 does not necessarily
imply very high filling pressures in this otherwise stable patient.
Fig. 12.37: Same patient as in Figure 12.36. E/e at lateral margin of
the mitral annulus (16.5) is lower than that at the septal margin but
is still way above normal. A lateral E/e 12 is indicative of diastolic
dysfunction.
Greater utility of E/e lies in patients with systolic
dysfunction as compared to those with pure diastolic
dysfunction.
In relatively younger patients, this ratio has greater
predictive value for filling pressure and symptoms
(Figs 12.36 and 12.37).
If E/e does not clearly indicate presence of diastolic
dysfunction, an e/a ratio < 1 can be used along with
other data (Fig. 12.38).
In elderly people, all normal-appearing mitral flow
patterns can not be regarded as pseudonormal.
An E/e may help define the degree of normalcy
(Fig. 12.39).
Diastolic Function 217
Fig. 12.36: Left panel shows normal transmitral flow, while mitral annular
velocity at septal margin is 5 cm/s and E/e ratio of 20 is indicative of
elevated filling pressures and most likely cause of dyspnea.
Fig. 12.38: An indeterminate E/e ratio from the septal edge is compli
mented by absolute e of 5 cm/s and e/a ratio < 1 in suggesting
diastolic dysfunction.
Fusion of mitral E- and A-waves may make E/e
calculation difficult (Fig. 12.40). Fusion occurs in
several conditions listed below.
Sinus tachycardia
Prolonged PR interval
Intraventricular dyssynchrony
Advanced diastolic dysfunction
In many disease states, post-systolic tissue waves may
mask tissue e, making it difficult to estimate E/e ratio
(Fig. 12.41).
Annular post-systolic positive waves may convert
severe diastolic dysfunction to mild by virtue of
changing transmitral flow pattern (Fig. 12.42).
218 Section 3: Systolic and Diastolic Function
Fig. 12.39: A 70-year-old healthy woman with normal mitral flow and
a septal edge E/e of 11.
Fig. 12.41: Post-systolic annular tissue wave masking e. This could
be called reversed e.
An E/e ratio may not be reliable in the presence of
atrial fibrillation, sinus bradycardia and first degree AV
block (Fig. 12.43).
LV diastolic function can be deciphered through
the evaluation not only of the relationship of the
amplitude of E to e but also through the evaluation of
the relationship of the timing of the onset of E to the
onset of e. Normally, mitral inflow is initiated with
rapid LV relaxation and suction of blood into the LV.
When this occurs, the onset of e will be slightly before
or simultaneous with the onset of E.25 If, however,
LA pressure is elevated and LV relaxation reduced, E
Fig. 12.40: Improbability of estimating E/e ratio due to fusion of
mitral E and A in presence of sinus tachycardia and absence of
annular e-wave (upper panel).
Fig. 12.42: Impaired relaxation pattern of mitral flow (upper panel)
in a patient with advanced heart failure. Post-systolic annular waves
extending into mid-diastole (lower panel).
velocity onset may precede the onset of e (Fig. 12.44).
These timing relationships have been correlated with
LV filling pressure.
PULMONARY VEIN FLOW AND
DIASTOLIC FUNCTION
PW Doppler flow pattern of pulmonary veins shows two
over-riding antegrade systolic waves (mostly seen as
one, S-wave), one antegrade diastolic wave (D) and a
retrograde wave during atrial contraction, Ar (Figs 12.45
to 12.47). First S-wave is due to atrial relaxation and the
 Diastolic Function 219

Fig. 12.43: E/e ratio of 7 (lateral) in an 84-year-old person with sinus Fig. 12.44: Mitral E preceding tissue e in a patient with Grade II dias-
bradycardia, first degree AV block with heart failure. tolic dysfunction.

Fig. 12.45: Pulmonary vein flow pattern in a normal subject. Patients Fig. 12.46: Equivalent pulmonary systolic and diastolic wave but with
with Grade I diastolic dysfunction have similar pattern. prolonged atrial flow reversal (Ar) suggestive of diastolic dysfunction.

second one (S2) due to descent of the mitral annulus

during systole. D-wave occurs during opened mitral valve.
Ar-wave occurs following atrial contraction when blood
has option of flowing antegradely into the LV as well as
back in pulmonary veins depending upon the relative
resistance.26
The pattern of pulmonary venous flow (systolic vs.
diastolic predominance) has been proposed as a pre
dictor of diastolic dysfunction (Figs 12.48 and 12.49).
However, diastolic preponderance is invariable in
children and young adults.
Ar velocity > 35 cm/s also indicates raised filling
pressures (Fig. 12.49).
Comparison of the duration of flow at atrial contraction
across the mitral valve (on the mitral inflow velocity
Fig. 12.47: Graphical representation of pulmonary vein flow in a curve) and the duration of reversal flow back into the
subject with raised left ventricle filling pressure.
pulmonary veins (on the pulmonary venous velocity
220 Section 3: Systolic and Diastolic Function
Fig. 12.48: Right upper pulmonary vein diastolic flow velocity and
velocitytime integral is greater than systolic filling fraction in a patient
with significant diastolic dysfunction.
Fig. 12.50: Atrial flow reversal (Ar) duration of pulmonary vein > mitral
A by > 30 milliseconds is suggestive of elevated LV end-diastolic
pressure.
curves) has been repeatedly demonstrated to reflect
the left ventricular end-diastolic pressure (Fig. 12.50).
If the duration of atrial reversal flow in the pulmonary
vein exceeds by more than 30 milliseconds the duration
of flow across the mitral valve, raised left ventricular
end-diastolic pressure can be diagnosed with high
specificity.
The major limitations to the use of the pulmonary
venous signals are that these signals are difficult
to obtain and interpret. The technical feasibility of
obtaining adequate signals has been reported at < 80%
of unselected patients.
Fig. 12.49: Right upper pulmonary vein atrial flow reversal (Ar) velocity
of 50 cm/s indicative of diastolic dysfunction.
Fig. 12.51: Upper panel shows mitral flow pattern and the lower
panel shows right upper pulmonary flow pattern. In the presence
of normal-appearing mitral flow, predominant systolic fraction and
short atrial flow reversal (Ar) indicate that the above pattern is of a
normal adult.
Pulmonary vein flow, when interpretable, is used to
refining the grades of diastolic dysfunction (Figs 12.51
to 12.53).
Longer duration of mitral atrial flow compared to that
of pulmonary vein atrial flow reversal velocity may
be found in Grade I diastolic dysfunction besides in
normal subjects.
Acquisition of Pulmonary Vein Flow Signals
Color flow imaging is useful for the proper location of
the sample volume in the right upper pulmonary vein.

Fig. 12.52: Equivalent pulmonary venous systolic and diastolic flow
fraction (lower panel) but with inspiratory decrease in D-wave (arrow)
is suggestive of normal filling pattern.
In most patients, the best Doppler recordings are
obtained by angulating the transducer superiorly such
that the aortic valve is seen.
A 2- to 3-mm sample volume is placed > 0.5 cm into the
pulmonary vein for optimal recording of the spectral
waveforms.
Wall filter settings must be low enough to display the
onset and cessation of the Ar velocity waveform.
Pulmonary venous flow can be obtained in > 80% of
ambulatory patients, although the feasibility is much
lower in the intensive care unit setting.
The major technical problem is LA wall-motion
artifacts, caused by atrial contraction, which interferes
with the accurate display of Ar velocity.
Spectral recordings should be obtained at a sweep
speed of 50100 mm/s at end-expiration and
measurements include the average of three or more
consecutive cardiac cycles.
Pulmonary Vein Flow Parameters
Measurements of pulmonary venous waveforms
include peak systolic (S) velocity, peak anterograde
diastolic (D) velocity, the S/D ratio, systolic and
diastolic filling fractions, and the peak Ar velocity in
late diastole.
Other measurements are the duration of the Ar
velocity, the time difference between it and mitral
A-wave duration (ArA).
D velocity DT. There are two systolic velocities (S1
and S2), mostly noticeable when there is a prolonged
Diastolic Function 221
Fig. 12.53: Upper panel: mitral flow, middle panel: pulmonary flow,
lower panel: septal annular velocities. There is hardly any S-wave in
pulmonary vein flow and E/e of 30 indicating advanced diastolic dys-
function.
PR interval, because S1 is related to atrial relaxation.
S2 should be used to compute the ratio of peak systolic
to peak diastolic velocity.
S1 velocity is primarily influenced by changes in LA
pressure and LA contraction and relaxation, whereas
S2 is related to stroke volume and PW propagation in
the pulmonary arterial tree.
D velocity is influenced by changes in LV filling and
compliance and changes in parallel with mitral
E velocity.
Pulmonary venous Ar velocity and duration are
influenced by LV late diastolic pressures, atrial preload
and LA contractility.
A decrease in LA compliance and an increase in LA
pressure decrease the S velocity and increase the
D velocity, resulting in an S/D ratio < 1, systolic filling
fraction < 40% and shortening of the DT of D velocity,
usually < 150 milliseconds (Figs 12.54 and 12.55).
However, DT of mitral E and pulmonary vein D may
not always be concordant as DT of D-wave tends to be
nonlinear more often (Fig. 12.56).
MITRAL FLOW PROPAGATION BY
COLOR M-MODE
Assessment of flow propagation into the LV is another
technique that provides better ability to predict filling
pressures.27,28
In the normal state, flow rapidly propagates into the
LV (Fig. 12.57). Early stage relaxation abnormalities show
a blunting of flow propagation.
222 Section 3: Systolic and Diastolic Function
Fig. 12.54: Upper panel: pulmonary vein flow, lower panel: transmi-
tral flow. Restrictive transmitral flow is negated by normal pulmonary
venous flow, although atrial flow reversal is 20 milliseconds longer.
Fig. 12.56: Upper panel shows short deceleration time (DT) of mitral
E, while DT of pulmonary vein D is longer (170 milliseconds) and non-
linear.
The propagation velocity (Vp) does not show a
pseudonormalization, and therefore, can be used in all
levels of diastolic dysfunction.
Similar to the tissue Doppler velocities, color M-mode
flow propagation has been combined in a ratio with the
mitral E velocity to provide an adjusted parameter (E/Vp)
with strong correlation to filling pressures and prognosis.
The chief limitations of this tool are lack of consensus
on technique and theoretical concerns that this will be
invalid in small left ventricular cavities.
Fig. 12.55: Pulmonary vein D-wave > S-wave with deceleration time
of 130 milliseconds indicating elevated left ventricular filling pressure.
Fig. 12.57: Mitral flow propagation velocity by M-mode.
Practical Tips
Acquisition is performed in the apical four-chamber
view, using color-flow imaging.
M-mode scan line is placed through the center of the
LV inflow blood column from the mitral valve to the
apex, with baseline shift to lower the Nyquist limit so
that the central highest velocity jet is blue.
Vp is measured as the slope of the first aliasing velocity
during early filling, measured from the mitral valve

Fig. 12.58: Vp of 31 cm/s in a patient with heart failure.
Fig. 12.60: Normal circumferential strain (right panel) in presence of
advanced diastolic dysfunction.
plane to 4 cm distally into the LV cavity, or the slope of
the transition from no color to color.
Vp > 4550 cm/s is considered normal (Fig. 12.58).
Should other Doppler indices appear inconclusive,
an E/Vp ratio 2.5 predicts PCWP > 15 mm Hg with
reasonable accuracy (Fig. 12.59).
Patients with normal LV volumes and EFs but elevated
filling pressures can have misleadingly normal Vp.
Peak velocity of early diastolic mitral flow propagation
velocity (Vp) has been used as an approximation for
ventricular suction.
Diastolic Function 223
Fig. 12.59: A 43-year-old female with recurrent pulmonary edema.
E/e of 12.5 (lateral) is inconclusive but E/Vp of 3.3 suggests raised
filling pressures.
LONGITUDINAL STRAIN, ROTATION AND
UNTWISTING RATE BY ACOUSTIC
SPECKLE TRACKING
Most patients with diastolic dysfunction have impaired
longitudinal strain by acoustic speckle tracking.
Impaired longitudinal strain (> 15%) is the first indi
cation of impaired diastolic function.29
Torsion and circumferential strain are normal in
patients with isolated diastolic dysfunction (Fig. 12.60).
Assessment of LV torsion has shown that untwisting
begins before aortic valve closure and might be an
important component of normal diastolic filling.28
Studies in human subjects using indirect indexes derived
from right heart catheterization have suggested a
relationship between constant of isovolumic relaxation
and measures of untwisting.
But the relationship between directly measured
diastolic function indexes with micromanometer
catheters and untwisting parameters has not been
established in human subjects.
Untwisting parameters are related to invasive indexes
of LV relaxation and suction but not to LV stiffness.
These data suggest that untwisting is an important
component of early diastolic LV filling but not of later
diastolic events.
224 Section 3: Systolic and Diastolic Function

Fig. 12.61: Diastolic stress test in a normal person. There is proportionate increase in mitral E and e.

Because most patients have limited functional capacity,

the workload starts at 25 W and increases in increments of
25 W every 3 minutes.
We need to record mitral inflow by pulsed Doppler
echocardiography at the level of the mitral tips, mitral
annular velocities by spectral Doppler echocardiography
and tricuspid regurgitation jet by CW Doppler (Fig. 12.61).

SUMMARY
Doppler echocardiography provides major insights into
the pathophysiology of diastolic LV dysfunction. So far,
however, no single Doppler echocardiographic index of
diastolic LV dysfunction has yielded a robust criterion
Fig. 12.62: A simplified schema to report diastolic function based upon for elevated LV filling pressures. A stepwise strategy with
pulsed wave Doppler mitral flow, annular velocities and pulmonary sequential use of multiple Doppler echocardiographic
vein flow. indexes reduces diagnostic sensitivity because it frequently
(DTI: Doppler tissue imaging).
leads to an indeterminate outcome. A multiparametric
approach with age and clinical situation in mind is the best
DIASTOLIC STRESS TEST way of using echocardiography in detection of diastolic
Many patients present with exertional dyspnea but have dysfunction because it is so complex and dependent
normal LV filling pressures at rest. upon multitude of variables (Fig. 12.62). Because of these
In these patients, it is important to evaluate filling persistent shortcomings, clinicians should continue to
pressure with exercise.30,31 make critical use of current Doppler echocardiographic
Exercise can be performed using a supine bicycle or estimates of LV filling pressures and should not hesitate
treadmill protocol. to implement invasive investigations to confirm their

clinical suspicions. Guidelines for assessing diastolic
function by echocardiography are continually being
updated. There is reasonable agreement estimating dias
tolic grade and LA pressure using current guidelines.
Further refinements in the definition of mild and moderate
dysfunction may improve agreement. There are a number
of limitations to these measurements, including the need
for high-quality signals, adequate flow visualization in the
apical views, experience in acquisition and analysis, and
so on.
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18. Nagueh SF, Middleton KJ, Kopelen HA, et al. Doppler
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 SEction 4
Muscle Mechanics

Chapters

Tissue Doppler Echocardiography: Current Status Rotation, Twist and Torsion

and Applications
Deformation Imaging: Theory and Practice
 Chapter Tissue Doppler

13
Echocardiography: Current
Status and Applications

CONCEPT OF TDI
In 1842, an Austrian scientist, Christian Doppler,
presented the concept of measuring distance of planets
from the earth by using what is now called Doppler
effect. A century later, at the University of Osaka, Japan,
S. Satomura first applied these principles to measure the
blood flow velocities in blood vessels. The pioneer of tissue
Doppler imaging is Karl Isaaz, a French man, who was the
first to realize the importance of clinical and diagnostic
potentials of tissue Doppler imaging. He hypothesized
that rate and direction of the heart tissue movement can be
obtained by using the tissue Doppler with the assumption
that the movement is parallel to the ultrasound beam
and within the beam. Movements of myocardial walls
Fig. 13.1: Concept of tissue Doppler echocardiography. Using a
include components of low velocity and short duration prespecified region for placement of sample volume, a Doppler
requiring a high sampling rate. Modifications to the filter spectrum is obtained as shown in the Figure depicting velocities in
settings on pulsed Doppler to image low-velocity, high- various phases of the cardiac cycle with preordained filter settings.
Velocities toward the transducer are positive and away from the
intensity myocardial signal rather than the high-velocity,
transducer are negative. Temporal resolution of various waves is due
low-intensity signal from blood flow allow tissue velocity to high frame rates (> 100 frames/s).
estimation. Tissue velocities are nearly one-tenth of the
intracardiac flow velocities. Measurement of myocardial LABELING OF TISSUE
tissue motion has created basis for detailed evaluation of VELOCITY WAVEFORMS
systolic and diastolic cardiac function not only in terms of
velocity, but also in terms of acceleration, displacement Two positive waves of myocardial shortening can
and deformation variables (Fig. 13.1). be recorded in systole. The first positive wave (S1)
230 Section 4: Muscle Mechanics

A B

C D
Figs 13.2A to D: (A) Tissue Doppler waveforms S1 and S2 are systolic velocities, while e and a are early and late diastolic velocities. There
are small biphasic velocities in isovolumic phases, which are normally not named. S1 represents longitudinal component, while S2 denotes
circumferential component of the systolic velocities. Conventionally, tissue velocities are labeled by lowercase letters; (B) Tissue Doppler wave-
forms of the actual tracing from the medial edge of the mitral annulus. There are two positive (systolic) and two negative (diastolic) waveforms;
(C) Lateral edge mitral annular tissue velocity profile showing two distinct systolic waves (S and S2) in a healthy young control. It is the S1
that represents contraction of longitudinal fibers that is usually measured; (D) Color Doppler myocardial imaging. After acquisition of image
containing velocity information, a sample volume of known length is placed (as here at basal inferior septum) and corresponding velocity
spectrum is obtained (shown on the right side).

occurs as a result of the longitudinal shortening of
the myocardial tissue during the phase of isometric
contraction. The second wave (S2) occurs due to
left ventricle (LV) shortening during LV ejection
(Figs 13.2A to C). Two peak velocities in systolic ejection
are commonly seen in free wall. These represent
functional switch-over from subendocardial longi
tudinal fibers contraction to circumferential fibers
shortening during ejection with a variable delay.
In healthy subjects, the shortening of the longitudinal
fibers predominates over that of the circumferential
fibers during early systole, whereas the shortening
of the circumferential fibers predominate over that
of longitudinal fibers in the ejection phase. However,
their relative importance remains ill-defined and,
therefore, both systolic waves should be measured and
mentioned. However, whenever two waves are seen, it is
not clear which one should be used. As S1 corresponds
 Tissue Doppler Echocardiography: Current Status and Applications
to contraction of subendocardial longitudinal fibers, it
is better to use it.
Early diastolic velocity, which correlates with active
relaxation, is labeled e. It is relatively much less load-
dependent.
Late diastolic velocity, which correlates with ventricular
stiffness, is labeled as a.
There is no consensus on labeling abnormal waves.
However, l wave is that recorded in diastasis.
A recoil wave can usually be seen after high-velocity
movements during isovolumic contraction, relaxation
or after early diastolic filling, and occurs in a direction
opposite to initial movement.
The rate of LV pressure decline during isovolumic
relaxation (IVR) becomes slower during the
development of most forms of cardiovascular disease
and also becomes slower during normal aging.
Prominent and prolonged IVR phase can be often
noticed in diseased states. It may be called IVR.
TERMS USED IN TISSUE
DOPPLER IMAGING
Velocity: speed of motion with direction (positive or
negative velocity).
Color velocity imaging shows red hue while shortening
and blue while lengthening. Velocity is a vector physical
quantity; both magnitude and direction are required to
define it.
Displacement: A displacement is the shortest distance
from the initial to the final position of a point. In ultrasound
terms, it is time integral of velocity (velocity time).
Displacement imaging, also called tissue tracking, uses
different hues for degree of displacement. TDI measures
only linear displacement.
Strain rate: regional myocardial velocity gradient.
Strain rate imaging (SRI) has several hues, for example,
green color denotes no strain rate, while orangered
hue indicates negative strain rate; blue color indicates
positive strain rate (color hues are reverse of tissue velocity
imaging (TVI)].
Strain: Integral of strain rate and time over a fixed
region measured in percent. Strain imaging has different
hues, for example, white means no strain.
Acceleration: Rate of velocity over a region (velocity/
time). Deceleration is called a negative acceleration.
Momentum: Integral of mass and velocity, rarely used
in TDI, although more common in flow Doppler studies.
231
Deformation: Change in shape and size of an elastic
object when a force is applied. Strain and strain rate are
examples of deformation imaging.
TDI or TVI: An imaging technique that provides
qualitative and quantitative information about regional
velocities using pulsed wave Doppler with good temporal
resolution.
Spectral pulsed TDI is online velocity determination
from a single point by placing a small sample volume. It
has the advantage of online measurements of velocities
and time intervals and an excellent temporal resolution
(8 milliseconds).
Color Doppler myocardial imaging (CDMI): An
imaging technique that provides qualitative or quantitative
information about spatial velocities using fast Fournier
algorithm of color flow mapping. Peak velocities measured
by this technique are approximately 2030% lower than
that of TDI, because these are mean velocities rather than
peak values (Fig. 13.2D).
Merely by turning on a knob, one can convert it to
displacement imaging or deformation imaging or tissue
synchronization imaging.
Curved anatomical M-mode TVI: High resolution
semiquantitative technique to study regional tissue
velocities and velocity-derived parameters. In M-mode
tracing, the derivative of the position versus time graph of
an object is equal to the velocity of the object.
TECHNICAL DETAILS OF TDI
TDI is an assessment of myocardial motion using
Doppler ultrasound imaging, often with color coding.
The fundamental units are velocity observed from the
echocardiographic transducer as a frame of reference.
Most systems have TDI software, which automatically
brings on tissue velocities once a sample volume is placed
in that image after activating the software. TDI information
is embedded in gray-scale images or the images are
colored.
Velocities are obtained from the selected sample
volume (single or multiple point velocity in reference
to the position of the transducer), which can be of
variable dimension. A sample volume of 25 mm is
optimum for spectral Doppler, while CDMI has a wide
but well-defined area (612 mm) from where velocities
can be obtained ex post facto.
Tissue velocities are usually < 25 cm/s.
A high sampling rate is essential for a proper rendering
of TVI signals (but introduces noise)too low frame
232 Section 4: Muscle Mechanics
Fig. 13.3: Spectral pulsed wave tissue velocities from the medial
edge of the mitral annulus. Velocities obtained from here are most
stable and commonly used for serial studies. This is because angle of
insonation is optimal.
rates result in underestimation (< 70 frames/s). To
ensure the optimal signal-to-noise ratio, temporal
filtering should be used with caution (usually 200
frames/s), governed by the awareness of the interplay
between sampling rate and temporal filters.
The influence of unfavorable insonation angle may
affect tissue Doppler measurements resulting in
underestimation of the true myocardial velocities.
Default gain settings of 50% saturation should be used
to measure velocities accurately. Overgaining results
in overestimation of tissue velocities by approximately
20%. Intervendor settings differences also should be
noted.
In clinical practice, annular velocities are used most
often because these are more reproducible (Fig. 13.3).
Usually, septal or lateral edges of the mitral annulus are
interrogated and can be used separately or by averaging
the two. Multiple points of the annulus can also be
used to enhance accuracy but are cumbersome and
are not recommended. The results of averaging mitral
annular velocities obtained from the four myocardial
walls do not differ from the average of using velocities
measured at the septal and lateral sites.
Color Doppler myocardial velocities are obtained ex
post facto and can be obtained from multiple sites
either in M-mode or two-dimensional (2D) format
(Figs 13.4 to 13.6).
Color Doppler obtained velocities are 20% to 30%
lesser than the pulsed wave Doppler velocities but
provide mean velocity estimation from several sites
simultaneously.
Temporal resolution is maximum in M-mode tissue
velocities, followed by pulsed wave TDI and then
CDMI (Fig. 13.5B).
TDI is used for assessing regional longitudinal
function. It is possible to obtain radial velocities, which
are mostly used for pattern reading and understanding
myocardial mechanics.
Systolic and early diastolic velocities decrease with
aging and hence normal values are age-dependent
when used in isolation.
Tissue velocities have a base-to-apex gradient and are
usually nearly absent close to the apex. Typical annular
tissue s and e velocities are 8 cm/s in healthy subjects
while a is less than e.
Lateral annular velocities are higher than medial
annular velocities (Fig. 13.6).
Tricuspid annular and right ventricular (RV) free wall
velocities are usually higher than mitral annular and
LV free wall velocities by approximately 2030%.
Tissue velocities have greatest utility for estimating
subclinical systolic and diastolic dysfunction and
prognosis. All waves have implications. Even s + e have
been used for prognosis. High temporal resolution
provides information about the behavior of the tissue
region over the entire cardiac cycle.
The isovolumic myocardial motion variables are
of considerable clinical interest since they appear
to be early markers of pathological phenomena
like ischemia-induced disturbances in myocardial
function. Post-systolic prominent positive velocities
usually indicate nonspecific myocardial diseased state
and are not specific to ischemia (Fig. 13.7).
Occasionally, there is a negative wave between e and
a during diastasis. This is called L-wave. L-wave is
mostly seen when heart rate is slow and represents
elevated diastolic pressures (Fig. 13.8).
TDI sometimes show phenomena that are of
physiological significance but are not present in flow
Doppler interrogation, for example, phasic or pan-
cyclic temporal or velocity alternans suggestive of
advanced myopathic process (Figs 13.9A and B).
Accurate measurement of myocardial tissues velocities
is of considerable clinical interest since it is accepted
 Tissue Doppler Echocardiography: Current Status and Applications 233

A B

C D
Figs 13.4A to D: (A) Color Doppler myocardial imaging from interventricular septum. Note velocity spectrum derivation from multiple points in
a single cardiac cycle. The tissue velocities decrease from base to apex; (B) Color Doppler myocardial imaging from interventricular septum.
Note velocity spectrum derivation from multiple points in a single cardiac cycle. The tissue velocities decrease from base to apex; (C) Right
ventricular free wall shows base-to-apex gradient of peak systolic velocities and diastolic velocities in a normal adult. (D) Color Doppler displacement
imaging of the interventricular septum. Average displacement of a myocardial wall is approximately 8 mm with a base-to-apex gradient. Note that
the apical segment (red curve) is nearly stationary while the basal segment moves a distance of 13.8 mm in systole.

that decreased peak systolic and early diastolic
velocities indicate failing myocardial function.
Attention should be paid to the site and size of sample
volume, frames rates, gain and angle of insonification.
Longitudinal systolic dysfunction (s velocities) might
be compensated by an increase of the radial function.
Therefore, in early disease states, there is no correlation
between systolic velocities and ejection fraction and the
two provide complimentary but different information.
Before TDI measurements, it is wise to perform cardiac
event marking defining aortic valve opening and
closure and mitral valve opening and closure.
Age, heart rate and LV dimensions account for between
20% and 70% of the variability seen in LV systolic and
diastolic velocities. Instead of relying upon normative
data from literature, each center should develop its
own normal values.
Mitral annular velocity measurement cannot be used
in patients with severe mitral annular calcification,
prosthetic ring or prosthetic mitral valve.
Apical segments cannot be assessed using TDI because
of limited movement of the apex and unfavorable angle
of incidence of apical myocardial motion with respect
to the transducer position.
Although TDI has become synonymous with velocity
measurement, in many cases it is not the frequency
shift (Doppler shift) of the received signal that is
measured, but the phase shift (when the received signal
234 Section 4: Muscle Mechanics

A B
Figs 13.5A and B: (A) M-mode color Doppler myocardial imaging in the apical four-chamber view of the left ventricle. Bright orange or red color
velocities are positive, while blue ones are negative. Note lack of any motion at the apex. Also note temporal heterogeneity of the septal wall in
this 50-year-old female with hypertrophic cardiomyopathy due to myofiber disarray. The walls are traced by curved anatomical M-mode method;
(B) M-mode Doppler myocardial imaging of the basal right ventricular free wall. Orange color are positive velocities, while blue are negative
velocities. Note the excellent temporal resolution. Positive velocity after early diastolic wave is due to recoil and is normal.

Fig. 13.6: Color Doppler myocardial velocities from basal septum
compared to basal lateral wall. Note that the velocities from the lateral
wall are higher.
Fig. 13.7: Tissue Doppler imaging of medial mitral annulus showing
prominent post-systolic positive wave (pst). A negative component
of similar magnitude is present during isovolumic relaxation. Post-
systolic wave indicates non-specific myopathic process but one
induced by stress are specific for ischemia.

arrives). This is used to study cardiac asynchrony and
cardiac phase-related myocardial performance index
(isovolumic phase duration/ejection phase duration)
and tissue alternans (Figs 13.9A and B).
MYOCARDIAL VELOCITIES IN SHORT AXIS
Myocardial velocities in the short axis are acquired
from the posterior wall and the interventricular septum
(Fig. 13.10). Short-axis TDI implies the possibility of
measuring a combination of longitudinal, radial and
circumferential, rather than the pure circumferential
motion.
Posterior wall waves resemble the waveforms of the
longitudinal plane with two systolic (S1 and S2) and
three diastolic waves (ivr, e and a).
The motion of the interventricular septum is more
complex as it is shared between the two ventricles.
Moreover, there is a hinge point in the septum,
proximal to which it moves away from the LV cavity in
 Tissue Doppler Echocardiography: Current Status and Applications 235

Fig. 13.8: Tissue Doppler imaging of the lateral edge of the mitral annulus. Note prominent L-wave at a heart rate of 61 beats/min. I-wave is
independent of E or A magnitude.

A B
Figs 13.9A and B: (A) Tissue Doppler imaging of the medial edge of the mitral annulus. Note temporal alternans during diastole (tissue diastole
in milliseconds is shown in each beat). Also note prominent post-systolic positive wave. Both alternans and positive isovolumic velocities are
indicative of advanced myopathic process; (B) A 14-year-old female child with heart failure (idiopathic dilated cardiomyopathy). Tissue Doppler
imaging at mitral annulus shows pan-cyclic Doppler alternans, which usually precedes flow alternans and is more specific than the latter. Note
alternation of peak velocities as well as duration of each wave. There is fusion of e and a in alternate cardiac cycle due to shortened tissue
diastole.

systole and toward the LV cavity in diastole. The part of
the septum distal to it moves in the opposite direction.
The tissue velocities in the later part of the septum
shows two inward movements in systole, the first (S1)
being due to isometric contraction, and the second
(S2) due to ventricular ejection. S2 wave in short axis is
bigger than in long axis.
The diastolic waves show a biphasic wave in early
diastole (e) and a wave of atrial contraction (a).
The systolic and diastolic waves occur earlier in the
septum as compared to the posterior wall and are
consistent with the pattern of electrical activation of
the septum. This information can be used to detect
ventricular pre-excitation.
The reason for the biphasic motion of the septum
in early diastole is not known. It may be because
of translational and/or RV influences (Fig. 13.11).
INTERNAL DEPENDENCY OF VELOCITIES
As systole is coupled with diastole, systolic velocities
are related to diastolic tissue velocities. s velocity
denotes longitudinal systolic function, while e denotes
myocardial relaxation. a is a reflection of ventricular
stiffness.
Systolic velocity (s) is positively correlated to the
early diastolic velocity (e). Increased longitudinal
contraction is able to improve early diastolic LV filling
through the effect of elastic recoil and vice versa.
236 Section 4: Muscle Mechanics
Fig. 13.10: Myocardial tissue velocities from the posterior wall in short
axis.
Fig. 13.12: Septal annular pulsed wave Doppler tissue velocity pattern
in an elderly subject. Both S and E are decreased (56 cm/s), while A
is increased (> 10 cm/s). This pattern indicates combined systolic and
diastolic dysfunction.
There is a negative correlation between early diastolic
(E) and late diastolic (A) velocities except in end-stage
disease, where both decrease (Fig. 13.12).
Therefore, S and A are independent predictors of
myocardial properties while e is dependent upon S.
E/A and S are more robust parameters of abnormal
physiology.
Limited data exist on isovolumic phase velocities and
their significance at rest. Stress-induced prominent
post-systolic positive velocities may be specific markers
of ischemia and correlate with extent of perfusion
Fig. 13.11: M-mode depiction of the color-coded tissue velocities of
the left ventricular short axis. Note the biphasic motion in the posterior
wall in isovolumic phases. Of note is the bidirectional and bilayered
pattern of contraction and relaxation in the interventricular septum.
defects. Prominent post-systolic velocities have also
been called delayed longitudinal contractions.
Regional myocardial tissue velocities, however,
represent the net effect of the contractile and elastic
properties of the area under investigation and traction
and tethering effects from other regions. Tissue motion
can be resolved by velocities but difference between
active or passive motion can not be made out. For this,
myocardial velocity gradient imaging (deformation
imaging) is used.
e/a ratio increases with increasing physiological stress
and exercise in healthy subjects. Abnormal response
could signify disease process or aging.
e is relatively independent of the effect of heart rate,
preload and afterload but is affected by age.
FUNDAMENTAL BASIS OF TDI
Heart as an organ continues to surprise us. The intricate
layout of muscle fibers from inside to outside, from right
to left and from base to apex is designed for mechanical
efficiency of extreme proportions at low energy
consumption (Fig. 13.13). TVI is one of the techniques that
has helped us in understanding this complexity. Heart is a
complex mechanical organ that undergoes cyclic changes
in multiple dimensions that ultimately effect a change
in chamber volume that results in ejection of blood. In
simple terms, it is called multidimensional motion or
movement. Primary motion of heart muscle secondary
to electromechanical coupling provides passive motion
to blood. Movement of blood or flow has been studied
 Tissue Doppler Echocardiography: Current Status and Applications
Fig. 13.13: Myo-architecture of the left ventricle from base to apex.
Subendocardial fibers (green line) descend toward the apex and then
make a figure of 8 as these ascend upwards as subepicardial fibers
(red line). Arrows represent circumferential component of the
motion, while other parts represent longitudinal motion.
Fig. 13.15: Tissue Doppler-derived strain rate imaging of the
basal septum in the apical four-chamber view over a fixed segment of
12 mm length. Systolic strain rates are negative (rate of longitudinal
shortening, esr), while diastolic strain rates are positive (rate of
diastolic lengthening). Note prominent post-systolic negative strain
rate (pssr), which usually indicates diseased segment.
for long by use of the Doppler principle. Application
of the Doppler principle to the heart tissue motion is
called tissue Doppler echocardiography (TDI) or tissue
velocity imaging. This requires a simple modification
of the settings used for flow velocity studies. Regardless
of imaging technique, the holy grail of heart motion or
action called ejection fraction, which is a sum total of
the heart motion, is unable to provide information on the
237
Fig. 13.14: Mean velocity gradient over a segment of fixed length
obtained by color Doppler myocardial imaging yields strain rate curves
as shown on the left side of the diagram. It is expressed as number/
second.
underlying myocardial mechanical activity. Also, ejection
fraction reflects the sum contribution of several regions
only during systole and does not provide information on
regional function. Regional function assessed visually is
subjective and prone to error. The most difficult part of
regional function by conventional imaging method has
been the study of diastolic function and isovolumic phase
function with temporal and spatial evaluation. Focal
estimation of the regional function has been the subject
of much research. Tissue Doppler imaging (TDI) is one
of the earliest such methods. Modifications to the filter
settings on pulsed Doppler to image low-velocity, high-
intensity myocardial signal rather than the high-velocity,
low-intensity signal from blood flow allows segmental
or regional assessment by ultrasound. The TDI method
depicts myocardial motion (measured as tissue velocity)
at specific locations in the heart. Tissue velocity indicates
the rate at which a particular point in the myocardium
moves toward or away from the transducer. Integration
of velocity over time yields displacement or the absolute
distance moved by that point. Although myocardial
velocity curves can be constructed either online from
spectral pulse TDI or offline from 2D color TDI, the latter
approach is preferable, because multiple segments can be
compared within the same heart beat. Further estimation
of myocardial velocity gradient by TDI over a fixed region
provides strain rate (rate of shortening or lengthening;
Figs 13.14 and 13.15).
238 Section 4: Muscle Mechanics
Fig. 13.16: Diagram depicting strain spectrum from mid-septum
obtained by integrating myocardial velocity gradient and time over a
fixed segment length. Strain is derived from color Doppler myocardial
imaging.
Time integral of the strain rate gives information about
strain (amount of shortening, thickening or lengthening).
Strain is dependent on preload, afterload, heart rate
as well as state of contraction. It correlates best with
dP/dt and to some extent with ejection fraction (Figs 13.16
and 13.17).
The validity of this approach for calculating strain has
been confirmed by the use of sonomicrometry and tagged-
magnetic resonance imaging as reference methods.
Tissue velocity per unit time provides regional
myocardial acceleration. All these above mentioned
parameters provide incremental assessment of the
function of regional and global heart muscle in health and
disease. TDI provided the greatest impetus to the study of
these parameters based upon non-Doppler methods when
limitations of TVI became obvious in certain situations.
Despite its obvious limitations, angle dependency,
inability to differentiate active versus passive motion and
nondiagnostic information about radial or circumferential
motion, it has found great utility in diagnosis, prognosis and
guiding therapy of a large number of clinical conditions.
Tissue velocity and strain data appear to be of optimal value
if the images are acquired carefully, analysis is meticulous
and the interpretation is judicious and balanced. In short,
tissue velocity and strain echocardiography allow detailed
interrogation of regional and global mechanics and offer
substantial incremental information on myocardial
function compared with conventional echocardiography.
Fig. 13.17: Tissue Doppler imaging-derived strain spectrum from
basal septum. Systolic strain is depicted in negative values (-11%).
There is additional -3% post-systolic strain. Post-systolic strain has
same significance as post-systolic velocity.
Both techniques characterize fundamental concepts in
cardiac physiology and represent a paradigm shift in the
application of echocardiography in clinical practice.
TISSUE DOPPLER DATA PROCESSING FOR
DEFORMATION IMAGING
Strain rate is calculated with a sample volume distance
of 812 mm.
A 16-segment model of the left ventricle is used, i.e.
each wall is subdivided into an apical, mid and basal
segment.
Strain rate curves are obtained from the center of the
segment and velocity curves are obtained from the
basal end.
Wall motion is manually tracked to keep midwall
position. Three heart cycles are temporally averaged to
improve the signal-to-noise ratio of the curves.
Displacement and strain curves are calculated by
integrating velocity and strain rate data, respectively,
and are baseline-corrected.
TVI and SRI curved M-modes can also be obtained
from all walls.
Timing of aortic and mitral valve opening (AVO, MVO)
and closure (AVC, MVC) is derived from the echo
recordings.
TVI parameters are positive if the region of interest
moves toward the transducer (for longitudinal
velocities usually systole) and negative if it moves away
 Tissue Doppler Echocardiography: Current Status and Applications
Fig. 13.18: Strain rate spectrum derived from basal lateral wall.
Negative waveform during systole is integrated with time to obtain
peak systolic strain. Note early diastolic strain rate, which is more than
systolic strain rate and correlates with diastolic function.
Fig. 13.20: Integration of strain rate with time to obtain strain of right
ventricular free wall. Peak longitudinal strain is normally around -20%
in left ventricular free wall and around -30% in right ventricular free wall
(RVFW) and its peaks at end systole in health and in diastole in dis-
ease. Peak systolic strain of -17% of RVFW suggests RV dysfunction.
from it. SRI parameters are negative in shortening
and positive in lengthening myocardium (Figs 13.18
to 13.20).
CLINICAL UTILITY OF TDI
TDI has found clinical application in a large number of
clinical situations. Of these, the important ones are listed
below:
Assessment of LV diastolic function and filling
pressures
239
Fig. 13.19: Anatomical M-mode description of strain rate of the
interventricular septum. Negative strain rate is shown redorange,
while blue color indicates positive strain rate. Green indicates no
strain rate.
Heart failure with normal ejection fraction (HFnEF)
Assessment of early LV systolic dysfunction
Constrictive pericarditis versus restrictive cardio
myopathy
Physiological versus pathological hypertrophy
Assessment of RV function
Phenomenon of aging
Study of exercise physiology
Utility in stress echocardiography
Study of atrial function
Correlation with genomics in hypertrophic cardio
myopathy (HCM), Fabry disease, etcetera.
Prognosis in various disease states
Study of muscle mechanics
Detection of intraventricular dyssynchrony
Left Ventricular Filling
Pressure and Diastolic Function
The early diastolic velocity of the longitudinal motion of
the mitral annulus (e) reflects the rate of myocardial
relaxation (Fig. 13.21). In normal subjects, e increases as
transmitral gradient increases with exertion or increased
preload, whereas in patients with impaired myocardial
relaxation, e is reduced at baseline and does not increase
as much as in normal subjects with increased preload.
Lateral annulus early diastolic velocity is usually higher
than septal annulus e. As e increases with increasing
transmitral gradient in healthy individuals, so that E/e is
similar at rest and with exercise (usually < 8).
240 Section 4: Muscle Mechanics
Fig. 13.21: Pulsed Doppler lateral edge mitral annular velocities in a
66-year-old subject with coronary artery disease. A ratio of e/a < 1
and e 12 cm/s suggests normal left ventricular filling pressures and
normal diastolic function.
Fig. 13.23: Pulsed wave mitral flow Doppler (above) and medial mitral
annular tissue velocities (below) in a 58-year-old hypertensive subject.
E/e is 10 and but e < a suggests presence of diastolic dysfunction.
Decreased e is one of the earliest markers for diastolic
dysfunction and is present in all stages of diastolic
dysfunction. However, not everyone with impaired myo
cardial relaxation has physiologically significant diastolic
dysfunction. Because e velocity remains reduced and
mitral E velocity increases with higher filling pressure,
the ratio between transmitral E and e (E/e) correlates
well with LV filling pressure or pulmonary capillary wedge
pressure (PCWP). The PCWP is 20 mm Hg if E/e is
15 and normal if E/e is < 8. Because PCWP has been
shown to be a prognostic indicator in patients with
heart failure (HF), it is reasonable to expect E/e to be
Fig. 13.22: Mitral annular velocities from medial edge (above) and
transmitral pulsed wave Doppler flow pattern. Transmitral flow pattern
can be normal or pseudonormal; however, reduced e (7 cm/s) and
E/e ratio of 20 indicates Grade II diastolic dysfunction.
a similarly powerful prognosticator in various cardiac
diseases. However, e is affected by adjacent wall motion
abnormality.
Kasner et al. who have conducted extensive research
correlating invasive versus noninvasive diastolic function
using diastolic pressurevolume loops versus early
diastolic tissue velocities have found e and a both to
be robust and reliable methods of assessing diastolic
dysfunction in health and disease. A combined data
showing e < a and E 8 cm/s at lateral edge of mitral
annulus correctly identifies 93% of the patients with
invasively proven diastolic dysfunction.
The recent guidelines have included E/e in grading
of diastolic dysfunction and have made the following
observations:
Mitral annular septal E/e 15 and lateral E/e 12
are indicative of significant diastolic dysfunction
(Fig. 13.22).
An average (septal + lateral edge) E/e 13 can also be
used as a marker of diastolic dysfunction.
E/e 8 is indicative of normal diastolic function.
E/e of 9 to 14 is of borderline significance needing
corroboration by other factors (Fig. 13.23).
Overall, E/e is the best predictor but does not
have adequate discriminative power in isolation in
predicting filling pressures.
TDI and Exercise Physiology: Heart Failure
with Normal Ejection Fraction
Heart failure with normal ejection fraction is present
in > 50% of all HF patients. The mortality and morbidity
 Tissue Doppler Echocardiography: Current Status and Applications
Fig. 13.24: Lateral mitral annular velocities in a 33-year-old hyperten-
sive female with dyspnea. elat (6 cm/s) and e/a (< 1) both are sug-
gestive of heart failure with normal ejection fraction with nearly 93%
accuracy.
of these patients may be quite elevated, and making the
diagnosis accurately is important. The gold standard
for assessing diastolic function remains the pressure
volume relationship, but it requires an invasive approach,
ideally with a conductance catheter system. Doppler
echocardiography and tissue Doppler imaging have been
studied and validated in patients with systolic dysfunction
and congestive HF and have been shown to be reliable in
assessing filling pressures. Kasner et al. have shown TDI to
be more accurate than conventional Doppler for detecting
impaired diastolic function in patients with HFnEF.
In general, the lateral annular velocities are more
closely related to the LV relaxation and compliance
indexes as determined by pressurevolume loop
analysis than the septal annular velocities.
TDI indexes elat and e/alat correlate more closely with
LV stiffness than any conventional echocardiography
index.
Similarly, the dimensionless E/e index shows the
best correlation with indexes of diastolic parameters
obtained by pressurevolume loop measurements.
Patients with HFnEF and E/elat > 8 have significantly
increased LV stiffness.
Both E/elat > 8 and E/alat < 1 detect HFnEF patients
with diastolic abnormalities equally well, but e/alat
showed lower sensitivity, yielding more false-negative
results than E/elat.
241
Combination of E/elat and e/a can detect diastolic
dysfunction in 93% of the patients with HFnEF
(Fig. 13.24).
Garca et al. and Meluzin et al. have demonstrated that
the peak systolic mitral annular velocity (s) belongs to
the most useful parameters for identifying HFnEF, having
even a higher predictive value than the peak early diastolic
mitral annular velocity (e). The following potential predi
ctors of HFnEF have been suggested by Meluzin et al.:
Exercise s < 10 cm/s with a sensitivity and specificity
of 83%
Exercise e < 10 with a sensitivity of 60% and specificity
of 87%
Exercise E/e > 9.5 cm/s with a sensitivity of 86% and
specificity of 83%
Rest E/e > 8 cm/s with a sensitivity of 83% and
specificity of 70%
Rest s < 8 cm/s with a sensitivity of 73% and specificity
of 72%
Assessment of Left Ventricular
Systolic Function
TDI s wave represents contraction of longitudinal
subendocardial fibers, which are most susceptible to any
disease process and ischemia. Hence, reduced s velocity
is the earliest sign of LV systolic dysfunction.
Because the LV apex is stationary, simple M-mode
measurement of mitral annulus excursion provides a
useful and sensitive measure of ventricular function,
which is rapidly affected by ischemia. The amplitude of
long-axis motion during systole also correlates well with
left ventricular ejection fraction (LVEF), which is also true
for the right ventricle.
Mitral and tricuspid annular systolic excursions have
been measured by M-mode echocardiography to assess
LV longitudinal function M-mode measurements of
the mitral or tricuspid annulus amplitude are more
laborious than measuring the peak systolic and
diastolic velocities by TDI, and the time course of this
movement is less readily obtained by M-mode.
Peak myocardial systolic velocity averaged from six
sites around the mitral annulus correlates well with
LVEF, and a cut-off of > 7.5 cm/s had a sensitivity of 79%
and a specificity of 88% in predicting normal global LV
function.
242 Section 4: Muscle Mechanics
Fig. 13.25: Medial edge mitral annular velocities in a 64-year-old
patient with asymptomatic severe mitral regurgitation. Note normal
diastolic velocities but lower S velocity suggestive of subclinical
systolic dysfunction. There is paradoxically increased E with
decreased S. This indicates that despite higher preload (increasing
E), left ventricular systolic function is depressed.
Similar data with color Doppler myocardial velocities
from four basal segments have defined a cut-off limit
of 5 cm/s for ejection fraction of 50%.
The peak systolic velocity is also a sensitive marker
of mildly impaired LV systolic function, even in those
with a normal LVEF or apparently preserved LV systolic
function, such as diastolic heart failure, or in diabetic
subjects without overt heart disease.
Reduced TDI velocities are present also in subjects
with HCM mutations at a time of subclinical disease
when cardiac hypertrophy is not present. Therefore,
TDI can be used for early identification of HCM.
In a group of asymptomatic patients with severe mitral
regurgitation but normal ejection fraction, Agricola
et al. showed that TDI of the lateral mitral annulus
systolic velocity could predict those who would develop
LVEF reduction after mitral valve surgery (Fig. 13.25).
Similar observations have been made in patients with
HF, post-transplant patients, etc.
Peak annular or basal systolic velocities are strong
predictors of outcome in several conditions. Wang et al.
followed a cohort of 518 subjects (353 with cardiac
disease and the rest normal) for 2 years after measuring
the average mitral annular velocities from four sites
(septal, lateral, anterior and inferior) from color-coded
TDI. Cardiac mortality was significantly higher when
both s and e were 3 cm/s [hazard ratios (HRs) 7.5
and 5.3, respectively].
Fig. 13.26: Tissue Doppler imaging of lateral edge of the mitral
annulus in a 42-year-old surgically proven case of constrictive
pericarditis. Note prominent e (> 26 cm/s) along with normal peak
systolic velocity (14 cm/s). Accentuated e is due to marked longi
tudinal expansion as transverse expansion is limited by the thick
pericardial shell.
There is a viewpoint that reduced s (< 8 cm/s) itself in
clinical syndrome of HF correctly characterizes cardiac
origin of dyspnea regardless of ejection fraction or E/e.
TDI in Constrictive Pericarditis and
Restrictive Cardiomyopathy
Constrictive pericarditis presents like a syndrome of
HF with essentially normal myocardial function except
in advanced state wherein, subepicardial fibers may
get involved. Pericardial constraint restricts transverse
motion of the heart, but longitudinal motion is preserved.
There is also some degree of RV dysfunction because of
compression. However, it is the study of the left ventricle
that gives clues about constriction in a patient with HF
with normal LVEF but elevated filling pressures. In these
patients, e is preserved or even accentuated even though
transmitral flow is restrictive (Fig. 13.26).
Therefore, E/e ratio is normal in constrictive
pericarditis while it is increased in other varieties of HF
syndrome. This phenomenon has been labeled annulus
paradoxus (Fig. 13.27). Several studies have reported that
mitral annular e 8 cm/s can differentiate constrictive
pericarditis from restrictive cardiomyopathy with a
sensitivity and specificity of > 90%. A recent study has
suggested an average of > 5.5 cm/s basal segment e
velocity to have 93% sensitivity in diagnosing constrictive
pericarditis. In some patients with constriction, regional
 Tissue Doppler Echocardiography: Current Status and Applications
Fig. 13.27: E/e of 6 in a 42-year-old patient with surgically proven
constrictive pericarditis. Normal E/e in a subject with clinical syndrome
of heart failure is called annulus paradoxus. Also respiratory variation
in transmitral flow is noted.
Fig. 13.29: Left and upper panel shows tissue velocities of the
medial mitral annulus, while the right lower panel shows the lateral
edge velocities, which are lower than at the medial edge (annulus
reversus).
mitral annular velocities may be decreased because of
concomitant myocardial disease, direct subepicardial and
midmyocardial scarring, compromise of coronary arterial
flow or pericardial calcification. It is, therefore, proposed
that tissue Doppler imaging from more than one wall of
the left ventricle would provide a more representative
global measure of longitudinal LV mechanics.
Idiopathic restrictive cardiomyopathy as a clinical
syndrome resembles constrictive pericarditis. However,
e is markedly reduced and annulus paradoxus is absent
(Fig. 13.28).
243
Fig. 13.28: A 62-year-old male with idiopathic restrictive cardio
myopathy and atrial fibrillation. Upper panel shows transmitral Doppler
flow, while the lower panel shows medial edge mitral annular veloci-
ties. Note markedly decreased e (first of the two negative waveforms)
and an E/e of 35. Prominent biphasic waveform during isovolumic
contraction shows a prominent negative component and a positive
component before s.
Another tissue Doppler phenomenon mentioned
in constrictive pericarditis is called annulus reversus.
Normally, septal edge mitral annular e is lower than
the lateral or free edge. In patients with constrictive
pericarditis, the lateral wall gets tethered to the thick
pericardium reducing its movements and hence e
recorded is lower on the lateral edge (Fig. 13.29).
Another tissue Doppler phenomenon observed in
constrictive pericarditis is multiple diastolic polyphasic
waveforms in the interventricular septum like diastolic
fluttering observed during gray-scale imaging (Fig. 13.30).
It has relatively high specificity for diagnosing constriction.
Significance of TDI in
Right Ventricular Function
It is difficult to estimate right ventricular function
because of its complex geometry. However, RV function
has prognostic significance in coronary artery disease,
pulmonary hypertension, congenital heart disease and in
postoperative cases.
The primary function of the RV free wall is to move the
atrioventricular valve ring toward the apex.
As compared with the evaluation of annular excursions,
the Doppler tissue imaging approach is quicker, simpler
and measurements can be made online within a very short
time interval.
Tricuspid annular velocities may be widely used
clinically because they can be obtained in nearly all
patients, and systolic velocities are independent of age.
244 Section 4: Muscle Mechanics
Fig. 13.30: Myocardial Doppler imaging of the interventricular
septum in short axis in a patient with constrictive pericarditis. Note three
positive waves during diastole. These can also be seen in radial
velocities of the posterior wall.
Fig. 13.32: Peak tricuspid annular systolic velocity of 7 cm/s in this
patient of operated tetralogy of Fallot indicates presence of right
ventricular dysfunction with an ejection fraction < 40%.
Tricuspid annular systolic velocities have found
excellent correlation with mean pulmonary pressure and
RV ejection fraction.
A cut-off value of peak tricuspid annular systolic
velocity of 11.9 cm/s differentiates those with RV ejection
fraction < 40% (Figs 13.31 to 13.33). Meluzin et al.
reported that tricuspid annular systolic velocity offers
obvious clinical benefit, enabling the prediction of RV
dysfunction with a good sensitivity of 90% and a specificity
Fig. 13.31: Pulsed wave tissue Doppler velocities from the free edge
of the tricuspid annulus in a normal 40-year-old subject. Note the peak
systolic velocity of 18 cm/s.
Fig. 13.33: A 66-year-old male with old inferior infarction and severe
right ventricular dysfunction as shown by peak systolic velocity of
5 cm/s and early diastolic velocity of 2 cm/s. Largest biphasic velocity
waveforms are during isovolumic contraction phase.
of 85% when a RV radionuclide ventriculographic ejection
fraction of 45% was taken as cut-off limit.
As there is hardly any circumferential arrangement
of fibers in the RV free wall, it is the s2 velocity that
represents systolic function during ejection (Fig. 13.32).
With onset of RV dysfunction, time-to-peak RV systolic
velocity increases and marked separation of two systolic
peaks can be a reasonable criterion of dysfunction but not
as good as RV s (Meluzin et al.) (Fig. 13.34).
 Tissue Doppler Echocardiography: Current Status and Applications 245

Fig. 13.34: Tricuspid annular tissue velocity profile in a 25-year-old Fig. 13.35: A 45-year-old farmer with unexplained left ventricular
female with hypoplastic right heart. Note separation of two systolic hypertrophy. s > 12 cm/s and e of 11 cm/s suggest that it is physio
waveforms with systolic velocities of 6 cm/s and prominent biphasic logical hypertrophy with normally functioning longitudinal subend
isovolumic relaxation waveform. ocardial fibers. The subject had global longitudinal strain of -30%.

Fig. 13.36: Left panel is parasternal long-axis view showing markedly thick left ventricular walls in a 26-year-old asymptomatic woman who had
closure of patent ductus arteriosus in early childhood. Medial mitral annular s is 8 cm/s and e is 6 cm/s suggesting pathological hypertrophy.

Physiological Versus Pathological

Left Ventricular Hypertrophy
Distinguishing physiological adaptive LV hypertrophy
(LVH) (Fig. 13.35) caused by exercise, as in athletes, from a
pathological process, as in HCM (Fig. 13.36), is important.
The key distinguishing feature of pathological versus
physiological LVH is the presence of diastolic dysfunction.
Long-axis systolic and early diastolic velocities are
decreased in patients with pathological hypertrophy but
preserved in athletes.
The best differentiation of pathological from
physiological hypertrophy is provided by a mean
systolic annular velocity < 9 cm/s (sensitivity 87%,
specificity 97%).
246 Section 4: Muscle Mechanics
Fig. 13.37: Conceptual tissue velocities in sarcomeric mutation-
associated subclinical hypertrophic cardiomyopathy (HCM). An E
13 cm/s has been shown to have > 90% sensitivity and specificity.
Mean early diastolic annular velocity < 9 cm/s has a
sensitivity of 73% but specificity of 97% (Fig. 13.37).
With increasing age, s and e velocities decrease and
A velocity increases. Hence, cut-off values for elderly
people will be different. Aging and athletics both can
cause LVH. No definite limits have been proposed for
older subjects.
TDI in Inherited Cardiomyopathies
Sarcomeric mutations are responsible for familial
cardiomyopathies that could be dilated, restrictive
or hypertrophic varieties. Metrics of systolic and/or
diastolic functions are reduced in carriers and subclinical
disease. Distinct cellular pathways are triggered early
in disease pathogenesis, based on how a mutation
fundamentally alters sarcomere function. These pathways
ultimately diverge to the development of HCM or dilated
cardiomyopathy (DCM). Tissue velocities, strain rates and
strain are reduced in cardiomyopathies and potentially
could be used for preclinical detection of several inherited
cardiomyopathies (Figs 13.34 and 13.35).
Systolic and diastolic velocities were significantly
reduced in transgenic rabbits with HCM.
Reduced systolic and diastolic velocities or reduced
early diastolic velocities only have been demonstrated
in patients with known mutations associated with
HCM without ventricular hypertrophy.
Mutation-positive carriers of DCM show reduced S
velocities with normal E velocities (Fig. 13.38). This is
Fig. 13.38: Conceptual tissue velocities in (DCM) sarcomeric mutation
-associated subclinical dilated cardiomyopathy. S is significantly
reduced but does not have enough predictive accuracy
Source: Lakadwala et al. 2012.
converse of what is seen in mutation-positive HCM
carriers.
Similarly, early diastolic strain rates are lower in HCM
than in athletes or normal control subjects, and they
are lower in restrictive than in normal or constrictive
cardiomyopathy.
Abnormal systolic and diastolic tissue velocities are
reported in subclinical Fabry disease patients without
ventricular hypertrophy. Systolic strain and strain rates
improve after enzyme-replacement therapy in Fabry
disease.
Tissue velocities and strain rates are reduced in
primary amyloidosis with and without evidence of
cardiac involvement.
Regional nonuniformity and paradoxical segmental
strain in SRI is another way of detecting subclinical
HCM (Fig. 13.39).
TDI in Detection of
Intraventricular Dyssynchrony
Electromechanical delay is caused by delay of electrical
propagation within the LV, resulting in mechanical
dyssynchrony. During propagation of the electrical
impulse in the LV, an area of functional electrical
conduction delay usually occurs in the anterior wall. This
results in a U-shaped endocardial activation pattern that
starts from the septum, curves around the apex and causes
delayed activation of the LV free wall. These patients will
have prolonged QRS duration, although this is not an
 Tissue Doppler Echocardiography: Current Status and Applications
Fig. 13.39: Curved anatomical M-mode of strain rate imaging in an
asymptomatic family member of a patient with hypertrophic cardio-
myopathy. Note paradoxically positive strain rate in midseptum due
to myofiber disarray coupled with negative strain rate in early diastole.
exclusive phenomenon. In heart failure (HF) subjects,
systolic dyssynchrony is potentially a marker for disease
severity and may act as a prognosticator. Therefore,
systolic dyssynchrony is now included as part of the HF
assessment by echocardiography.
Echocardiography is the most widely used tool to
assess mechanical dyssynchrony, and TDI has been found
to be the most useful among different echocardiographic
modalities. Although myocardial velocity curves can
be constructed either online from spectral pulse TDI
or offline from 2D color TDI, the latter approach is
preferable, because multiple segments can be compared
within the same heart beat (Fig. 13.40). To assess systolic
dyssynchrony, the time-to-peak or onset of systolic velocity
is measured from individual segments. In addition, other
parameters of systolic dyssynchrony, such as strain
dyssynchrony, can be derived from these raw data.
Several reports have examined the significance
of demonstrating mechanical dyssynchrony and
its possible use in predicting response to cardiac
resynchronization therapy (CRT).
Almost all of these studies used TDI-based criteria to
evaluate dyssynchrony and have generated a number
of potential dyssynchrony indices.
In general, these indices demonstrate either a time
delay in mechanical activation between segments
of the LV (septal to lateral wall delay in time-to-peak
systolic tissue velocity) or substantial dispersion of
mechanical activation (standard deviation of time-to-
peak systolic tissue velocity).
247
Fig. 13.40: Tissue synchronization imaging (a modification of TVI with
colorization of graded delay in peak contraction). Peak velocity of the
basal septum comes much earlier than that of lateral wall showing a
septolateral delay of about 120 milliseconds during ejection phase.
A number of small, mostly single-center studies have
suggested that a septal to lateral or opposing segment
delay of 65 milliseconds predicts response to CRT.
Similarly, a standard deviation of time-to-peak
tissue velocity 32 milliseconds of 12 basal and mid
segments appears to predict response. Response in
most studies was defined by clinical improvement and/
or presence of reverse remodeling as demonstrated by
echocardiography.
In these small, nonrandomized, nonblinded and
retrospective studies, the reported cut-off values
appear to be superior to QRS duration and several
other conventional echocardiographic parameters in
predicting response to CRT.
These findings suggest that echo-derived parameters
may be an efficient method of selecting patients for
CRT.
More recently, however, two recent large, multicenter,
prospective studiesPredictors of Response to CRT
(PROSPECT) and Resynchronization Therapy in
Narrow QRS Study (ReThinQ) used echocardiographic
criteria to select patients for CRT and found no
correlation between echo-based indices of mechanical
dyssynchrony and CRT benefit, raising questions about
the need for echocardiography in selecting patients
for CRT. The relative value of TDI versus strain/strain
rate in predicting response to resynchronization has
not been fully resolved. Although these studies are
limited by small numbers of patients, they provide no
248 Section 4: Muscle Mechanics
Fig. 13.41: Measuring septolateral activation delay by color-coded
Doppler imaging in a 70-year-old post-coronary artery bypass grafting
patient with QRS duration of 140 milliseconds. Lack of dyssynchrony
indicates that this patient is unlikely to improve with cardiac resynchro-
nization therapy.
convincing evidence supporting the hypothesis that
mechanical dyssynchrony predicts response to CRT.
Tissue velocity signals are generally more robust than
strain.
However, in either parameter, it is not unusual to move
the sample region minimally to find wide variations in
signal quality with significant differences in amplitude
and phase (timings), with obvious implications for its
clinical implementation.
With multiple lines of evidence to demonstrate
its superiority in analysis of dyssynchrony, tissue
velocity analysis can be used to select patients for CRT
especially if standard criteria for CRT are not met or
vice versa (Fig. 13.41).
Pulsed TDI traces may be challenging for timing
measurements, because they often do not yield
distinct peaks. Similarly, multiple systolic peaks in the
TDI signal are often difficult to adjudicate. Although
recommendations have been made that the earlier and
larger of the peaks is the true peak, this approach is not
totally immune to error, because moving the sample often
changes the amplitude and character of the peaks. The
angle of insonation does influence timing of TDI events
when angles exceed 20.
There is controversy with regard to value of TVI versus
strain imaging in detecting dyssynchrony. Yu et al. have
not found it useful while Miyazaki et al. have shown better
results with strain imaging. Time-to-peak strain was able
to differentiate patients with dyssynchrony better than
TDI in Miyazakis study. However, such data need further
validation having come from small sample size.
Possibly a multifactor dyssynchrony score will likely
emerge as the best predictor of response to CRT. This
score will incorporate clinical factors, QRS duration and
multiple imaging parameters. Imaging parameters may
not be restricted to intraventricular dyssynchrony alone
and may include flow Doppler and TDI measurements
of interventricular dyssynchrony. Such an approach will
likely reveal that the presence of myocardial dyssynchrony
is a weighted component in this score and possibly a
required substrate.
TDI in Coronary Artery Disease and
Stress Echocardiography
Detection of myocardial ischemia by visual assessment
of wall motion is fraught with variability and low
reproducibility. Wall motion can be quantified by TDI or
strain echocardiography, respectively.
Low systolic tissue velocities correlate with
angiographic or echocardiographic wall motion
abnormality. Tissue velocities decrease with reduced
regional perfusion, recover on reperfusion and
differentiate between transmural and nontransmural
infarction.
Global systolic and diastolic performance by TDI (in
terms of global s and E/e) are negatively correlated to
the number of vessels with significant stenoses.
Both regional and global s is significantly reduced in
patients with three-vessels disease.
Regional strain rates and strain are reduced in ischemia
and infarction. Strain and strain rate identify infarcted
segments and correlate with extent of transmural
infarction and extent of ischemia (Figs 13.42 and 13.43).
Strain and strain rate are less susceptible to cardiac
translational motion and tethering. The term tethering
is used to describe the dragging of an akinetic basal
segment toward the apex by normally functioning
mid or apical segments. This theoretical advantage of
strain/strain rate has been confirmed in the clinical
setting.
The stress response of TDI has been studied as an
adjunct to wall motion scoring for the prediction of
outcome in patients undergoing dobutamine stress
echo. Color TVI and tissue tracking are performed
in the basal and middle segments of the heart, the
apex being ignored because tissue velocity in that
 Tissue Doppler Echocardiography: Current Status and Applications 249

Fig. 13.42: Strain rate imaging in curved anatomical M-mode of the lateral wall at peak dobutamine dose during stress echocardiography. Note
reduction and positivity of strain rate in mid and basal segments at heart rate of 148 beats/min, indicating ischemia.

A B

Figs 13.43A to C: Two-chamber view (2CV)-tissue Doppler imaging

in a patient with acute anterior mycadial infarction (MI). Note markedly
decreased peak systolic velocity (A); strain (B); and strain rate (C); of
the mid-anterior wall along with delay in peaking of velocity and strain.
Of note is that corresponding inferior wall segment shows reduced
systolic velocity (2 cm/s, tethering effect) but nearly normal strain
and strain rate (cut-off for abnormal strain is -13% and for strain rate
C -0.9 sec-1).

area is close to 0 (Fig. 13.44). Peak velocities derived
from postprocessing of color images are averaged, to
account for the contractile response not only in the
area with abnormal wall motion but also the ability of
remote segments to compensate.
Typically, peak systolic velocities should increase
> 2 cm/s in normal segments on exercise or during
pharmacological stress. There should be increase or
no change in early diastolic velocities. A decrease in e
on stress is suggestive of ischemia. However, at faster
250 Section 4: Muscle Mechanics
Fig. 13.44: Response of basal septal segment to dobutamine stress. Peak velocity increases from 5 to 10 cm/s at heart rate of 144 beats/min,
indicating normal response.
heart rates, early and late tissue velocities tend to fuse
and make it difficult to assess e.
The average peak systolic velocity in patients with
events is significantly lower than in those without
events. Similarly, the average tissue displacement in
patients with events is significantly lower than in those
without events.
Post-systolic shortening evidenced either by TDI or
strain imaging has been considered a marker of viability
and ischemia when induced during stress. However,
when present in resting state, its exact significance has
not been clarified. Post-systolic strain and strain rate are
sensitive indicators of myopathic or ischemic process, but
specificity is modest.
PROGNOSTIC VALUE OF TDI IN
DIVERSE CARDIAC DISORDERS
Tissue Doppler imaging is evolving as a useful
echocardiographic tool for quantitative assessment of
LV systolic and diastolic function. Recent studies have
explored the prognostic role of TDI-derived parameters
in major cardiac diseases, such as HF, acute myocardial
infarction and hypertension. In these conditions,
myocardial mitral annular or basal segmental (s) systolic
and early diastolic (e) velocities have been shown to
predict mortality or cardiovascular events. In particular,
those with reduced s or e values of < 3 cm/s have a very
poor prognosis. In HF and after myocardial infarction,
noninvasive assessment of LV diastolic pressure by
transmitral to mitral annular early diastolic velocity ratio
(E/e) is a strong prognosticator, especially when it is
15. In addition, systolic intraventricular dyssynchrony
measured by segmental analysis of myocardial velocities
is another independent predictor of adverse clinical
outcome in heart failure subjects, even when the QRS
duration is normal. In HF patients who received CRT, the
presence of systolic dyssynchrony at baseline is associated
with favorable LV remodeling, which in turn predicts a
favorable long-term clinical outcome. Finally, TDI and
derived deformation parameters improve prognostic
assessment during dobutamine stress echocardiography.
A high mean systolic velocities value in the basal segments
of patients with suspected coronary artery disease is
associated with lower mortality rate or myocardial
infarction and is superior to the wall motion score.
Tissue velocities of the interatrial septum atrial free
wall and aorta are being studied in patients with aortic
disorders and in atrial fibrillation. Study of aorta might help
in understanding the physiology of aging, predilection for
aortic aneurysms and so on. Atrial wall strain and strain
 Tissue Doppler Echocardiography: Current Status and Applications
rate is being evaluated to detect who will maintain sinus
rhythm following cardioversion in atrial fibrillation.
LIMITATIONS OF TDI
A significant limitation of tissue Doppler imaging is
marked angle dependency, more so than for other
Doppler modalities. This is due to the fundamental
difference between measurement of fluid velocities,
where particles move freely, and tissue velocities in
solid structures, where deformation in one direction
is always associated with deformations in other
directions to keep the mass of the structure constant.
Other technical limitations include signal noise,
signal drifting, spatial resolution, sample volume and
tethering artifacts.
Mitral annular velocities also can be reduced
erroneously by mitral annular calcification, surgical
rings or prosthetic valves.
Regional myocardial tissue velocities represent the net
effect of the contractile and elastic properties of the
area under investigation and traction and tethering
effects from other regions. Therefore, these do not
necessarily represent intrinsic regional myocardial
function.
Because of cardiac motion and the lack of fixed
reference points in the myocardium, it is not possible
to maintain identical sampling points throughout the
cardiac cycle. In this regard, the Doppler method is
inferior to magnetic resonance tissue tagging.
Strain rate signal derived by tissue Doppler has
significant noise. This is mainly a result of random
noise in the velocity signal, and this noise is magnified
when differences are measured instead of absolute
velocities.
SUMMARY
Tissue velocity imaging has revolutionized the concept
of parametric imaging in echocardiography. It offers the
promise of an objective measure to quantify regional
and global cardiac function through the assessment
of myocardial velocity data. Besides definite clinical
utility, there has been a phenomenal increase in our
understanding of heart muscle mechanics, physical
principles that it obeys and the complex geometric
changes that accompany the heart motion.
In daily practice, tissue Doppler echocardiography
(TDI or TVI) is used to estimate LV filling pressures,
categorize diastolic dysfunction, identify patients with
251
HFnEF, differentiate constrictive pericarditis from
restrictive cardiomyopathy, to prognosticate acute
coronary syndrome, valvular heart disease, syndrome of
HF, correlate exercise capacity and symptoms, differentiate
physiological versus pathological hypertrophy, assess
intraventricular dyssynchrony, regional and global
systolic and diastolic properties, estimate of RV function
and identify possible carriers of genetic cardiomyopathies
like Fabry disease and HCM. Its role in adding incremental
value to stress echocardiography, subclinical dysfunction
evaluation, cardiac transplant rejection, cardiotoxicity of
anticancer drugs, predicting occurrence and reversion of
atrial fibrillation, predicting aortic catastrophies, and so
on, although very encouraging, has not found many users.
It was intuitively considered invaluable in detecting subc
linical myocarditis, acute rheumatic fever, Chagas disease
and localization of atrioventricular accessory pathways
with manifest conduction, but could not find prime time
readiness. In a similar manner, tissue-velocityderived
deformation parameters have not found prime time use
despite making great inroads into the mysteries of muscle
mechanics. Part of the problem lies in their emphasis
on unidirectional information of a structure, which is
essentially multidimensional. The other problems have
been angle-dependency and low signal-to-noise ratio in
deformation imaging, which has restricted its use to highly
experienced operators rather than more democratic
use. Validation studies did indicate its great potential.
TDI-derived imaging paved the way for non-Doppler
multidimensional deformation imaging, which is slowing
gaining ground.
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256 Section 4: Muscle Mechanics
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 Chapter
14
Deformation Imaging:
Theory and Practice
Introduction
Objective quantification of the heart muscle segmental
function is needed in clinical and preclinical arena.
Heart muscle is arranged as a syncytium with viscoelastic
character and changes its size and shape with every phase
of cardiac cycle. It is incompressible and has a definite
architecture. It is an almost synchronous generator of
bidirectional force for suction and ejection. Cohesive
and sequential integration of motion and deformation
optimizes filling and ejection, the two of its fundamental
functions. To some extent, it follows the laws governing
material deformation. The deformation parameters can
be assessed by echocardiography and can be applied
to clinical conditions to get information, which is
otherwise not available from images and intracardiac
flow. Myocardial deformation is the complex resultant
of intrinsic contractile forces and extrinsic loading
forces applied to tissue with varying elastic properties.
Deformation parameters provide incremental and unique
information of the heart muscle. There is a progressively
greater use of these data in clinical practice, although a lot
still needs to be learned. Detection of subclinical systolic
and/or diastolic dysfunction has significant use in clinical
medicine. The areas in which deformation imaging is finding
utility include heart failure, systolic and diastolic function,
stress echocardiography, myocardial fibrosis, viability,
ischemia, intraventricular dyssynchrony, monitoring
cardiotoxic drug therapy, heart transplant rejection, and
so on. The understanding of architecture (form) and its
deformation (function) provides important insights into
pathogenesis, therapy and prognosis. Its superiority over
tissue Doppler imaging (TDI) lies in providing functional
information in multidimensional format without angle-
dependency. Although not yet sufficiently proven for
routine clinical use, two-dimensional/three-dimensional
(2D/3D) strain methods offer the long-term potential for
more complete, accurate and reproducible assessment of
myocardial function.
MYOCARDIAL DEFORMATION
Sarcomere is the fundamental unit of contraction in
the heart muscle. Each sarcomere is attached to at least
15 other sarcomeres. Following electromechanical
activation, the myocardium deforms during systole due to
sarcomere shortening.1 Sarcomeric unidirectional short
ening results in multidirectional change in size and shape
of the tissue and this is called myocardial deformation
(Fig. 14.1).
With the onset of systole, there is sarcomere shortening
resulting in reduction of intracavitary size and
myocardium deformation2 (Fig. 14.2).
Since the myocardial tissue is almost incompressible,
the volume of ventricular wall and the myocardial
mass remain constant in every phase of cardiac cycle.
The deformation occurs in three dimensions that
are expressed along three ventricular coordinates:
a longitudinal and circumferential shortening and
a radial thickening (Figs 14.3 to 14.6) (Table 14.1).
258 Section 4: Muscle Mechanics
Fig. 14.1: Diagram showing a sarcomere, which is a unit of
contraction.
Fig. 14.3: Depiction of three co-ordinates of deformation. Deformation
in three different planes occurring simultaneously are X-Xo/X, Y-Yo/Y
and Z-ZO/Z.
The ventricular myocardium simultaneously shortens
in the longitudinal and circumferential planes
and thickens in the radial plane, with reciprocal
changes in diastole.
The fourth form of deformation is rotation, which is
the angular motion at two ends of the ventricle and the
difference between the two, is twist or torsion. Rotation
or torsion are indicators of shear strain (Figs 14.7A
and B).
The deformation is calculated based on the relative
change of the length of myocardial fibers during
cardiac cycle3,4 and is expressed in a unidimensional
parameter termed strain () (Figs 14.8A and B).
Fig. 14.2: Graphical description of deformation (strain). Strain is
spatial derivation of displacement.
Fig. 14.4: Graphic diagram showing a single myofiber and its length
during diastole (L) and at end-systole (L0). Percentage longitudinal
shortening is strain and rate of shortening is strain rate.
The local end-systolic strain value reflects the regional
ejection fraction (EF) and the global left ventricle (LV)
end-systolic strain reflects the overall systolic function3
(Fig. 14.9).
The cardiac deformation can also be represented
graphically with high temporal resolution when
obtained by Doppler method (Fig. 14.10). S-wave
represents the negative deflection occurring during
systole with the peak negative deflection representing
maximal longitudinal myocardial shortening
(or peak systolic strain). With the start of diastole,
the myocardial fibers start regaining their original
length. Graphically, it is represented in three phases:

Fig. 14.5: Graphical description of myofiber width (short-axis
diameter) during diastole (R) and during end-systole (R0). Radial strain
is the percentage increase in width.
Table 14.1: Vectors of cardiac movement
Longitudinal shortening (compression strain) and lengthening
(tensile strain)
Transverse or radial thickening and thinning
Circumferential shortening and lengthening
Rotation (twist and untwist)
(1) the early, or rapid filling phase (E-wave) followed
by (2) a plateau phase, or diastasis and finally (3) atrial
filling (A-wave).
The speed at which the myocardial deformation
occurs is the strain rate (SR) and is expressed as unit/s.
SR depicts the change in strain over a period of
time3-4 (Fig. 14.10).
Two-dimensional strain imaging requires high
quality gray-scale images5 with frame rate exceeding
50 frames/s (usually 50100 frames/s). Doppler-
derived deformation has much greater temporal
resolution because of imaging at about 200 frames/s.6
To obviate through plane motion, 3D strain estimation
has been developed for which the minimum frame rate
is 25 frames/s.7 Multibeat acquisition is the preferred
way to achieve these frame rates.
Deformation parameters can be estimated by multiple
methods (Table 14.2). But fundamental knowledge is
method-independent.
Deformation during active contraction is an interaction
between contractility (developed force) and the load.
Deformation is not a measure of pure contractility.8
Active contraction occurs only during very early part of
systole, but deformation keeps occurring throughout
systole and a little beyond.3
Deformation Imaging: Theory and Practice 259
Fig. 14.6: Simultaneous graphical depiction of three vectors of the
heart muscle motion.
(R: Radial; C: Circumferential; L: Longitudinal).
Table 14.2: Methods for the study of deformation
Doppler-derived deformation imaging
Echocardiographic acoustic speckle tracking two-dimensional
strain (including velocity vector imaging)
Echocardiographic acoustic speckle tracking three-dimensional
strain
Sonomicrometry
Tagged magnetic resonance imaging
The strain and SR subtracts motion due to the effects of
neighboring segments.
Strain and its rate values are deformation per length
and do not need to be corrected for heart size.9
Deformation parameters depict volume changes of
the pressurevolume loop and hence do not provide
complete information about the cardiac function.
Strain in three dimensions is interrelated, so strain in
one direction is representative of regional deformation
in more than one direction.10
Two basic facts to be remembered are: apex is stationary
and the outer boundary of the heart is unchangeable
(constant). Action is at the base and within the walls
and the boundary is invariate (the heart has constant
volume and outer boundary (Fig. 14.11).
Isometric function can not be defined by deformation
parameters. However, isometric strain wave-forms
have clinical applications.
Peak velocity and SR are early-systolic measures, and
more closely related to contractility (dP/dt) during
active contraction, while displacement and strain
260 Section 4: Muscle Mechanics

A B
Figs 14.7A and B: Myocardial twist. During systole, base rotates clockwise, while the apex rotates counterclockwise when viewed from the
apex.

A B
Figs 14.8A and B: Arrangement of myocardial fibers in systole (A) and in diastole (B). The muscle fibers descend longitudinally from the base in
the subendocardium and make a figure of 8 near the apex before starting the ascent subepicardially (helical configuration).

Fig. 14.9: Longitudinal strain of the basal and midanterior interventricular septum by speckle tracking method (two-dimensional strain) in a
subject with anterior myocardial infarction. There is hardly any strain during systole, but there is post-systolic strain (shortening).

Fig. 14.10: Strain rate over a fixed segment derived from tissue
Doppler method. Lower panel shows various waveforms at a frame
rate of approximately 200/s.
Fig. 14.12: Diagram showing peaks of strain rate and longitudinal
strain with regard to aortic valve closure (AVC). Note early peaking
of strain rate.
are end-systolic measures related to the total stroke
volume and EF.
Normal myocardium shows the highest SR in the first
third of the ejection period, whereas the maximal
deformation mostly occurs at aortic valve closure
(AVC) (Fig. 14.12).
DESCRIPTIVE TERMS
Deformation: It is the change in the metric properties
of a continuous body. If after a displacement of the
continuum, there is a relative displacement between
particles, a deformation has occurred.
Deformation Imaging: Theory and Practice 261
Fig. 14.11: Depiction of the cavity without walls in diastole and
systole. It is the cavity that gets smaller in systole without any change
in outer contour (not shown). As the outer contour is constant, longitu-
dinal shortening is coupled with radial thickening and circumferential
shortening.
Elasticity: It describes materials that return to their
resting shape after the force is removed.
Viscoelastic: A viscoclastic material can be simply
modeled as an elastic component coupled with a
viscous component, which acts as a damper that
delays the stress-strain response (time-dependent
stress-strain relationship). The healthy myocardium
has viscoelasticity (hysteresis on contraction and
relaxation).
Strain: Strain is a normalized measure of deformation
representing the displacement between particles
in the body relative to a reference length. Strain is
dimensionless and is usually expressed as a decimal
fraction, a percentage or in parts per notation. Strain
measures how much a given deformation differs locally
from a rigid body deformation. Thus, strain is a tensor
quantity (Fig. 14.2).
Meaning of strain: Tissue strain is a surrogate for tissue
stiffness. Low tissue strain corresponds to high tissue
stiffness and vice versa. Tissue stiffness corresponds to
ischemia, fibrosis, muscle fiber disarray, infiltration,
and so on.
Components of strain: The amount of stretch or
compression along line elements or fibers is the
normal strain, and the amount of distortion associated
with the sliding of plane layers over each other is
the shear strain (Fig. 14.13), within a deforming
body (Table 14.3). Area Strain is the combined
262 Section 4: Muscle Mechanics

Table 14.3: Types of strain Table 14.4: Normal values of various left ventricular peak systolic
Normal Strain Shear Strain strains and strain rates

a. Longitudinal a. Longitudinalcircumferential Longitudinal strain -15% to -25%

b. Radial b Longitudinalradial Longitudinal strain rate 1.01.4 s-1

c. Circumferential c. Circumferentialradial Radial strain 5070%

d Radialcircumferential Radial strain rate 3.14.1 s-1

e Radiallongitudinal Circumferential strain 1530%

f. Circumferentiallongitudinal Area strain -30% to -50%

Fig. 14.13: Diagram showing complex motion of a natural acoustic Fig. 14.14: Circumferentialradial shear strain at the apex. Note that
reflector in different planes during a single cardiac cycle. Length and this shear strain is greater at the subepicardial region compared to
direction of the arrow denotes the quantum of displacement. It is subendocardial region leading to apical counterclockwise rotation.
tracked by sum-of-absolute differences algorithm. Right panel: angle represents the shear strain.

longitudinalcircumferential normal strain in a given
area and measured by 3D imaging.
Acoustic Speckle Tracking
Intramural displacement of a natural tissue reflector
(speckle or a group of 3040 pixels called kernel) located
in an area of interest on a gray-scale image is measured
using a phase-sensitive correlation-based speckle tracking
approach (Figs 14.14 to 14.16). It is also called 2D strain
imaging. Essentially, it is automatic tracking of interference
patterns from conventional gray-scale B-mode images
during the cardiac cycle.11
Longitudinal Strain
Typical global longitudinal strain of the LV is -15% to
-25% (Table 14.4). This is based upon the assumption
that normal mitral annulus systolic excursion is
1120 mm and the normal length of the base-to-apex
LV is 89.5 cm.
Longitudinal strain increases from base to apex in
proportion to the wall stress (Figs 14.16 and 14.17).
However, this is not a consistent or universally resolved
fact.
Abnormality of the longitudinal strain is the earliest
sign of myocardial disease including ischemia.12
Differences in wall stress due to differing wall curvatures
between longitudinal, radial and circumferential axes
(by Laplace Law) may possibly explain the more freq
uently observed abnormal systolic longitudinal strain.
The high sensitivity of longitudinal strain to detect
functional impairment due to subtle ischemia or early
dysfunction could be also explained by the predominant
longitudinal orientation of subendocardial fibers,
which are more susceptible to ischemia.
Longitudinal strain decreases with age, with increasing
wall thickness and obesity.13 Strain is relatively
independent of maturational changes, lending it as
a tool for cardiac evaluation across differing ages in
pediatric subjects.

Fig. 14.15: Longitudinal strain estimation in apical four-chamber view
by acoustic speckle tracking in a normal control. Longitudinal strain of
the speckles within the region of interest (outlined) is depicted as an
average of six segments (-30%).
Speckle-derived strain values are lower than those
derived by the Doppler method, because the latter has
higher temporal resolution. It is also possible because
there is greater noise in tissue Doppler method near
the peak values.
In early stage of disease, radial function acts as a
compensatory phenomenon to the decrease in longi
tudinal deformation to maintain a normal LVEF.
Therefore, reduced global longitudinal strain with
normal EF is a subtle sign of dysfunction.
Different tracking algorithms potentially produce
different results. Inter-vendor differences could be
significant.1417 This is the major limitation for prime
time use.
Orthogonal Strain
Circumferential and radial strains represent orthogonal
strains of the myocardium and are obtained from short-
axis images (Fig. 14.18). These are affected late in a
disease process when the latter becomes transmural.
Three principal strains are interrelated and convey similar
information about volume deformation.18
Circumferential Strain
Circumferential strain does not reflect circumferential
fiber contraction. There would be circumferential
shortening even without circumferential fibers.
Circumferential strain is mainly the inward movement
of midwall circumference as the wall thickens
(Fig. 14.19).
Deformation Imaging: Theory and Practice 263
Fig. 14.16: Two-dimensional longitudinal strain in a modified apical
long axis. Note base-to-apex gradient of the anterior septum (-18, -31,
-41) and the posterior wall (-21, -25, -37).
The regional circumferential strain may be affected in
different ways, depending on the degree of transmural
involvement. Subendocardial infarct affects the
midwall circumferential fibers to a very small extent,
if any, with little or no effect on circumferential force.
Endocardial circumferential shortening is greater than
midwall circumferential shortening, which is greater
than epicardial circumferential shortening. Mean
circumferential strain must be taken to mean midwall
circumferential shortening.
Circumferential function plays a pivotal role in
maintaining LV structure and tensile strength.
Subepicardial organization of collagen structure seems
to differ from that in the midwall and subendocardial
regions accounting for the transmural strain gradients.
Circumferentiallongitudinal shear, also known as
torsion, has been shown to depend strongly on the
transmural variation of the helix angle.
In patients with early systolic dysfunction or heart
failure with normal EF, longitudinal strain is reduced,
while circumferential strain remains normal or gets
enhanced.
Radial Strain (Transmural Strain)
Radial strain means wall thickening, but there are
no myocardial fibers going in the radial direction
(Fig. 14.20). Wall thickening is a function of wall shortening
to maintain normal muscle volume, as the heart muscle is
incompressible. Increased radial function (meaning wall
thickening) as compensation for decreased longitudinal
264 Section 4: Muscle Mechanics

Fig. 14.17: Right ventricular longitudinal strain by acoustic speckle tracking within the region of interest in apical four-chamber view in a normal
person. Note that the right ventricle free wall has greater longitudinal strain compared to the interventricular septum.

function actually does not exist, it seems to be a theoretical

impossibility.
Clinically, radial strain (time-to-peak strain) has been
used to detect intraventricular dyssynchrony19 (Fig. 14.21).

Velocity Vector Imaging

Velocity vector imaging (VVI) is an echocardiographic
method that is based on speckle tracking.17 In gray-scale
images, interference by backscattered ultrasound from
neighboring structures results in a random, speckled
pattern. This gives each small area a unique pattern that
remains relatively constant from one frame to the next.
With the optimized pattern-matching algorithm, VVI can
accurately track these speckles frame by frame, and by
Fig. 14.18: Vectors of orthogonal strains in short-axis direction.
reconstructing the deformation and motion, the motion of
 Deformation Imaging: Theory and Practice 265

Fig. 14.19: Short-axis view is used to extract circumferential strain, which like longitudinal strain is normally negative and nearly of the same
value. Fixed reference point is kept in the center of the cavity from where relative shortening and lengthening in circumferential axis are
measured.

Fig. 14.20: Short axis at various levels is used to extract radial strain, which normally is a positive quantity in systole (thickening) with reference
point at the center of the cavity.
266 Section 4: Muscle Mechanics
Fig. 14.21: Left panel shows radial strain waveforms in a patient with heart failure but no intraventricular dyssynchrony. Right panel shows
marked dispersion in time-to-peak radial strain indicating presence of intraventricular dyssynchrony. An anteroposterior segmental peak radial
strain delay 130 milliseconds is suggestive of significant intraventricular dyssynchrony.19
Fig. 14.22: Longitudinal strain estimation in four-chamber view by
velocity vector imaging. In early systole, different velocity vectors are
depicted.
flow and tissue can be analyzed. VVI is more precise, self-
updating, faster and gives simultaneous information about
regional and global EF. The algorithm works as follows:
For each pixel in the image, angle-independent
velocity estimation is performed by selecting a search
pattern around that pixel in one frame and looking for
a matching pattern in a search region around that pixel
of the following frame.
The search pattern is placed at different positions in
the search region, and the similarity is measured for
the overlapping area.
The position where the highest similarity is found
determines the in-plane frame-to-frame displacement
relative to its initial position.
A fine grid is automatically positioned within the
selected region of interest (ROI) with an intergrid point
distance of variable size (Fig. 14.22).
For each frame, the position of each grid point is
updated on the basis of the underlying velocity vector.
The deformation of the grid follows the deformation of
the underlying myocardium.
Drifting is compensated for by forcing all grid points to
return to their initial positions at the end of the heart
cycle (Fig. 14.23).
Various strains can be estimated from the distance
changes between grid points as a function of time9,13,20
(Fig. 14.24).
Layer-specific strains can be obtained by placing grids
in the subendocardium, midwall and subepicardial
region. However, this is an area of research with no
clear clinical application.
HOW TO PERFORM TWO-DIMENSIONAL
STRAIN IMAGING?
Two-dimensional images of apical four- and two-
chamber views, as well as the apical long-axis view and
the LV parasternal short-axis view (at base, mid and
apex) are recorded.

Fig. 14.23: Velocity vectors shown at end-diastole in apical four-
chamber view.
Fig. 14.25: Point-and-click method to extract longitudinal strain curves in apical views. Marking three points on the endocardium (left panel)
generates the region of interest (ROI), which can be manually adjusted and strain values can be derived after accepting the ROI.
Three consecutive cardiac cycle loops are recorded at
end expiration.
Images are recorded with an acoustic method that
provides information frame by frame. The frame rate is
kept between 50 frames and 100 frames/s. By reducing
imaging depth and insonation angle without reducing
spatial resolution, frame rate can be optimized.
The imaging sector is optimized to complete
visualization of the structure under consideration.
The 17-segment LV model of the American Society of
Echocardiography is used to analyze regional cardiac
function.21
The long-axis ventricular walls are divided into three
levels: base, middle and apical.
Deformation Imaging: Theory and Practice 267
Fig. 14.24: Velocity vectors seen in short axis of the left ventricle
showing circumferential strain. Velocity vectors also suggest possi
bility of clockwise rotation.
Using a point-click approach, a number of points are
placed along the endocardium or the middle layer
of myocardium. The software automatically traces
epicardium.
The number of points is decided depending on the
radian of the endocardium.
In apical views, three points are placedmedial edge
of the mitral annulus, lateral edge of the mitral annulus
and the apical endocardium (Fig. 14.25).
The correct tracking of border zones is visually
controlled and manually corrected.
Peak positive or peak negative strain is extracted from
each strain curve. Strain curves and numbers are
obtained by off-line analysis.
268 Section 4: Muscle Mechanics
Fig. 14.26: Three-dimensional strain by acoustic speckle tracking. Bulls eye map is marked X in boxes for mid and basal posterior segments
because of unacceptable image quality.
In the VVI analysis, a relatively static reference point is
placed at the apical location in the long-axis view and
at the center of the ventricle in the short-axis view.
Segments for which no adequate image quality can
be obtained are rejected by the software and excluded
from the analysis (Fig. 14.26).
The ROI is defined by tracing the endocardium in a still
frame (default at end systole).
The ROI width is set to match the myocardial thickness.
This has to be performed manually most often.
Bulls eye map depiction is possible for all types of
strain, time-to-peak strain and extracted post-systolic
strain (Figs 14.27 and 14.28).
Three-dimensional strain is less time-consuming and
provides global longitudinal, radial, circumferential
and area strain from a single pyramidal volume by just
tracking the endocardium in systole and diastole.22
It is crucial that the tracking algorithm is able to track
the tissue correctly. Factors that affect the tracking
accuracy include image quality, frame rate and line
density.22
EFFECTS OF ISCHEMIA ON REGIONAL
DEFORMATION METRICS
Acute ischemia induces systolic thinning, decreases
systolic deformation and increases post-systolic
thickening (PST). These changes are directly related to
perfusion.23
With acute total vessel occlusion, systolic deformation
is totally ablated and replaced by systolic lengthening
(paradoxical strain).
An acute increase in afterload exaggerates the effects
on deformation induced by ischemia, whereas an
increase in preload diminishes it.24
Reperfusion restores deformation to near-normal,
but some early systolic lengthening and PST remain
present in the early phase as a result of stunning.

Fig. 14.27: Bulls eye map showing longitudinal strain in 17-segment model in a normal subject.
Fig. 14.28: Bulls eye map of longitudinal strain in a patient with
hypertrophic cardiomyopathy and resting intraventricular gradient of
64 mm Hg. Note significantly decreased strain in anterior septum and
anterior wall.
Deformation Imaging: Theory and Practice 269
Late systolic thinning can also occur during ischemia
just before the start of PST.25
Strain shows a biphasic response to physiological
stress and decreases at peak stress due to lower stroke
volume as a consequence of higher heart rates.3,26
EARLY SYSTOLIC LONGITUDINAL
LENGTHENING (PARADOXICAL
LONGITUDINAL SYSTOLIC STRAIN)
During isovolumic contraction, there may be a brief systolic
lengthening due to contraction of basal circumferential
fibers and this is a normal phenomenon (Fig. 14.29).
During the isovolumic contraction phase, segments
with reduced rate of force development might demonstrate
significant and prolonged systolic lengthening (Fig. 14.30).
This is possible because of reversible dysfunction
as in ischemia, late activation of the segment due to
270 Section 4: Muscle Mechanics
Fig. 14.29: Two-dimensional longitudinal strain of the right ventricle. Note waves (arrow) of longitudinal positive strain for a brief period.
conduction block or segmental fibrosis resisting the
development of force.
Duration of early systolic lengthening may provide
incremental value over peak systolic longitudinal
strain for the identification of patients with significant
systolic dysfunction.27
Duration of early systolic lengthening has been shown
to be a strong and independent predictor of significant
coronery artery disease (CAD).
POST-SYSTOLIC LONGITUDINAL
SHORTENING
Post-systolic shortening (PSS) means that the segment
continues shortening after the AVC, often after a short
relaxation giving one or two peaks a systolic and a
post-systolic, or a single peak after AVC as shown in
Figure 14.31.
The definition of shortening as post-systolic is depen
dent on the location of AVC, which can be done by TDI.
A small amount of PSS may be present in up to
one-third of normal segments but not more than 3%.
Pathological strain is concomitant with reduced systolic
strain and higher post-systolic strain (in magnitude) as
well as later peak PSS.
PSS and post-systolic thickening are to some degree
equivalent, due to the incompressibility.
Presence of PSS is mainly a measure of inhomogeneity
of force development, due to differences in activation,
load or contractility, and not as specific marker of
ischemia.
 Deformation Imaging: Theory and Practice 271

Fig. 14.30: Two-dimensional longitudinal strain in a patient with idiopathic dilated cardiomyopathy in apical four-chamber view. Arrow points to
paradoxical positive strain for nearly half of systole in all the segments.

Fig. 14.31: Left panel shows longitudinal strain from apicoseptal segment and the right panel from the basal and midlateral wall. Note markedly
reduced end-systolic strain and significant post-systolic strain in the right panel. The patient had critical stenosis of the left circumflex artery.
272 Section 4: Muscle Mechanics
The new concept of mechanical dispersion, meaning
unequal duration of the shortening phase, seems to be
due to variable amount of PSS within the ventricle.
Presence of PSS may give asynchrony between walls.
Presence of PSS in a segment leads to a delay in the
onset of segmental lengthening compared to the
normal segments, so the finding is equivalent to the
delayed compression/expansion crossover.
PSS is mainly the reduced, but prolonged contraction
of a segment due to ischemia and/or relative load
increase in the early diastolic interaction with normally
relaxing segments.
Stretch recoil is a mechanism for PSS, especially
in segments that do not show systolic shortening.
Therefore, PSS is not always suggestive of viability or
ischemia.
The degree of this thickening is expressed as the
post-systolic index (i.e. post-systolic increment divided
by systolic strain).
Fig. 14.32: Holosystolic longitudinal stretch with post-systolic shortening in apical four-chamber view in a child with dilated cardiomyopathy.
Post-systolic motion is reported in > 30% of myocardial
segments in normal subjects, but can be identified
as pathological if there is a concomitant reduction
of systolic strain, especially if the PST is marked
(e.g. index > 2535%).
PST or PSS presence actually implies that tissue
elasticity is preserved, which means that no important,
irreversible fibrosis is present.
PST can also occur in normal myocardium, especially
with increased afterload (aortic stenosis, hypertension),
myocardial storage diseases and abnormal activation.28
PARADOXICAL STRAIN PATTERNS
Holosystolic stretching in longitudinal or circumferential
plane is an extension of the early systolic lengthening
found in diseased states, especially in scarred tissue,
dilated cardiomyopathy (indicative of dyssynchrony
(Fig. 14.32) and in left bundle branch block (septal
holosystolic stretch).

RIGHT VENTRICULAR DEFORMATION
The right ventricle (RV) has complex geometry with
mainly longitudinal/circumferential fiber orientation in
the free wall and minimal radial function due to thin walls.
Longitudinal deformation of the RV free wall provides
assessment of systolic function (Figs 14.33 to 14.35), which
does correlate with RVEF as well as strain estimate by
sonomicrometry.29
Apical views are used to obtain RV free wall longitudinal
strain.
RV free wall longitudinal strain is 510% more than the
LV free wall.
A base-to-apex gradient is also seen but is not a
consistent finding.
RV free wall deformation assessment is feasible in
> 90% cases.
There is a reasonably good correlation with tissue
Dopplerderived strain.
Fig. 14.33: Right ventricle free wall longitudinal strain in a patient with type I pulmonary hypertension. Note markedly decreased end-systolic
strain (-5%) and 50% post-systolic strain.
Deformation Imaging: Theory and Practice 273
Global RV strain, however, has modest correlation with
EF.
Significant utility of RV free wall strain lies in assess
ment of ambiguous conditions like arrhythmogenic
dysplasia, noncompaction, pulmonary embolism,
Friedrichs ataxia, and so on.30
LEFT ATRIAL FUNCTION
BY DEFORMATION IMAGING
Deformation imaging is a good method for assessing
reservoir function of the left atrium.31 The reservoir
function (lengthening or increase in volume during
ventricular systole) is coupled with longitudinal function
of the LV (Figs 14.36 and 14.37). Reduced left atrial
diastolic longitudinal strain is an indicator of left atrial
dysfunction. However, many conditions are associated
with predo minant left atrial dysfunction with some
decrease in LV longitudinal function.
274 Section 4: Muscle Mechanics

Fig. 14.34: Right ventricle free wall longitudinal strain in a case of suspected pulmonary embolism. Note early systolic positive strain (systolic
stretching) with markedly reduced end-systolic (-4%) strain and also post-systolic strain.

It may provide incremental information about
subclinical atrial pathology like likelihood of developing
atrial fibrillation, left atrial thrombus, paroxysmal atrial
fibrillation recurrence after ablation, and so on. It is still
an investigational tool but with great promise (Fig. 14.37).
Marked decrease in reservoir function (either with
reduced strain or paradoxical shortening) is commonly
found in patients with heart failure with or without systolic
dysfunction and is an indicator of left atrial dysfunction.
aorta are not well understood. Deformation imaging of
the aorta aids in understanding the mechanical properties
of aorta and may be a great tool in future (Fig. 14.38).
The aortic circumferential strain can be measured with
2D strain echocardiography and is a new tool that can be
used to directly and easily evaluate aortic stiffness.
Normative age-specific data are yet to be reported in
adequate numbers. Also, through-plane motion remains a
major handicap as of now.

MECHANICAL PROPERTIES OF THREE-DIMENSIONAL/FOUR-

THE AORTA
Understanding the mechanical behavior of the arterial
wall and its spatial variations is essential for the study
of vascular physiopathology. Although it is generally
accepted that the aortic wall gets stiffer along its length,
the spatial variations in the mechanical behavior of the
DIMENSIONAL DEFORMATION IMAGING
Three-dimensional/four-dimensional (4D) strain is a
postprocessing research tool that tracks inherent features
in a 3D image called natural acoustic markers from
frame to frame in three dimensions over time (Fig. 14.39).
Three-dimensional strain uses a tracking algorithm based
 Deformation Imaging: Theory and Practice 275

Fig. 14.35: Comparison of tissue Dopplerderived strain at basal right ventricle free wall (-6%) and the basal septum (-36%) in the same patient
as in Figure 14.34. Increased basal septal strain may be a compensatory phenomenon.

on frame-to-frame block matching performed in three

dimensions. This involves successively searching for a
match between 3D patterns found in one 3D frame and in
the next. The 3D strain ROI is automatically generated in the
end-systolic frame and is built up from an endocardial and
an epicardial mesh. The epicardial mesh is automatically
generated from the epicardial mesh used in the LV mass
stage. A 4D mapping (three spatial dimensions + time)
of myocardial SR would help to describe the mechanical
properties of the myocardium.
Three-dimensional strain performs tracking over time
in three dimensions, which also means there is no
out-of-plane motion issue.
It is less time-consuming as it provides global
Fig. 14.36: Mid-septal left atrial longitudinal strain. Upper panel is a deformation in a quick fashion.
normal subject with a strain value of +42% (typically twice of left ven-
This method exclusively provides the area strain, which
tricle longitudinal strain). Middle panel shows a left atrial strain (+33%)
of a patient with diastolic dysfunction with normal ejection fraction and is a combination of longitudinal and circumferential
lower panel shows left atrial strain (+3%) in a patient with diastolic strain. Area strain is superior to any single strain in
heart failure with atrial fibrillation. detecting myocardial function.
276 Section 4: Muscle Mechanics
Fig. 14.37: Left atrial longitudinal strain during ventricular systole (left panel) and the left ventricular longitudinal strain in four-chamber view in a
patient with heart failure and normal ejection fraction. Reservoir function of the left atrium is markedly reduced (-6% longitudinal strain compared
to > +40% in normal subjects).
Fig. 14.38: Circumferential strain of the ascending aorta in a subject
with hypertension.
If more than three segments are rejected because
of poor tracking, global strain values will not be
calculated.
Radial strain is estimated from the area strain assuming
that the segment has a constant volume. This way, it is
more accurate than the 2D strain method.
Strain values in 2D bulls eye map are the peak systolic
values, including positive peaks, while in 3D strain it is
the strain values from the end-systolic frame that are
used.
CLINICAL APPLICATIONS OF
STRAIN AND STRAIN RATE IMAGING
Technical and vendor-related differences do not allow,
at the moment, wide-spread clinical use of strain and SR
imaging except, perhaps, the longitudinal strain, which
is more robust and reproducible and has been used in
various clinical situations.32,33 Following are the fields
wherein strain/SR imaging has been used:
In CAD to detect ischemia, viability, reperfusion, extent
of transmural infarction.
To detect subclinical systolic dysfunction in valvular
heart disease like asymptomatic aortic stenosis, aortic
regurgitation, mitral regurgitation,34 and so on.
Detection of intraventricular dyssynchrony.
Understanding diastolic dysfunction and heart failure
with normal EF.
Incremental value in prognosticating heart failure and
ischemic heart disease.
Detecting earliest evidence of cardiotoxicity of
chemotherapeutic agents.
Heart transplant rejection.
Study of right ventricular function.
Differentiating physiological hypertrophy from the
pathological one.
Predicting extent of myocardial fibrosis noninvasively.

Fig. 14.39: Three-dimensional (3D) radial strain in a normal subject. All 17-segment strain curves can be simultaneously shown with the average
value (interrupted line) and Bulls eye map. The 3D data set is sliced to show three apical and three short-axis slices, allowing inspection of the
tracking of each segment both in apical and short-axis directions.
Limitations
Two-dimensional/three-dimensional speckle tracking
echocardiography is generally more smoothed and,
therefore, less influenced by artifacts than TDI-derived
strain but also less sensitive to detect small regions of
pathology.
Despite noise reduction by increased smoothing and
despite an anticlutter filter, dropout is still problematic
and stationary reverberations are sometimes still
tracked or interfere with the frame-by-frame tracking,
resulting in drift or incorrect calculation of strain
and SR.
A clear delineation of the endocardial border is also
important for a reliable radial and transverse tracking.
Since spatial resolution is lower in the transverse
Deformation Imaging: Theory and Practice 277
direction, tracking perpendicular to the ultrasound
beam becomes less robust.
At present, the optimal frame rate for speckle tracking
seems to be 5070 frames/s, which is lower compared
to TDI; this could result in undersampling, especially
in patients with tachycardia.
Rapid events during the cardiac cycle (e.g. isovolumic
phases) may disappear all together, and peak SR and
velocity values may be reduced due to under-sampling,
especially in isovolumic phases and in early diastole.
Higher frame rates could reduce the under-sampling
problem, although this will result in a reduction of
spatial resolution.
Speckle tracking software uses a frame-by-frame
approach to follow the myocardial movement and
searches each consecutive frame for a speckle
278 Section 4: Muscle Mechanics
pattern closely resembling and in close proximity to
the reference frame. With a too-low frame rate, the
speckle pattern could be outside the search area, again
resulting in poor tracking. This can be obviated by
3D strain imaging.
Optimal tracking of the ROI is not only dependent on
optimal image quality, but also on the implemented
tracking algorithm. Software programs designed for
speckle tracking are relatively new and are subjected
to periodical improvements. Different tracking
algorithms potentially produce different results.
Visualization of the myocardial wall needs to be
optimal, with a clear delineation of myocardial tissue
and extracardiac structures and avoidance of dropout
since this will result in unacceptable ROI tracking and
drift.
The optimal balance between temporal and spatial
resolution is achieved when adjusting the image sector
slightly wider than the interrogated wall.
Near-field clutter can be reduced with the
implementation of dual-focus imaging when artifacts
are prominent.
For parasternal recordings (for radial and circum
ferential function on the short axis), small angle
recordings are not possible; all myocardial segments
need to be in the image field.
For any recording, it should be kept in mind that all
myocardial segments need to be visualized optimal,
since poor tracking of any segment often affects
tracking of the adjacent segments.
Inaccurate results are obtained near boundaries
between different kinds of tissues and this may limit
the window size for cross-correlation.
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 Chapter
15 Rotation, Twist and Torsion
Introduction
The study of vectors of motion of the heart provides new
insight into the intricate functioning of the heart muscle
and detection of subclinical disease. In the left ventricle
(LV), fibers in the subepicardium run in a left-handed
direction, fibers in the midlayer run circumferentially
and fibers in the subendocardium run in a right-handed
direction. These myocardial fibers are connected to each
other, with a smooth transition from subendocardium
to midlayer, and then to subepicardium, about the long
axis. Helical orientation of the heart muscle fibers creates
several vectors of motion. Rotation is one of these along
its long axis. Rotation is angular movement about the
center of the mass in the left ventricular short-axis image.
If a longitudinal structure like the LV has two ends, which
rotate in different directions, the net angular movement is
called twist. The LV twists in systole and untwists in diastole.
Twisting produces ejection and also storage of potential
energy. Untwisting is the recoil of twisted muscle due to
release of potential energy. The terms torsion and twist
refer to the same phenomenon and define the base-to-apex
gradient in rotation. Torsion is the net twist angle divided
by the long-axis dimension. Ejection is predominantly a
result of the twist as longitudinal shortening is not capable
of ejecting a normal stroke volume. Twist and torsion are
gaining grounds as robust and valid mechanisms of the
heart muscle function. Although of limited clinical utility
at the moment, it is necessary to understand these vectors
of motion for greater future applications. Disturbed
LV torsion may be considered as a marker for cardiac
disease. In addition, quantification of LV torsion might
be helpful in clinical decision making. It might indicate
proper timing of aortic valve replacement or response to
cardiac resynchronization therapy. Also, it could be used
to monitor the effect of therapy.
Rotation is angular movement about the center of
the mass in the left ventricular short-axis image. Looking
from the apex, counterclockwise rotation is expressed
with positive values and clockwise rotation with
negative values, in units of degrees. Rotation of two ends
(base and apex) occurs in opposite direction and this
wringing motion is called twist. Torsion is more accurately
defined as the base-to-apex gradient in rotation angle
along the long axis of the LV, expressed in degrees/cm.
Others express torsion as the axial gradient in rotation
angle multiplied by the average of the outer radii of apical
and basal planes. In echocardiographic examinations,
torsion is nothing but net twist angle.
FUNDAMENTALS OF TORSION
Torsion is the stress or deformation caused when one
end of an elastic object is twisted in one direction and the
other end is either held constant or rotated in the opposite
direction (Fig. 15.1).
Torsion of the LV is the wringing motion of the ventricle
around its long axis, induced by contracting myofibers in
the wall.

Fig. 15.1: Graphical depiction of torsion when the twisting force is
applied at two ends of an elastic object in different directions.
Fig. 15.3: Graphical depiction of the left ventricle short axis at the base
(left side) and at the apex (right side). When viewed from the apex,
the base rotates clockwise in systole and the apex rotates counter-
clockwise. The net difference in the angular movements (radians) is
the twist.
A flexible elastic structure like myocardium stores
mechanical energy when it is twisted. It also exerts a
force in the opposite direction. The twisting force is
proportionate to the angle it is twisted at. The stored energy
is released during untwisting like a spring. Thus, the left
ventricular muscle is like a helical torsion spring due to the
arrangement of its muscle fibers (Fig. 15.2).
Subendocardial fibers are right-handed and have
smaller radii than the subepicardial fibers, which are left-
handed.13 The two helixes rotate in opposite direction, but
Rotation, Twist and Torsion 281
Fig. 15.2: Arrangement of myocardial fibers. The muscle fibers
descend longitudinally from the base in the subendocardium and
make a Fig. of 8 near the apex before starting the ascent subepi-
cardially (helical configuration). In the middle, the fibers are arranged
circumferentially.1-4
the rotation of the subepicardial fibers dominates because
of greater angular amplitude. The arrangement of fibers
is such that subendocardial fibers rotate clockwise at the
apex during ejection but are overpowered by the
subepicardial fibers with bigger radii, which rotate
counterclockwise.2 At the base, the phenomenon gets
reversed (Figs 15.3 to 15.7). During initial isovolumic
contraction, the apex and the base both rotate in a counter
clockwise direction when viewed from apex to base.
These muscle mechanics can be studied either by
tagged magnetic resonance imaging (MRI) or by two-
dimensional (2D) or three-dimensional (3D) echocardio
graphic strain imaging using acoustic speckle tracking
algorithms. Although considered more accurate, MRI
requires considerably more time for acquisition, has less
temporal resolution and is less affordable and accessible
in most research and clinical environments. Indeed,
the recent surge in interest evaluating LV rotation has
coincided with the arrival of ultrasound tissue tracking.
Torsional deformation is sensitive to changes in
endocardial and epicardial contraction, concentric
remodeling and the fibrous architecture of the heart.
Three factors govern rotation and torsion, and
alteration in any of these will disturb twisting.
Arrangement of muscle fibers as two helixes running
down and up from the apex each separated by about
60 angle from the long axis.4
Inotropy and lusitropy of muscle fibers and all the
factors that affect these like preload, afterload,
catecholamines, and so on.5
282 Section 4: Muscle Mechanics
A B
Figs 15.4A and B: (A) Rotation of the base-to-apex from end diastole to end systole; (B) Angular motion of the left ventricle long axis. Normally,
near base, it rotates about 4 clockwise, while at apex, it rotates 12 counterclockwise in systole producing a net twist of 16.
Fig. 15.5: Twist depicted graphically with simultaneous shortening
in circumferential (C-C) and longitudinal (L-L) planes along with the
net shortening in oblique plane (O-O). Net shortening is greater than
longitudinal or circumferential shortening and correlates with ejection
fraction. Net twist is 90-.
Relative balance between subepicardial versus suben
docardial muscle fibers.
Therefore, distorted anatomy, reduced contraction
and nontransmural involvement in a diseased process will
all affect torsion.
As mentioned previously, subepicardial myocardial
fibers run in a left-handed direction, and contraction
of these fibers causes the base to rotate in a clockwise
direction and the apex to rotate in a counterclockwise
direction. Myocardial fibers in the subendocardial region
run in a right-handed direction, and contraction of these
fibers causes the base to rotate in a counterclockwise
direction and the apex to rotate in a clockwise direction
(Figs 15.4 and 15.5). Radius of rotation of the subepi
cardium is greater than that of subendocardium and
hence normally, the net effect is dominated by the
action of subepicardial fibers. Conditions like cons
trictive pericarditis, which predominantly affect
subepicardial fibers, produce hypo rotation,6 while
initial stages of pathological hypertrophy, which mainly
affects subendocardium will result in hyper-rotation.7
Torsion gives rise to a principal shortening direction
(i.e. direction of maximum contraction, O in Figure 15.5),
which is oriented obliquely to the short-axis plane, in
the approximate direction of the subepicardial muscle
fibers. The direction of the principal shortening is
relatively constant across the wall, despite the large
change in fiber angle, so that the maximum contraction
in the subendocardial wall is approximately orthogonal
to the fiber direction. There is a constant relationship
between torsion and shortening. Torsion to shortening
relationship is a measure of intrinsic contractility and is
load-independent7 (Figs 15.6 to 15.8).
Acoustic speckle tracking has made estimation of
twist and torsion easy.8 However, before LV torsion can
be used as a clinical tool, the physiology of the torsional
deformation should be well understood. Mean values for
systolic peak rotation, systolic basal and apical rotation,
peak systolic twist, twist rate, peak torsion, diastolic peak
untwist, untwist rate and time-to-peak untwist are usually
measured.

Fig. 15.6: Basal rotation (mauve color) versus apical rotation (green
color) giving rise to net twist (white color) throughout a cardiac cy-
cle in a normal subject. Clockwise rotation is shown below the base-
line (negative) and the counterclockwise rotation is shown above the
baseline (positive). Net twist is 16 [11-(-5)]. Also note that during
isovolumic contraction, the rotation vectors are opposite to that seen
during ejection.
Fig. 15.8: Rotation of the left ventricle apex by velocity vector
imaging. All segments show counterclockwise rotation (above the
baseline) during systole.
Torsion represents the myocardial rotation gradient
from the base to apex of the LV.
LV systolic torsion is an important mechanism of wall
thickening and a primary component of normal systolic
function. Mere longitudinal shortening of 1520%
cannot produce ejection fraction of 6070%.1
It acts to normalize LV wall stress by minimizing trans
mural gradients of fiber strain and thereby, increase
energy efficiency by reducing oxygen demand.
Rotation, Twist and Torsion 283
Fig. 15.7: Rotation of the left ventricle base in a normal subject by
velocity vector imaging. Radians of all four segments are shown below
baseline (negative) during ejection, indicating clockwise rotation. Note
the heterogeneity of segments.
Greater torsion occurs in the presence of increased
concentricity (decreased radius/thickness ratio) due
to increased mechanical torque advantage of subepi
cardial fibers over subendocardial fibers.
LV torsion is followed by rapid isovolumic untwisting
of the ventricle. During contraction, potential elastic
energy is stored in the collagen matrix and cytoskeletal
proteins (titin); its release (recoil) causes rapid
untwisting and contributes to active suction of blood
from the atria.9
Normalized twist can be twist divided by distance
from base to apex or individual rotation divided by
corresponding radii.
LV torsion is directly related to the circumferential
longitudinal shear angle.
Both twist and shear angles were counterclockwise as
seen from the apex and greater in anterolateral regions
than in posteroseptal regions.
Rotation occurs around the center of mass of the
entire heart, which would be located more toward the
inferoseptal region, instead of only around a centroid
in the LV.
Besides the magnitude of rotation, its timing also
provides physiological information.9
There is a positive relation between torsion and stroke
volume, and ejection fraction. However, contraction
and torsion are two independent phenomena.
284 Section 4: Muscle Mechanics
Fig. 15.9: Graphical depiction of twisting rate (100/s) and untwisting
rate (138/s) in a normal subject.
Fig. 15.11: Apical rotation (counterclockwise, shown above baseline)
by velocity vector imaging. Note the lack of smoothening of curves.
LV untwisting rate is related to the peak twisting angle
and the LV end-systolic volume, both in patients
with decreased ejection fraction and in patients with
diastolic dysfunction.10
Left ventricular untwisting is the dominant deformation
during relaxation and links systole with early diastolic
recoil. There is a relationship between the LV pressure
drop during isovolumic relaxation (recoiling), which
generates diastolic suction, and untwisting.9,10
Significant amount of untwisting occurs prior to the
opening of mitral valve. Relaxation of torsion is a direct
measure of the deactivation of myocytes and release
of stored elastic energy, both of which facilitate rapid
filling (Fig. 15.9).
Fig. 15.10: Rotation of base and apex in opposite directions during
ejection with net twist in white by acoustic speckle tracking.
ECHOCARDIOGRAPHIC METHODS OF
STUDYING TWIST
Myocardial tissue velocities can be tracked at the base and
apex in the short-axis plane, allowing for the determination
of rotational velocities by tissue Doppler imaging (TDI).
The tissue Doppler technique of assessing torsion has
been shown to correlate quite well with MRI; however, as
with all Doppler recordings, there is concern about angle
dependency. Therefore, torsion estimation using TDI is
rarely used in clinical practice.
Rotation, twist or torsion can be studied by two
different algorithms of 2D strain.
1. Acoustic speckle tracking (which tracks acoustic
reflectors of a region of interest in time and space).
2. Velocity vector imaging (incorporates myocardial
featuring, which tracks speckle as well as endocardial
border simultaneously).
The values derived by the two methods have modest
correlation with each other and can not be used
interchangeably.11 There is a better validation of acoustic
speckle tracking against tagged MRI. The speckles are
tracked throughout the cardiac cycle to quantify the
rotational displacement of the myocardium (Figs 15.10
and 15.11).
Methodological Details
Short-axis 2D images are acquired at the apex and base
(mitral valve level) using frame rates of 50100 Hz and
at least three cardiac cycles are stored. The width of the
region of interest is adjusted as required to fit the wall
thickness.

Fig. 15.12: Counterclockwise rotation of the six equidistant apical
segments in degrees with the average value shown as dotted line
curve in a normal subject.
Fig. 15.14: Net twist in a healthy elderly person 70 years of age. Note
that net twist is increased (24) with increased basal rotation.
After manually tracing the endocardial boarder,
computer software is used to automatically select
speckles and then track them frame by frame using
the sum of absolute difference algorithm. Verify
visually adequate tracking quality of endocardial and
epicardial borders by the system.
Circumferential motion (in degrees) and rates of
rotation (degrees/s) are provided by the software for
both a mean measure and for six equidistant regions
around the circumference (Fig. 15.12).
The software depicts net twist in degrees with time
activity curve as well as rotational velocities.
Using the algorithm, twisting and untwisting rate can
be easily estimated (mean as well as segment-wise)
as shown in Figure 15.9.
Rotation, Twist and Torsion 285
Fig. 15.13: Difference in apical rotation values at true apex (17, left
panel) versus near the apex (11, right panel).
Rotational deformation delay is determined and
defined as the magnitude of the time difference
between time-to-peak basal rotation and time-to-peak
apical rotation.
It is also possible to estimate transmural torsion (endo
cardium, midmyocardium and epicardium). However,
it has limited clinical utility.
With low frame rates, the myocardial motion is too
large frame to frame, and with frame rates that are too
high, the opposite occurs.
Speckle tracking-derived torsion and twist depend
on numerous factors that require technical care,
making the acquisition of high-quality images at the
appropriate LV levels susceptible to error.
Limitations of Speckle Tracking
Method to Assess Torsion
High-quality images are required, which are not always
possible.
2D strain suffers from limitation of through-plane
motion.
Imaging true apex remains a challenge (Fig. 15.13).
CLINICAL APPLICATIONS OF TORSION
Torsion is an important index of cardiac function
and provides additional information on myocardial
performance over and above standard pump function
indices. However, there are no large valid and robust
clinical studies and the most information is in the realm
of research, physiology and hypothesis-generating. The
importance of measuring LV rotation lies in its potential
286 Section 4: Muscle Mechanics
Fig. 15.15: Increased torsion of 25 in a subject with nonobstructive
hypertrophic cardiomyopathy.
for early detection of pathology. Systolic twist acts to
limit myocardial energy expenditure by creating high
intraventricular systolic pressures with minimal muscle
shortening, resulting in efficient LV contraction. Reduced
twist will, then, be associated with inefficient contraction.
Increased torsion or twist, on the other hand, may be
a compensatory phenomena or just a reflection of an
imbalance between subepicardial versus subendocardial
muscle fiber function.
AGING AND TORSION
Aging is associated with increased LV torsion secondary
to reduced rotational deformation delay and increased
peak basal rotation.12 Aging is associated with a decrease
of contractile function in the subendocardium relative
to that in the subepicardium without changes in ejection
fraction. This impairment of subendocardial contractile
function may be secondary to subendocardial fibrosis,
asymptomatic subendocardial infarction or reduced
subendocardial perfusion. The net effect is increased LV
torsion due to unopposed action of subepicardial fibers
and the preservation of ejection fraction in the elderly and
reduced myocardial oxygen demand. Time-to-peak apical
rotation occurs later in systole and closer to the timing of
peak basal rotation with advancing age (Fig. 15.14).
Torsion may represent a compensatory mechanism to
maintain an adequate stroke volume and cardiac output
in the face of progressively reduced LV volumes and
myocardial shortening associated with aging.
Fig. 15.16: Increased torsion (28) in an asymptomatic patient with
aortic stenosis.
AORTIC STENOSIS, HYPERTENSION AND
HYPERTROPHIC CARDIOMYOPATHY
Elevated torsion and/or torsion-shortening ratios have
been detected almost exclusively in patients with LV
hypertrophy13 caused by increased hemodynamic loading
conditions (i.e. aortic valve stenosis or hypertension),
and in patients with hypertrophic cardiomyopathy
(Figs 15.15 and 15.16). However, elderly patients with
normal LV wall dimensions also show increased left
ventricular torsion, indicating that age-related myocardial
alterations contribute to changes in the pattern of
contraction in this population.
Increased torsion is generally regarded as the result of
impaired contraction of predominantly subendocardial
myofibers (due to relative hypoperfusion of the thickened
wall), leading to increased counteraction of contracting
epicardial fibers, which have a longer lever arm. However,
increased basal rotation has been observed more often in
hypertrophic cardiomyopathy (Fig. 15.15).
A similar observation of increased LV torsion
with unaltered circumferential strain in asymptomatic
type I diabetes mellitus patients without morphological
evidence of cardiac disease, contributes to the idea that
intrinsic disease-related pathology might be responsible
for differences in myocardial deformation.14
Increased torsional deformation also exists in healthy
mutation carriers of hypertrophic cardiomyopathy, even
in the absence of hypertrophy.15

Fig. 15.17: Dilated cardiomyopathy in a young male showing reduced
rotation and torsion. There is prolonged unidirectional counterclock-
wise rotation during isovolumic contraction.
Fig. 15.19: Solid body rotation in a patient with left ventricle noncom-
paction cardiomyopathy.
HEART FAILURE
Torsion differentiates two phenotypes of heart failure.
Torsional deformation is reduced in heart failure with
reduced systolic function (Fig. 15.17) but is preserved in
patients with normal ejection fraction (Fig. 15.18).
Heart failure with LV dilatation and reduced ejection
fraction is characterized by spherical remodeling. This
results in greater angle between the LV long axis and the
helixes. Torsion is reduced as a result of more transverse
orientation of the muscle fibers.16
Heart failure with normal ejection fraction (HFnEF) is
characterized by normal torsion, although untwisting rate
may be slowed in some cases.17
Rotation, Twist and Torsion 287
Fig. 15.18: Torsion in a 63-year-old male with heart failure with normal
ejection fraction and Class IV symptoms. Note that rotation and net
twist are maintained.
Fig. 15.20: Negative net twist of -4 in a patient with end-stage systolic
heart failure. Note reversed rotation of the base and the apex.
In advanced heart failure with spherically remodeled
hearts, rotation at the two ends may be in the same direction
with no net twist (Figs 15.19 and 15.20). This phenomenon
is called solid body rotation.18,19 Solid body rotation was
initially considered specific for genetic cardiomyopathy
like noncompaction, mitochondrial myopathy, etcetera,
but of late has been shown to exist in any advanced heart
failure.
Other patterns of rotation in heart failure are being
explored (Figs 15.21 to 15.23).
CONSTRICTIVE PERICARDITIS
Constrictive pericarditis may have involvement of
subepicardial muscle fibers either by fibrosis and
288 Section 4: Muscle Mechanics
Fig. 15.21: Unusual biphasic rotation in heart failure with reduced ejec-
tion fraction due to markedly prolonged isovolumic contraction phase.
Fig. 15.23: Mitochondrial cardiomyopathy in a 12-year-old boy show-
ing solid body rotation in first half of systole followed by reduced
torsion and prolonged time-to-peak torsion.
calcification or tethering.6 This can result in hyporotation
and reduced twist (Figs 15.24 to 15.26).
Pericardium plays a significant role in maintaining
myocardial muscle mechanics. Patchy involvement of
pericardium with affliction of the underlying subepicardial
fibers can produce several different patterns of rotation.
Even unidirectional basal and apical rotation has been
shown due to marked tethering at one or the other site
(Fig. 15.26).
HFnEF has normal torsion but reduced longitudinal
strain (Fig. 15.27).
Fig. 15.22: Noncompaction left ventricle cardiomyopathy showing
reduced twist and markedly prolonged time-to-peak twist.
Fig. 15.24: Study of basal rotation in a patient with surgically proven
constrictive pericarditis. Mean clockwise rotation is reduced (-1) due
to paradoxical counterclockwise rotation of the tethered left ventricle
free wall segments.
TORSION AND CARDIAC
RESYNCHRONIZATION THERAPY
In patients with LV dyssynchrony due to heart failure,
LV twist and torsion are negatively correlated with
radial dyssynchrony.20
Torsion improves after resynchronization (Fig. 15.28).
Twist and torsion may be predictors of response to
resynchronization therapy.21
The difference in response may be due to lead
placement, since LV leads positioned in midventricular

Fig. 15.25: Reduced apical rotation (+6) in a patient with constrictive
pericarditis. Note significant reduction in counterclockwise rotation of
the free wall segments. There is also post-systolic rotation.
Fig. 15.27: Endomyocardial fibrosis in a 40-year-old female with heart
failure. Note preserved twist despite restrictive mitral flow pattern.
and apical regions can exhibit a larger increase in
systolic LV twist than LV leads positioned in the basal
regions of the LV free wall.
ACUTE AND CHRONIC ISCHEMIA
In acute ischemia, apical rotation may be initially
increased due to relative impairment of subendocardial
fibers.22
Rotation, Twist and Torsion 289
Fig. 15.26: A 25-year-old male with constrictive pericarditis. Reduced
twist due to both apex and base showing counterclockwise rotation.
Ejection fraction was preserved due to normal apical counterclockwise
rotation.
Fig. 15.28: Apical rotation in a 60-year-old female with heart failure
and left bundle branch block before (left panel) and after (right panel)
resynchronization therapy. Apical rotation is shown, which improves
significantly after therapy, although time-to-peak rotation is still pro-
longed.
In regional ischemia or myocardial infarction, torsion
is typically impaired in relation to the regional nature
of the disease.
In patients with myocardial infarction, twist is reduced
and untwisting is delayed and prolonged.22
Apical myocardial infarction can produce solid
body rotation, which tends to normalize after
revascularization over time.
Regional heterogeneity in ischemia can show varying
patterns of twist and rotation.
290 Section 4: Muscle Mechanics
Fig. 15.29: Apical hypertrophic cardiomyopathy with early diastolic
dysfunction. Note enhanced torsion due to basal rotation.
GRADES OF DIASTOLIC
DYSFUNCTION AND TWIST
Significant increase in apical rotation, basal rotation,
twist and twist rate occurs in those with Grade I
diastolic dysfunction (impaired relaxation), while
those with more severe diastolic dysfunction are not
different from controls23 (Fig. 15.29).
Systolic-diastolic rotational coupling is always present.
There are a variety of other cardiac conditions where
twist mechanisms are being studied to understand cardiac
physiology and consequences of procedures, which alter
the helical geometry of the LV like ventriculectomy,
cardiac transplantation, and so on.
SUMMARY
Relative to end diastole, the apex of the LV rotates
anticlockwise about its central axis, as viewed from the
apex, at a relatively constant rate throughout systole, to a
maximum value of approximately 10. The base, initially
rotating anticlockwise, reverses direction to give a net
clockwise rotation by end systole of approximately 3. The
resulting end-systolic torsion is the difference between two
rotations. During diastole, most untwisting or restoration
of angular motion occurs in isovolumic relaxation.
LV torsion is circumferentiallongitudinal shear angle
corrected for length or radius. Amount and timing of LV
torsion are directly related to the structure and function
of the myocardium and myocytes. The proof of concept is
there, but some methodological and validation issues still
remain. Torsion has been calculated as relative rotation
(degrees), rotation per length (degrees/mm), torsional
shear angle (degrees) and shear strain (dimensionless).
A unified way to describe LV torsion should be
independent of the measurement method. Noninvasive
measurement methods such as cardiovascular magnetic
resonance tissue tagging and speckle tracking echocardio
graphy must provide reproducible and comparable
measurements of LV torsion, before they can be used as
clinical tools for detection of myocardial dysfunction.
It might be difficult to incorporate the circumferential
longitudinal shear angle approach in echocardiography,
due to the lack of a reference coordinate system. However,
new methods such as 3D speckle tracking might be able to
overcome this problem.
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method for assessment of left ventricular rotation: speckle
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3. Notomi Y, Lysyansky P, Setser RM, et al. Measurement of
ventricular torsion by two-dimensional ultrasound speckle
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manipulations, heart rate, and contractility on left ventri
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Disparate patterns of left ventricular mechanics differenti-
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8. Phillips AA, Cote AT, Bredin SS, et al. Heart disease and left
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 SEction 5
CHD, Aorta and Pericardium

Chapters

Congenital Heart Disease in Adults Pericardial Diseases

Aorta: Congenital and Acquired Disorders
 Chapter

16
Congenital Heart
Disease in Adults

Introduction
Most congenital heart diseases (CHDs) of consequence
present in early childhood and are managed appro
priately. Some CHDs are detected for the first time in
adults either because of their natural course or because
these were neglected in childhood. There is also a large
pool of patients who have been operated for CHD in
childhood but become symptomatic in adult life because
of arrhythmias, heart failure or recurrence, or residual
lesions.13 Echocardiography is an integral tool in managing
such patients. Spatial anatomy is difficult to assess in CHD
and three-dimensional echocardiography has become an
important part of echocardiographic assessment.
The most common congenital heart disorders affecting Fig. 16.1: Schematic diagram of the right atrium showing location of
various types of atrial septal defect (ASD).
adults are:2,3 (SVC: Superior vena cava; IVC: Inferior vena cava; CS: Coronary
Congenital valve defects (discussed in section on sinus; RV: Right ventricle; TV: Tricuspid valve).
valvular heart disease).
Atrial and ventricular septal defects. ATRIAL SEPTAL DEFECT
Patent foramen ovale (PFO). Three types of atrial septal defect (ASD) can occur
Patent ductus arteriosus. (Fig. 16.1): 46
Anomalous pulmonary veins. 1. Ostium secundum is the most common type (70%).
Coarctation of the aorta discussed in section on Aorta. It can be large, but usually does not affect the
Ebstein anomaly. atrioventricular valves.
Tetralogy of Fallot (TOF). 2. Ostium primumthe hole is situated close to the
Transposition of the great arteries. atrioventricular valves and can be associated with an
Pulmonary hypertension (Eisenmenger syndrome). atrioventricular septal defect.
296 Section 5: CHD, Aorta and Pericardium
Fig. 16.2: Transesophageal echocardiographic long axis view with
rightward probe deflection showing secundum atrial septal defect
(arrow length).
Fig. 16.4: Transesophageal echocardiographic anatomic relationship
of the secundum atrial septal defect with left-to-right shunt (interrupted
line).
3. Sinus venosus is a defect situated near the entrance of
the superior vena cava (SVC) or inferior vena cava (IVC)
to the right atrium.7 It is unusual and is often associated
with partial anomalous pulmonary venous drainage
(usually drainage of the right upper lobe into the SVC).
The shunt of blood from the left atrium to the right
atrium results in:
Increased volume load and dilatation of the right
atrium and right ventricle (RV).
Fig. 16.3: Ostium secundum atrial septal defect shown in transes
ophageal echocardiographic bicaval view (left panel) and the
schematic diagram (right panel).
Fig. 16.5: Transthoracic echocardiographic apical four-chamber view
in end-systole. Two rims of the atrial septal defect are shown (arrows).
Increased pulmonary blood flow and enlargement of
the pulmonary arteries.
Increase in size of the pulmonary veins.
Reduced filling of the left ventricle (LV) and aorta.
The ostium secundum ASD is the most common
type of ASD, and comprises 610% of all CHD (Figs 16.2
to 16.6). About 70% of the ASD are ostium secundum type.
Stretched ASD dimensions are best measured in
systole (Fig. 16.6).

Fig. 16.6: Apical four-chamber view with color Doppler interrogation
of atrial septal defect. Supero-inferior diameter is much bigger in
ventricular systole (left panel) compared to that in diastole (right
panel).
Fig. 16.8: Subcostal long-axis view showing bidirectional flow across
a large secundum atrial septal defect (arrows).
The secundum ASD usually arises from an enlarged
foramen ovale, inadequate growth of the septum secun
dum, or excessive absorption of the septum primum. Ten
to twenty percent of individuals with ostium secundum
ASDs also have mitral valve prolapse.
If the ostium secundum ASD is accompanied by an
acquired mitral valve stenosis, that is called Lutembachers
syndrome.
Subcostal views or right low parasternal views are the
best to visualise ASD because in these transthoracic views,
the interatrial septum is perpendicular to the ultrasound
beam (Figs 16.7 and 16.8). However, obtaining adequate
views in adults may be a challenge.
Congenital Heart Disease in Adults 297
Fig. 16.7: Subcostal four-chamber view showing rims of secundum
atrial septal defect (arrows).
Atrial septal defect is assessed by parasternal short-
axis, apical and subcostal four-chamber views in
transthoracic echocardiography (TTE). In transesophageal
echocardiography (TEE), multiple views are used to
estimate rims of the ASD and its relationship with adjoining
structures (Figs 16.9A to D).
Earlier, it was sufficient to categorise ASD by
transthoracic and transesophageal imaging, give its appro
ximate size in multiple views, estimate left-to-right shunt
along with pulmonary artery pressures and associated
anomalies. With advent of transcatheter closure of
ASD, it has become important to identify and measure
rims of ASD all around and study their characteristics.8
3D TTE and TEE plays a stellar role in this aspect
(Figs 16.10 to 16.13). The key points to be examined are:
Size, shape and number of ASDs.
Panoramic view of the rims.
Relationship to adjoining structures.
Advantages of the real-time 3DE are:8
Unlimited viewing of the interatrial septum.
Possibility to create an en face view.
Examination from both right atrium and the left atrium.
Appreciating the change in size and shape of the
ASD during cardiac cycle (largest size during atrial
relaxation or ventricular systole). Size can vary by
about 50%.
Feasibility for transcatheter closure and monitoring
during the procedure.
Number of defects with their relationships.
298 Section 5: CHD, Aorta and Pericardium

A B

C D
Figs 16.9A to D: Multiple transesophageal echocardiographic views to assess shape, size and margins of the secundum atrial septal
defect (ASD). Comparison of upper panels with lower panels indicates that the ASD is elliptical and posterio-inferior margin (left upper panel) is
deficient.

Fig. 16.10: Real-time 3DE right atrial view with atrial septal defect Fig. 16.11: 3D transthoracic echocardiographic image showing
(ASD) in the center to show various relationships. en face view of the atrial septal defect (ASD).
 Congenital Heart Disease in Adults 299

Fig. 16.12: Real-time 3D transesophageal echocardiographic view Fig. 16.13: Real-time 3D transesophageal echocardiographic en face
from the left atrium. view of the interatrial septum with atrial septal defect (ASD).

On echocardiography, there may not be any shunting

of blood noted except when the patient coughs. However,
shunting can be easily appreciated by contrast injection.6
It is possible to visualize PFO by real-time 3D TEE
(Fig. 16.14).
There is debate within the neurology and cardiology
communities about the role of a PFO in cryptogenic
(i.e. of unknown cause) neurologic events such as strokes
and transient ischemia attacks without any other potential
cause.9 Some data suggested that PFOs may be involved
in the pathogenesis of some migraine headaches.10 It can
also be associated with fossa ovalis membranous
aneurysm (Fig. 16.15).
Fig. 16.14: Real-time 3D TEE examination showing patent foramen Patent foramen ovale can be visualized by injecting
ovale (PFO) (arrow) during straining. agitated saline in a peripheral vein either during
transthoracic examination but more often during TEE.
Atrial septal defect rims can be seen in the following
Immediate appearance of contrast in the left atrium after
manner:
it is seen in the right atrium (usually in < 3 cardiac cycles)
Aortic or anterosuperior rim.
is highly suggestive of PFO (Fig. 16.16). Sometimes,
Mitral or anteroinferior rim.
Valsalva manouvre or cough or sniff can be used to
Superior or SVC rim.
augment the effect.
Posteroinferior or IVC rim.
Occasionally, small secundum ASD can occur in oval
Posterior rim along posterior right atrial wall.
fossa following atrial puncture and dilatation (Fig. 16.17).
Inferior or coronary sinus rim.
These are usually restrictive with appreciable pressure
gradients.
PATENT FORAMEN OVALE
A PFO is a small channel that has some hemodynamic OSTIUM PRIMUM ATRIAL SEPTAL DEFECT
consequence; it is a remnant of the fetal foramen ovale. A defect in the ostium primum is occasionally classified
Clinically, it is linked to: as an ASD but it is more commonly classified as an
Decompression sickness. atrioventricular septal defect (Figs 16.18 and 16.19).
Paradoxical embolism. Ostium primum defects are less common than ostium
Migraine. secundum defects.
300 Section 5: CHD, Aorta and Pericardium
Fig. 16.15: Aneurysm of the patent foramen ovale membrane (arrow)
seen in apical four-chamber view.
Fig. 16.17: Apical four-chamber view showing small atrial septal defect
in oval fossa (arrow) following transcatheter mitral commissurotomy.
SINUS VENOSUS ATRIAL SEPTAL DEFECT
A sinus venosus atrial septal defect is a type of ASD in
which the defect in the septum involves the venous inflow
of either the SVC or the IVC (Fig. 16.20).
A sinus venosus ASD that involves the SVC makes up
23% of all interatrial communication.5 It is located at
the junction of the SVC and the right atrium (Fig. 16.20).
It is frequently associated with anomalous drainage of
the right-sided pulmonary veins into the right atrium
(instead of the normal drainage of the pulmonary veins
into the left atrium).
Sinus venosus defects are better appreciated by TEE
and need to be differentiated from the secundum ASD
(Fig. 16.21).
Fig. 16.16: Apical four-chamber view showing apparently intact atrial
septum with contrast appearance in the left-sided chambers.
Fig. 16.18: Apical four-chamber view showing ostium primum atrial
septal defect (ASD) (arrow).
COMMON OR SINGLE ATRIUM
Common (or single) atrium is a failure of development of
the embryologic components that contribute to the atrial
septal complex. It is frequently associated with heterotaxy
syndrome or tricuspid atresia (Fig. 16.22).
VENTRICULAR SEPTAL DEFECT
Ventricular septal defect (VSD) is the most common
congenital heart defect (20% of all CHD) and frequently
seen in adults either as a small defect or as a part of
repaired but residual complex CHD. Its prevalence
in adults is low, fundamentally due to spontaneous
closing of some defects and to the fact that the majority
 Congenital Heart Disease in Adults 301

Fig. 16.19: Complete atrioventricular septal defect with primum defect Fig. 16.20: Sinus venosus atrial septal defect (ASD) showing override
(spot) seen in four-chamber view. There is no central fibrous body and of superior vena cava (SVC) and right upper pulmonary vein.
inferior interatrial and superior ventricular septa are deficient.

A B
Figs 16.21A and B: 2D transesophageal echocardiographic caval view showing sinus venosus atrial septal defect. Note that the posterior wall
of the superior vena cava is deficient and right pulmonary artery is jutting the defect.

of symptomatic defects are closed surgically during
childhood. Symptoms depend on the size of the defect
and the age of the patient. Small VSDs are usually
asymptomatic and compatible with a normal life (in fact,
about 40% close spontaneously in early childhood). If a
large shunt does not produce symptoms during infancy,
there is usually little disturbance until late adolescence or
early adult life when the patient develops high pulmonary
vascular resistance, breathlessness, fatigue and cyanosis.
There is progression to effort syncope, recurrent
hemoptysis and heart failure.
The interventricular septum has a complex and curved
shape (Figs 16.23 to 16.25). The ventricular septum is
directed obliquely backward to the right, and curved
with the convexity toward the RV; its margins correspond
with the anterior and posterior longitudinal sulci.11 It is
composed of:
Membranous part near the central fibrous body.
Muscular Septum.
Outlet septum or infundibular septum or aorto
pulmonary septum that is spiral in orientation.
Upper and posterior part, which separates the
aortic vestibule from the lower part of the right atrium
and upper part of the RV, is thin and fibrous, and is
termed the membranous ventricular septum (septum
membranaceum).
The muscular part of the interventricular septum
derives from the bulboventricular flange that is developed
due to differential growth of primitive ventricle and
bulbous cordis.
302 Section 5: CHD, Aorta and Pericardium
Fig. 16.22: Common atrium in an adult subject with tricuspid atresia
shown in apical four-chamber view.
Fig. 16.24: En face view of the interventricular septum (IVS).
MORPHOLOGY OF VSD
Four types are described below:1215
Perimembranousmost common type in adults (80%)
(Figs 16.26 and 16.27)
Muscularmost common type in young children
(Figs 16.28 to 16.30)
Complete atrioventricular septal (endocardial
cushion) defects (Figs 16.19 to16.31)
Supracristal (subarterial) (Fig. 16.32)
Fig. 16.23: Relationship of the membranous septum to the aortic
annulus and the left ventricular outflow tract (LVOT).
Fig. 16.25: Site-specific classification of the ventricular septal defect
(VSD).
PATHOPHYSIOLOGY OF VSD
Restrictive VSD is typically small, such that a significant
pressure gradient exists between the LV and RV
with small shunt (Qp/Qs 1.4: 1) (Fig. 16.33).
Moderately restrictive VSD moderate shunt (Qp/Qs
1.4 to 2.2: 1).
Large/nonrestrictive VSD large shunt (Qp/Qs
> 2.2: 1). There is enlargement of LA and LV as well
(Fig. 16.34).
 Congenital Heart Disease in Adults 303

Fig. 16.26: Schematic diagram of the short-axis transthoracic Fig. 16.27: Transesophageal echocardiography long-axis view
echocardiographic image showing location of perimembranous versus showing perimembranous ventricular septal defect (arrow).
subarterial ventricular septal defect (VSD).

Fig. 16.28: Apical muscular ventricular septal defect (arrow) in Fig. 16.29: Restrictive muscular ventricular septal defect with left-to-
modified short-axis view. right shunt.

Fig. 16.30: Large muscular ventricular septal defect in posterior Fig. 16.31: 3D transthorasic echocardiographic showing atrioven
septum (arrow). tricular septal defect (arrow).
304 Section 5: CHD, Aorta and Pericardium
Fig. 16.32: Subarterial ventricular septal defect in transthoracic
echocardiography short-axis image.
Fig. 16.34: Large perimembranous ventricular septal defect with
transventricular peak gradient of 30 mm Hg indicating presence of
significant pulmonary hypertension.
Eisenmenger VSD irreversible pulmonary hyper
tension and shunt may be reversed (i.e. R L)
Defect size is often compared to aortic annulus:14
Large: > 50% of annulus size (Figs 16.35 and 16.36)
Medium: 2550% of annulus size (Fig. 16.37)
Small: < 25% of annulus size
Real-time 3DE has great utility in assessing size and
location of VSD (Fig. 19.38). En face view from the left
side identifies VSD more accurately.
EBSTEINS ANOMALY
Ebsteins anomaly is the downward displacement of a
portion of the tricuspid valve with atrialization of a large
Fig. 16.33: Restrictive muscular ventricular septal defect with
100 mm Hg transventricular peak gradient.
Fig. 16.35: 15 mm ventricular septal defect (VSD) size compared to
25 mm of aortic annulus (large VSD).
part of the RV.1618 There is often an associated ostium
secundum ASD. The atrialized portion of the ventricle
hinders rather than helps the forward flow of blood and
there is tricuspid regurgitation. Occasionally, Ebsteins
anomaly is asymptomatic, but it generally presents in
childhood or early adulthood with dyspnea, fatigue, signs
of tricuspid regurgitation and right-sided cardiac failure.17
In the normal heart, the tricuspid valve has three
leaflets: anterior, posterior and septal. Ebsteins anomaly is
a malformation of the tricuspid valve and RV characterized
by (Fig. 16.39).
Adherence of the septal and posterior leaflets to the
underlying myocardium (failure of delamination).

Fig. 16.36: Large ventricular septal defect (VSD) 25 mm in tetralogy of
Fallot with secundum ASD in apical four-chamber view.
Fig. 16.38: En face view of atrioventricular septal defect from the right
side (arrow).
Downward (apical) displacement of the functional
annulus (septal>posterior>anterior).
Dilatation of the atrialized portion of the RV, with
various degrees of hypertrophy and thinning of the wall.
Redundancy, fenestrations and tethering of the
anterior leaflet.
Dilatation of the right atrioventricular junction (true
tricuspid annulus).
In normal human hearts, the downward displacement
of the septal and posterior leaflets in relation to the anterior
mitral valve leaflet is < 8 mm/m2 body surface area. The
spectrum of the malformation in Ebsteins anomaly may
range from:
Congenital Heart Disease in Adults 305
Fig. 16.37: 8 mm ventricular septal defect (VSD) size compared to
24 mm of aortic annulus (moderate VSD).
Fig. 16.39: Ebsteins anomaly in an adult in parasternal long-axis
view. Note enlarged right atrium (RA), dilated annulus, small atrialised
portion, septal leaflet (SL) displacement and sail-like anterior tricuspid
leaflet (ATL).
Minimal displacement of the septal and posterior
leaflets
Imperforate membrane
Muscular shelf between the inlet and trabecular zones
of the RV.
The anterior leaflet is generally redundant and may
contain several fenestrations. Its chordae tendineae are
generally short and poorly formed. The anterior leaflet of
the tricuspid valve (ATL) may be severely deformed, so
that the only mobile leaflet tissue is displaced into the right
ventricular outflow tract, where it may cause obstruction
or form a large sail-like intracavitary curtain (Fig. 16.40).
306 Section 5: CHD, Aorta and Pericardium
Fig. 16.40: Ebsteins anomaly with large, redundant and deformed
anterior tricuspid leaflet (ATL) attached by short aberrant chords to the
right ventricle (RV) free wall.
Fig. 16.42: Type B Ebsteins anomaly.
In Ebsteins anomaly, the RV is divided into two regions:
1. Atrialized Ventricle: The part directly involved with
the malformation (i.e. the inlet portion), which is
functionally integrated with the right atrium
2. Functional RV: The part that is not involved by the
anomaly, which consists of the other two components
of the RV, namely the trabecular and outlet portions
that constitute the functional RV.
The atrialized portion of the RV (i.e. the inlet
component) can become disproportionately dilated and
may account for more than half of the right ventricular
volume in extreme cases instead of the usual one third of
the total right ventricular volume.
Fig. 16.41: Type A Ebsteins anomaly.
Fig. 16.43: Type C Ebsteins anomaly. Note the right ventricular out
flow tract (RVOT) obstruction caused by anterior leaflet (arrow).
CARPENTIER CLASSIFICATION OF
EBSTEINS ANOMALY19
Type A: The volume of the true RV is adequate
(Fig. 16.41).
Type B: A large atrialized component of the RV exists,
but the ATL valve moves freely (Fig. 16.42).
Type C: The ATL is severely restricted in its movement
and may cause significant obstruction of the right
ventricular outflow tract (RVOT) (Fig. 16.43).
Type D: Almost complete atrialization of the ventricle
except for a small infundibular component (Fig. 16.44).

Fig. 16.44: Type D Ebsteins anomaly with very small residual
functional right ventricle.
Fig. 16.46: Double-chambered right ventricle (RV; arrows) shown in
modified short-axis view. A peak systolic gradient of 150 mm Hg was
observed (right panel)
(PC: Proximal chamber; DC: Distal chamber).
DOUBLE-CHAMBERED RV
In this disorder, the RV is divided into a high-pressure
proximal chamber and lower-pressure distal chamber by
anomalous muscle bundles, creating a double-chambered
RV (Figs 16.45 and 16.46).
The morphological features may be variable and
the particular muscle bands involved vary from an
anomalous septoparietal band, an anomalous apical
shelf (Fig. 16.47), or an abnormal moderator band.20
The distance between the moderator band and the
pulmonary artery may be abnormally short.
Congenital Heart Disease in Adults 307
Fig. 16.45: Double-chambered right ventricle (RV) in parasternal long-
axis view (arrows). (DC: Distal chamber).
Fig. 16.47: Shelf-like obstruction proximal to pulmonary valve (PV).
(PC: Proximal chamber; DC: Distal chamber LA: Left atrium; PA:
Pulmonary atresia).
The RVOT obstruction is generally believed to be an
acquired one and to be progressive over time, although
the basic anatomic features are congenital.
In 75% of cases, it is associated with a perimembranous
VSD that is usually, but not always, below the level of
the muscular obstruction (Fig. 16.48).
In some instances, there is greater RV dysfunction
when the VSD is restrictive or closes.
Other associations include valvular pulmonary
stenosis (PS), TOF and double-outlet RV (Fig. 16.49).
There is subaortic obstruction in a variable number of
these patients.
308 Section 5: CHD, Aorta and Pericardium
Fig. 16.48: Double-chambered right ventricle (yellow arrows) with
aneurysm of the membranous ventricular septal defect (green arrow).
Fig. 16.50: 3DE cross-section showing three aortic sinuses.
The anomaly is rare, occurring in 1% of patients
with congenital heart disease. It has been reported to
develop in 3% of patients with repaired TOF and in
310% of patients with a VSD.
SINUS OF VALSALVA ANEURYSMS
The three sinuses of Valsalva are located in the most
proximal portion of the aorta, just above the cusps of the
aortic valve (Figs 16.50 and 16.51). The sinuses correspond
to the individual cusps of the aortic valve. These structures
contained within the pericardium are easily revealed using
Fig. 16.49: Double-chambered right ventricle (yellow arrows) with
pulmonary valve stenosis (right panel, white arrows).
Fig. 16.51: Suprasternal long-axis view showing right and left aortic
sinuses. Anterior to right sinus is the right ventricular outflow tract
(RVOT).
echocardiography as distinct but subtle outpouchings of
the aortic wall just above the valve. The sinuses end in the
area of the sinotubular junction, and the tubular portion of
the aorta begins here.
Aneurysm of the aortic sinus, also known as the
sinus of Valsalva, is comparatively rare. Frequency of
involvement is:2125
Aneurysm of the right sinus (6585%) (Figs 16.52
and 16.53).
Aneurysm of the noncoronary sinus (1030%) (Figs 16.54
and 16.55.
Left sinus aneurysm (< 5%).
 Congenital Heart Disease in Adults 309

Fig. 16.52: Aneurysm of the right sinus of Valsalva (arrow) seen in Fig. 16.53: Aneurysm of the right sinus of Valsalva (arrow) shown in
parasternal long-axis view. parasternal short-axis view

Fig. 16.54: Aneurysm of the noncoronary sinus (arrow) in transes Fig. 16.55: Aneurysm of the noncoronary sinus opening into the right
ophageal view at 80. atrium (arrow) 3D transthoracic echocardiography.

This type of aneurysm is typically congenital and may separation between the aortic media and the annulus
be associated with heart defects. It is sometimes associated fibrosus.
with: Rupture of the dilated sinus may lead to intracardiac
Marfan syndrome shunting (Fig. 16.56) when a communication is established
LoeysDietz syndrome with the right atrium [Gerbode defect (10%)] or directly into
the RV (6090%). Cardiac tamponade may occur if the
EhlersDanlos syndrome
rupture involves the pericardial space. Rupture is the event
Atherosclerosis
that makes the patient seek medical attention although
Syphilis rarely, RVOT obstruction can occur. Various sites of
Cystic medial necrosis rupture are shown below: (Figs 16.57 to 16.60)
Chest injury Associated congenital defects with aneurysm of sinus
Infective endocarditis of Valsalva are:
Congenital aortic sinus aneurysm is caused by a Ventricular septal defect (3060%, more often
dilatation, usually of a single sinus of Valsalva, from a subarterial type).
310 Section 5: CHD, Aorta and Pericardium

A B

C
Fig. 16.56: Schematic diagram showing relationship of the aortic Figs 16.57A to C: Panel A shows aneurysm of right aortic sinus open
sinuses with intracardiac structures and possible sites of comm ing into the RVOT. Panel B shows color Doppler interrogation and
unication when rupture occurs. panel C shows systolic-diastolic continuous flow across the defect.

A B
Figs 16.58A and B: Transesophageal echocardiographic view showing noncoronary sinus aneurysm opening into the right atrium
(left panel, arrow). The right panel shows color Doppler interrogation of the flow.

Fig. 16.59: Transesophageal echocardiographic long-axis view showing communication of the left aortic sinus with the left atrium (arrows) with
out any aneurysm formation.
 Congenital Heart Disease in Adults 311

A B
Figs 16.60A and B: Aneurysm of noncoronary aortic sinus communicating with the right atrium. 2D transesophageal echocardiographic color
Doppler flow mapping (panel A) compared to 3D transthoracic echocardiographic imaging (arrow).

Fig. 16.61: Parasternal long-axis view showing large subaortic Fig. 16.62: Modified short-axis view showing infundibular obstruction
ventricular septal defect and override of the aortic root due to anterior (arrow) and mild hypoplasia of the pulmonary arteries. The peak
deviation of the infundibular septum. systolic gradient of 100 mm Hg by continuous wave Doppler is shown
in the right panel.

Aortic insufficiency (2030%). TETRALOGY OF FALLOT

Bicuspid Aortic Valve (10%).
Coarctation.
Aortic sinus aneurysms are more common among
men than women and among Asians than other ethnic
groups. Nonruptured aneurysms may be asymptomatic
and incidentally discovered, or they may be symptomatic
and manifest acutely with mass effect on adjacent cardiac
structures. Ruptured Valsalva sinus aneurysms result
in an aorto-cardiac shunt and may manifest as acute or
insidiously progressive congestive heart failure, severe
acute chest pain with dyspnea, or, in extreme cases,
cardiac arrest.21
A significant number of patients with TOF survive to
adulthood. The proportion of children reaching adulthood
is predominantly determined by the magnitude of the
hypoxia. TOF, the most common cyanotic malformation in
adults, represents a spectrum from mild RVOT obstruction
to complete pulmonary atresia.
Tetralogy of Fallot is diagnosed using recognized
morphological criteria.24 TOF is a cono truncal defect
resulting from anterior malalignment of the infundibular
septum. This single morphologic defect gives rise to the
four main components of TOF (Figs 16.61 to 16.63).
312 Section 5: CHD, Aorta and Pericardium
Fig. 16.63: Subcostal four-chamber view showing biventricular origin
of the aortic root due to aortic override.
Fig. 16.65: Complete atrioventricular septal defect with a large right
ventricle (RV) in tetralogy of Fallot.
1. Anterior deviation of the infundibular septum
2. Ventricular septal defect
3. Obstruction to right ventricular outflow
4. Right ventricular hypertrophy
Malalignment of the infundibular septum to the
trabecular septum is present, resulting in a malalignment
VSD (Fig. 16.63).
Anterior displacement of the bulbotruncal region has
been postulated to cause the infundibular stenosis.
MORPHOLOGICAL VARIANTS OF TOF
TOF with pulmonary atresia (Fig. 16.64).
TOF with atrioventricular septal defects (Fig. 16.65).
Fig. 16.64: Tetralogy of Fallot with atretic outflow tract.
Fig. 16.66: Double-outlet right ventricle (RV) variant of tetralogy
of Fallot. Note malalignment ventricular septal defect (arrow) with
> 50% aortic override.
Double-outlet RV variant (Fig. 16.66).
Absent pulmonary valve syndrome (Fig. 16.67).
Double-outlet RV requires at least 50% of each great
vessel to arise from the morphological RV. This broad
definition covers lesions from TOF to those with single-
ventricle physiology. The VSD is typically large and has
four potential locations: subaortic, subpulmonic, doubly
committed or remote. The insertion and location of the
outlet septum define which great vessel is related to the
VSD.
Tetralogy of fallot with absent pulmonary valve
syndrome is a rare cardiac malformation, usually
associated with a number of other defects.25 Congenital
absence of the leaflets of the pulmonary valve is

Fig. 16.67: Double-Outlet RV variant of tetralogy of Fallot with absent
pulmonary valve. There is narrowing of the pulmonary annulus and
pulmonary artery is aneurysmally dilated.
Fig. 16.69: Transthoracic echocardiographic short-axis view show
ing large ventricular (VSD) and absent right ventricular outflow tract
(RVOT) in a case with truncus arteriosus.
less common when the ventricular septum is intact.
Characteristic features of the syndrome include dysplasia
or absence of the pulmonary valvar leaflets, permitting
severe pulmonary regurgitation and aneurysmal dilation
of the pulmonary artery (Fig. 16.67).
In TOF adults, evaluation of surgical residua and
sequelae includes imaging of:26
Aortic-to-pulmonary arterial palliative shunts.
Detection of residual VSD.
Patch leaks.
Right ventricular outflow tract obstruction.
Definition of extracardiac conduit patency.
Quantitation of ventricular function and valvular
regurgitation.
Congenital Heart Disease in Adults 313
Fig. 16.68: Parasternal long-axis view showing Type 1 truncus
arteriosus.
In pulmonary atresia, persistence of descending
thoracic branches accounts for the abnormal pulmonary
arterial supply in this condition. Major aortopulmonary
collateral arteries may anastomose at any site in the
pulmonary vascular tree. Most frequently, the right and left
pulmonary arteries are patent and maintain free comm
unication with each other; they are termed confluent
pulmonary arteries. The pulmonary arteries may also be
hypoplastic and nonconfluent. No antegrade blood flow is
present from the RV to the pulmonary arteries. The ductus
arteriosus is often an important source of blood supply,
although it is occasionally absent.
TRUNCUS ARTERIOSUS OR
COMMON ARTERIAL TRUNK
Truncus arteriosus or common arterial trunk is a very
uncommon lesion in adults, and essentially all adult
patients will have had surgical intervention (Figs 16.68
and 16.69).
It consists of a single arterial trunk giving origin to the
pulmonary arteries, coronary arteries and the systemic
circulation.27
It is rare even among congenital heart lesions, occu
rring in only 1%.
The Society of Thoracic Surgeons classification simply
combines Types 1 and 2 (main pulmonary trunk or
branches coming off the trunk).
The common trunk is large, and cystic medial necrosis
is usually present, resulting in further dilatation as the
patient ages.
314 Section 5: CHD, Aorta and Pericardium
Fig. 16.70: Paraternal long-axis view showing subaortic membrane
(arrow). The right panel shows peak gradient of 64 mm Hg across the
membrane with regurgitation as well.
Fig. 16.72: Cleft anterior mitral leaflet (AML) (single yellow arrow) with
subaortic membranous orifice (white arrows).
The common trunk usually overrides the VSD and is
committed to both ventricles.
The VSD is large and nonrestrictive and results from
absence of the infundibular septum. It lies between the
two limbs of the septomarginal trabeculation.
The truncal valve may have from 1 cusps to 6 cusps.
In 1 study, 61% had a tricuspid truncal valve, 31% a
quadricuspid valve and 8% a bicuspid valve.
Poor valve function (mostly incompetence) usually
results in early heart failure and death in infancy.
The coronary arteries may arise above the truncal
leaflets in a variety of positions, although many are
normally located.
Fig. 16.71: 3DE en face view of the orifice of the membrane (arrows)
in the left ventricular outflow tract (LVOT) (left panel) compared to
profile view in 2DE long-axis view (right panel).
SUBAORTIC MEMBRANOUS STENOSIS
Subaortic membrane (SAM) is a form of fixed subaortic
obstruction in which a fibrous membrane is located below
the aortic valve (Fig. 16.70).
Subaortic membrane may involve the ventricular
septum, the anterior leaflet of the mitral valve, and the
aortic valve itself (Fig. 16.71).28 It may be associated with
other structural anomalies of the aortic valve such as:
bicuspid aortic valve
abnormalities of the left ventricular outflow tract,
such as in atrioventricular canal (Fig. 16.72) or tunnel
subaortic stenosis.
Ventricular septal defect can also be associated with
SAM (Fig. 16.73).
PHYSIOLOGY AND PATHOLOGY
The subaortic stenosis causes problems in several different
ways. It may obstruct left ventricular outflow and cause
subaortic stenosis. The resultant effects are essentially
the same as valvular aortic stenosis: left ventricular
hypertrophy from the pressure overload, myocardial
ischemia.
A SAM may alter left ventricular outflow dynamics and
harm the aortic valve without any significant obstructive
component. The abnormal flows cause aortic insufficiency
and permanent structural damage to the aortic valve.
There may be other effects from SAM as well, including
permanent damage to the mitral valve and direct damage

Fig. 16.73: Subaortic stenosis (white arrow) with subaortic ventricular
septal defect (yellow arrow) with color flow map.
Fig. 16.75: Flow regurgitation from the membrane in diastole.
to the aortic valve, if the membrane grows up into the
aortic valve itself.
The abnormal flow characteristics that initiate the
growth of a SAM may allow the regrowth of the membrane,
even after complete resection.
Echocardiographic features are:
Direct visualization of the membrane at varying
distance from the aortic valve (Fig. 16.74).
A high systolic flow velocity in the LVOT.
Increased turbulence in the LVOT begins proximal to
the aortic valve.
Varying degree of aortic regurgitation (Fig. 16.75).
Real-time 3DE has considerably advanced our
understanding and visualization of the subaortic stenosis.29
Note only the rims of the membrane can be seen well
Congenital Heart Disease in Adults 315
Fig. 16.74: Subaortic membrane very close to the aortic valve (arrow)
with aortic regurgitation (see inset).
Fig. 16.76: Real-time 3DE in parasternal long-axis view showing the
membrane (arrow) and its relationship to the aortic valve.
(Fig. 16.76), the membrane can be seen en face as well and
the area can be planemetered.
TRANSPOSITION OF GREAT VESSELS
In adults, it is not unusual to see corrected transposition
of great vessels and operated complete transpositions.30
This may be asymptomatic or may present with left-sided
tricuspid valve regurgitation or heart blocks (Figs 16.77
and 16.78).
In simple transposition, usually such patients are seen
with Mustard repair or Senning atrial switch (Figs 16.79
and 16.80).
It is necessary to study atrioventricular and ventri
culoarterial relationships to identify the transpositions.
Some patients with single ventricle with malpositions
also survive into adulthood (Fig. 16.81).
316 Section 5: CHD, Aorta and Pericardium

Fig. 16.77: Atrioventricular discordance. Fig. 16.78: Ventriculoarterial discordance.

Fig. 16.79: Complete transposition of great vessels with Senning Fig. 16.80: Direction of pulmonary venous blood flow through the
operation. Baffle is seen draining pulmonary venous blood into the baffle after Senning operation.
right-sided circulation.

Fig. 16.81: Morphologically left ventricle (LV) type of single ventricle. Fig. 16.82: Same patient as in Figure 16.81. Both great vessels come
out off the single ventricle (SV) with infundibular pulmonary stenosis
and D-malposition of great vessels.

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 Chapter

17
Aorta: Congenital and
Acquired Disorders

Introduction
There is increasing awareness of acute and chronic aortic
disorders and the pivotal role of echocardiography in
diagnosis and monitoring prognosis. There is a variety
of congenital and heritable disorders that affect aorta.
Acute aortic disorders presenting in emergency include
aortic dissection, intramural hematoma and aortic ulcer,
and rarely traumatic aortic transection. Longitudinal
progression of chronic aortic diseases and appropriate
timing of open or endovascular surgery are usually
derived from serial noninvasive imaging studies including
echocardiography. Echocardiography, especially tran
sesophageal one, is an ideal imaging modality for
detecting precisely, safely and rapidly suspected acute or
Fig. 17.1: Graphical description of anatomy of aorta.
chronic pathology of ascending aorta with quantitative
information on aneurysm formation and progression,
as well as on tear location, extent and type of dissection diameter, and after ascending for a short distance, arches
including evaluation for imminent complications. Ultra backward and to the left side, over the root of the left
sound techniques for imaging of the aorta include lung; it then descends within the thorax on the left side
transthoracic echocardiography (TTE), transesophageal of the vertebral column, passes into the abdominal cavity
echocardiography (TEE), abdominal ultrasound and through the aortic hiatus in the diaphragm and ends,
intravascular ultrasound. However, echocardiography considerably diminished in size (approximately 1.75 cm in
has limited role in detecting aortic pathology at sites other diameter), opposite the lower border of the fourth lumbar
than ascending aorta. vertebra, by dividing into the right and left common iliac
arteries (Fig. 17.1).
Structure of Aorta
Parts of Aorta
The aorta is the main trunk of vessels, which conveys
the oxygenated blood to the body. It commences at the Aortic root: The root is the beginning of the aorta.
upper part of the left ventricle, where it is about 3 cm in Starting from the aortic valve (annulus) and becoming
 Aorta: Congenital and Acquired Disorders 319

Fig. 17.2: Graphic view of aortic root, sinotubular junction and ascen Fig. 17.3: Suprasternal long-axis view showing aortic root, ascending
ding aorta. aorta and its arch.
(LVOT: Left ventricular outflow tract; RPA: Right pulmonary artery). (IA: Innominate artery; LPA: Left pulmonary artery; RPA: Right
pulmonary artery; LV: Left ventricle).

The ascending aorta is covered at its origin by

the pulmonary trunk and the right atrial appendage
and, higher up, is separated from the sternum by the
pericardium, the right pleura, the anterior margin of the
right lung, some loose areolar tissue and the remains of
the thymus; posteriorly, it rests upon the left atrium and
right pulmonary artery (Fig. 17.4). On the right side, it is
in relation with the superior vena cava and right atrium,
the former lying partly behind it; on the left side, with the
pulmonary artery.
Aortic arch: The arch represents the curved portion
at the top of the aorta. The innominate, left common
carotid and left subclavian arteries, which supply
blood to the head and upper body, branch from the
Fig. 17.4: Tilted parasternal long-axis view showing aortic root and arch. It is outside the pericardial sac and generally has
ascending aorta with posterior relationship. better support from surrounding structures (Fig. 17.5).
The aortic arch is divided into proximal (immediately
distal to the innominate artery) and distal (immediately
slightly wider in diameter (sinuses of Valsalva), it gives distal to the left common carotid artery) segments.
rise to two coronary arteries and ends at the beginning Descending aorta: This section begins just beyond the
of the ascending aorta (sinotubular junction) (Fig. 17.2). origin of left subclavian artery at a relatively narrower
Ascending aorta: This segment of 5 cm length extends portion called isthmus. The descending aorta ends
upward from the aortic root to the point where the at the diaphragm. It contains the intercostal arteries
innominate artery branches off the aorta, and the that feed the spinal cord. The beginning portion of the
aorta begins to form an arch (Fig. 17.3). It is within descending aorta is vulnerable to intimal tear during
the pericardium and no arteries branch from it. There deceleration conditions (Fig. 17.6).
is little support from surrounding tissue and it must Thoracoabdominal aorta: This section begins at the
face the entire cardiac output volume, making the diaphragm and ends at the visceral vessels (celiac,
ascending segment the most vulnerable part of the superior mesenteric and renal arteries) (Figs 17.7
aorta. and 17.8).
320 Section 5: CHD, Aorta and Pericardium
Fig. 17.5: Suprasternal long-axis view showing end of the arch at
origin of the left subclavian artery and beginning of the descending
thoracic aorta.
Fig. 17.7: Thoracoabdominal aorta in subcostal long-axis view.
Abdominal aorta: The abdominal aorta begins below
the renal arteries. The aorta ends where it divides into
the two iliac arteries. It contains a small artery named
the inferior mesenteric artery.
Functions of Aorta
Aorta and its proximal branches act as an elastic buffering
chamber beyond the left ventricle (the Windkessel
function) and store about 50% of the left ventricular stroke
volume during systole. In diastole, the elastic forces of the
aortic wall forward this 50% of the volume to the peripheral
circulation, thus creating a nearly continuous peripheral
blood flow (Fig. 17.9).
Fig. 17.6: Descending thoracic aorta begins just beyond the origin
of the left subclavian artery. The segment between the arch and the
descending thoracic aorta is called isthmus.
Fig. 17.8: Thoracoabdominal aorta viewed in subcostal long-axis view
showing celiac axis and superior mesenteric artery (SMA).
This systolicdiastolic interplay represents the
Windkessel function, which results in reduction of left
ventricular afterload and better coronary blood flow and
left ventricular relaxation.1
The elastic resistance (or stiffness), which the aorta sets
against its systolic distention, increases with aging, with an
increase in blood pressure, and with pathological changes
such as atherosclerosis.
This increased stiffness leads to an increase in systolic
blood pressure and a decrease in diastolic blood pressure
at any given mean pressure, an increase in systolic blood
velocity, an increase in left ventricular afterload and a
decrease in subendocardial blood supply during diastole.

Fig. 17.9: Windkessel phenomenon in proximal aorta shown
graphically.
Fig. 17.11: Normal measurements of aorta.
The elastic properties of the aortic Windkessel can
be assessed in vivo in humans in several ways including
tissue velocity imaging and deformation imaging. With
reduced elasticity, positive circumferential strain tends to
decrease (Fig. 17.10).
Normal Aortic Measurements and
Imaging Views
Using different windows, the proximal ascending aorta
is visualized in the left and right parasternal long-axis
views (Fig. 17.4) and, to a lesser extent, in basal short-axis
views. The long-axis view affords the best opportunity for
measuring aortic root diameters by taking advantage of
the superior axial image resolution. In all patients with
Aorta: Congenital and Acquired Disorders 321
Fig. 17.10: Study of aortic circumferential strain by velocity vector
imaging.
suspected aortic disease, the right parasternal view is
recommended for estimating the true size of the ascending
aorta.
The ascending aorta is also visualized in the apical long-
axis and modified apical five-chamber views; however,
in these views, the aortic walls are seen with suboptimal
lateral resolution.
Measurements of aortic diameter by echocardiography
are accurate when care is taken to obtain a true perpen
dicular dimension and gain settings are appropriate.
Standard measurement conventions established the
leading edge-to-leading edge diameter in end diastole
and the normative data published in the literature were
obtained using the leading edge technique. Some favor
inner edge-to-inner edge diameter measurements to
increase reproducibility and match those obtained by
other methods of imaging the aorta. However, recent
improvements in echocardiographic image quality
and resolution minimize the differences between these
measurement methods.
Normal measurements of various aortic segments are
shown in Figure 17.11.
In a normal ascending aorta, the diameter at sinus
level is the largest, followed by the sinotubular junction
and the aortic annulus.24
Suprasternal view depicts the aortic arch and the
three major supra-aortic vessels (innominate, left carotid
and left subclavian arteries), with variable lengths of
the descending and, to a lesser degree, ascending aorta
(Fig. 17.6).
322 Section 5: CHD, Aorta and Pericardium
Fig. 17.12: Visualization of mid portion of descending thoracic aorta in
parasternal long-axis view.
(LV: Left ventricle; LA: Left atrial)
The entire thoracic descending aorta is not well
visualized by transthoracic windows. A short-axis view of
the descending aorta can be imaged posteriorly to the left
atrium in the parasternal long-axis view. From the apical
window, a short-axis cross-section of the descending aorta
is seen lateral to the left atrium in the four-chamber view
and a long-axis stretch in the two-chamber view. By 90
transducer rotation, a long-axis view is obtained and a mid
part of the descending thoracic aorta may be visualized
(Fig. 17.12).
Transesophageal echocardiography is an ideal
modality to image ascending aorta, part of the arch
and descending thoracic aorta. The most important
transesophageal views of the ascending aorta, aortic root
and aortic valve are the high transesophageal long-axis (at
120150) and short-axis (at 3060) views (Fig. 17.13).
A short segment of the distal ascending aorta, just before
the innominate artery, remains unvisualized owing to
interposition of the right bronchus and trachea.
Like the ascending aorta, the descending aorta often
produces an artifactual pseudoaorta located posteriorly to
the true aorta (double-barrel aorta) in TEE views.4
Etiopathogenesis of
Aortic Disorders
Although most aortic disease is associated with
atherosclerosis and hypertension (i.e. aneurysms and
dissection), the spectrum of aortic disease is vast and
includes various congenital and acquired entities.
Fig. 17.13: Simultaneous long axis and short axis of the aortic root
obtained by three-dimensional transesophageal echocardiography.
(LV: Left ventricle)
The congenital group includes patent ductus arteriosus,
aortic hypoplasia, aortic coarctation, interrupted aortic
arch, aortopulmonary (AP) window, common arterial
trunk, supravalvular aortic stenosis (SAS), aneurysms of
sinus of Valsalva and vascular rings.
The acquired disorders include aortic dissection due
to extension of a coronary artery dissection, Marfan synd
rome, large-vessel vasculitis such as Takayasu arteritis,
mycotic aneurysms, aneurysms of sinus of Valsalva, and
so on.
Specific conditions associated with therapeutic
manoeuvre, such as recoarctation, stent-graft rupture and
endoleaks are also evaluated by echocardiography.
Congenital Disorders of Aorta
Unicuspid and Bicuspid Aortic Valve and
Associated Aortopathy
The bicuspid aortic valve is the most common congenital
abnormality of the human heart, affecting approximately
1% to 2% of the general population.
Unicuspid and bicuspid aortic valve are an inherited
anomaly and commonly associated with proximal aortic
dilatation.5,6 Unicuspid or bicuspid aortic valve is associated
with abnormal flow patterns and asymmetrically increased
wall stress in the proximal aorta (Figs 17.14 to 17.16).
In persons with bicuspid aortic valve (and also the
unicuspid aortic valve), the dimensions of the proximal
aorta (especially the tubular ascending aorta) are
significantly larger than those in persons with tricuspid
 Aorta: Congenital and Acquired Disorders 323

Fig. 17.14: Bicuspid aortic valve with proximal aortic dilatation in parasternal long-axis view.

A B

Figs 17.15A to C: Unicuspid aortic valve (A: TEE image and B: three-
dimensional echo in short axis) with aortic dilatation in TEE long-axis
view.
C (TEE: Transesophageal echocardiographic).
324 Section 5: CHD, Aorta and Pericardium
Fig. 17.16: Dilatation of the ascending aorta with normal aortic root in
an 18-year-old boy with unicuspid aortic valve.
Fig. 17.18: Graphical representation of aortic coarctation (left panel)
contrasted with actual echocardiographic picture.
aortic valve, even in the absence of significant valvular
hemodynamic disturbance. This has been empirically
linked to an increased risk of acute aortic complications
like aneurysm formation, dissection and rupture. Larger
dimensions of the ascending aorta at the time of aortic
valve surgery (i.e. 45 mm) might be associated with the
increased rate of late aortic events.
Aortic Coarctation
Aortic coarctation involves aortic narrowing in the
region of the ligamentum arteriosum just distal to the left
subclavian artery (Figs 17.17 and 17.18).
Aortic coarctation represents 7% of congenital heart
disease. It has a male predominance. The stenotic segment
frequently develops in a juxtaductal location but may show
Fig. 17.17: Suprasternal long-axis view showing tubular narrowing of
the descending thoracic aorta.
extension into the aortic arch and isthmus. The previous
classification into preductal (infantile) and postductal
(adult) is less commonly used because aortic coarctation
is always periductal.
Aortic coarctation occurs as a solitary lesion in 82%
of cases but has multiple associations, including Turner
syndrome, bicuspid aortic valve (seen in 2242% of cases),
intracranial aneurysms (10% of cases), ventricular and
atrial septal defects and Shone complex (i.e. left ventricular
outflow tract obstruction and parachute mitral valve).
Aortic coarctation may also be associated with aortic
hypoplasiaisolated isthmic hypoplasia, isolated aortic
arch hypoplasia or isthmic and aortic arch hypoplasia.7,8
A significant coarctation is when the ratio of
diameter of the coarct segment to aortic diameter at
diaphragm is 0.5. Examination by continuous wave
Doppler echocardiography is an effective noninvasive
method of assessing the severity of coarctation of the
aorta, particularly when systolic and diastolic events are
considered together (Fig. 17.19). Peak systolic gradient
of 40 mm Hg and diastolic pressure half time of 100
milliseconds are highly specific for severe coarctation.
Diastolic parameters are much more useful in assessing
severity. Recoarctation is defined by the presence of peak
systolic gradient 10 mm Hg.
Interrupted aortic arch is defined as a complete luminal
and anatomical discontinuity between the ascending and
descending aorta (Fig. 17.20). It is rare, accounting for only
1% of congenital heart diseases. It is of three types.8
Type A: It is defined as an interruption distal to the left
subclavian artery.

Fig. 17.19: Continuous wave Doppler interrogation of coarct segment
(left panel). Graphical description (right panel) shows systolodiastolic
gradients.
A B
Figs 17.21A and B: Type A aortic interruption with low-velocity continuous flow in thoracoabdominal aorta through aortopulmonary collaterals.
Type B: The absent segment is between the left
common carotid artery and left subclavian artery.
Type C: It is defined as an interruption distal to
the innominate artery. Descending thoracic aorta
reconstitutes from the pulmonary artery collaterals
(Fig. 17.21).
Aneurysm of Sinus of Valsalva
The Valsalva sinuses are three subtle dilatations of the
aortic root wall that arise between the aortic valve annulus
and the sinotubular ridge (Fig. 17.22).
Each sinus is associated with a corresponding right,
left or noncoronary aortic valve cusp.
Aneurysm of aortic sinuses, also known as aneurysm of
sinus of Valsalva, is a rare congenital disorder.
Aorta: Congenital and Acquired Disorders 325
Fig. 17.20: Type A aortic interruption (arrow) with hypoplastic pulmo
nary artery (PA) shown in suprasternal long-axis view.
Congenital aneurysm of sinus is caused by a dilatation,
usually of one sinus of Valsalva, due to a separation
between the aortic media and the annulus fibrosus
(Figs 17.23 to 17.26).
Right sinus is commonly involved (85%) and the left
sinus is least involved (< 5%).
Aneurysm of sinus of Valsalva may rupture into cardiac
chambers to establish aortocameral fistulae. The right
sinus usually ruptures in or communicates with the right
ventricular outflow tract, noncoronary sinus aneurysm in
right atrium and the left sinus of Valsalva may rupture into
the left ventricle, left atrium, pulmonary artery or in the
pericardium.9,10
The abnormality is usually congenital but may be
associated with Marfan Syndrome, Ehlers-Danlos
326 Section 5: CHD, Aorta and Pericardium
Fig. 17.22: Three-dimensional short-axis view showing all three
sinuses of Valsalva.
Fig. 17.24: Transthoracic parasternal long-axis view showing
aneurysm of right sinus of Valsalva (arrow).
Syndrome, cystic medial necrosis, trauma, infective endo
carditis, tuberculosis, syphilis and also atherosclerosis.
Aneurysms of the sinus of Valsalva are usually
diagnosed after an acute rupture into an adjacent cardiac
structure (Figs 17.25 to 17.27). Prior to rupture, aneurysms
of the sinus of Valsalva may present with conduction-
system abnormalities attributable to erosion into the
interventricular septum, thromboembolism originating
in the aneurysm sac, myocardial ischemia attributable
to coronary compression and aortic regurgitation
(Fig. 17.28).
Functional aortic regurgitation is related to the aortic
annulus/root mismatch. Aortic root dilatation, whether
symmetrical or asymmetrical, causes leaflet tethering.
Fig. 17.23: Aneurysm of right sinus of Valsalva shown in short-axis
view (arrow).
Gerbodes shunt, wherein the aneurysm communicates
with the right atrium, is the second commonest anomaly
(Figs 17.29 and 17.30).
Nonruptured aneurysms may be asymptomatic and
incidentally discovered, or they may be symptomatic
and manifest acutely with mass effect on adjacent
cardiac structures.
Ruptured Valsalva sinus aneurysms result in an
aortocardiac shunt and may manifest as insidiously
progressive congestive heart failure, severe acute chest
pain with dyspnea or, in extreme cases, cardiac arrest.
Cardiac tamponade may occur if the rupture involves
the pericardial space.
Aortic sinus aneurysm is more prevalent in Asian
countries and correlates with more supracristal
ventricular septal defects (VSDs; ~ 60%).
Associated structural defects in congenital aortic sinus
aneurysms included supracristal or perimembranous
VSD (3060%), bicuspid aortic valve (1520%) and
aortic regurgitation (4450%). Approximately 10% of
patients with Marfan syndrome have some form of
sinus dilatation (Fig. 17.31).
Two-dimensional (2D) Doppler echocardiography
easily makes this diagnosis, but real-time three-
dimensional (3D) echocardiography allows for complete
visualization of the aneurysm neck and its relation to
the surrounding structures, including the aortic valve
(Figs 17.32 and 17.33).
The criteria for diagnosing a Valsalva sinus aneurysm
include:
Origin above the aortic annulus.
Saccular shape.
 Aorta: Congenital and Acquired Disorders 327

A B
Figs 17.25A and B: Three-dimensional echocardiographic short-axis images showing windsock effect of aneurysm of right sinus of Valsalva
(arrows).

A B
Figs 17.26A and B: Color flow Doppler interrogation showing communication between the aneurysm of the right sinus with right ventricular
outflow tract (upper panel) in modified long-axis view. Continuous wave Doppler spectrum with continuous flow at high velocities is shown in
lower panel.

Fig. 17.27: Ruptured aneurysm of right sinus of Valsalva into the right ventricular outflow tract (arrow) with prominent diastolic flow accentuation
due to venturi effect (right panel) in the spectrum of systolodiastolic flow.
328 Section 5: CHD, Aorta and Pericardium

Fig. 17.28: Unruptured aneurysm of the right sinus of Valsalva (arrow) Fig. 17.29: Transesophageal echocardiographic view at 80 showing
with flail aortic leaflets due to loss of support to the aortic annulus. aneurysm of noncoronary sinus of Valsalva protruding into the right
atrium (arrows).

A B
Figs 17.30A and B: (A) Ruptured aneurysm of noncoronary sinus communicating with the right atrium just below the posterior tricuspid valve
leaflet. Figure B shows the color flow jet extending toward the tricuspid valve.

Fig. 17.31: Transthoracic short-axis view showing dilatation of all three Fig. 17.32: Three-dimensional echocardiographic view of aneurysm of
sinuses in a patient with Marfan syndrome. right aortic sinus (arrow).
 Aorta: Congenital and Acquired Disorders 329

Fig. 17.33: Three-dimensional echocardiographic short-axis view Fig. 17.34: Transesophageal echocardiographic midesophageal short
showing collapsed aneurysm of aortic sinus (white arrow) with axis showing communication between the right atrium and noncoro
incomplete aortic valve coaptation causing regurgitant orifice (red nary aortic sinus by color flow mapping (yellow arrow). Note aneurysm
arrow). of atrial septum with small jet of atrial septal defect (white arrow).

Table 17.1: Normal values of aortic dimensions It is an uncommon entity, representing approximately
Aortic annulus 13 1 mm/M2 0.1% of all congenital heart disease. It is explained by
Aortic root 19 1 mm/M2
incomplete fusion or malformation of right or left cono
truncal rings.
Sinotubular junction 15 1 mm/M2
Its pathophysiology shares similar hemodynamic
Ascending aorta 15 2 mm/M2
features with patent ductus arteriosus and truncus
Arch 15 2 mm/M2
arteriosus, and a frequent clinical manifestation is heart
failure.
Normal dimensions of the adjacent aortic root and Types of Aortopulmonary Window
ascending aorta (Table 17.1).
The above criteria differentiate the aortic sinus Type I or proximal communication occurs near the
aneurysm from the aneurysm of the membranous septum semilunar valves.
and subannular aortic pseudoaneurysms. Type II or distal communication involves the
Less commonly observed anomalies include pulmonary bifurcation at the level of the right pulmonary
pulmonary stenosis, coarctation and atrial septal defects artery.
(Fig. 17.34). In type III, there is a wide communication between the
Acquired aortocameral communications can be with aorta and pulmonary artery owing to total absence of the
or without aneurysmal dilatation of the aortic sinuses AP septum.
(Figs 17.35A and B).
Truncus Arteriosus
Aortopulmonary Window
Truncus arteriosus, also known as common arterial trunk,
Aortopulmonary window is defined as a communication is characterized by a single great artery that arises from the
between the ascending aorta and the pulmonary trunk, or base of the heart and supplies the systemic, coronary and
right pulmonary artery (Fig. 17.36). pulmonary blood flow and by a VSD (Fig. 17.37).
It is characterized by the presence of well-defined and This anomaly results from a septation failure during
separate aortic and pulmonary valve apparatuses, unlike development of the ventricular outlets and the proximal
in truncus arteriosus, where only an isolated truncal valve arterial segment of the heart tube. Four types of trunks are
is noted.10 described.
330 Section 5: CHD, Aorta and Pericardium

A B
Figs 17.35A and B: Communication between left coronary sinus and the left atrium following aortic valve replacement. Transesophageal
echocardiographic picture (A) with continuous wave Doppler flow across the hole.

Fig. 17.36: Type II aortopulmonary window (arrow) seen in low Fig. 17.37: Transthoracic parasternal long-axis view showing type I
parasternal short-axis view with some tilt. (RVOT: Right ventricle out truncus arteriosus. Arrow points to the ventricular septal defect.
flow tract; MPA: Main pulmonary artery; LPA: Left pulmonary artery;
RPA: Right pulmonary artery).

In type I, the main pulmonary trunk arises from the
truncal artery just distal to the truncal valve.
In types II and III, the pulmonary trunk is absent and
the right and left pulmonary branches arise posteriorly.
Type IV corresponds to pulmonary atresia with VSD
and multiple major AP collateral arteries.
The presence of a common truncal valve allows
differentiation from AP window, in which two separate
valves are noted. The truncal valve is often abnormal,
typically being stenotic or insufficient.
often involving the entire ascending aorta (15% of cases)
(Fig. 17.38).
Aortic or peripheral arterial system involvement is
not common. The other entities in this group are bicuspid
aortic valve, aortic coarctation and subaortic stenosis.11
Supravalvar aortic stenosis (SAS) is commonly associated
with WilliamsBeuren syndrome, an autosomal dominant
multisystemic disorder that may manifest with SAS
(71% of cases), mitral valve prolapse and pulmonary
artery stenosis.

Supravalvular Aortic Stenosis Patent Ductus Arteriosus

Supravalvular aortic stenosis is a focal or diffuse narrowing The patent ductus arteriosus is a vascular structure that
of the aorta starting at the sinotubular junction and connects the proximal descending aorta to the roof of the

Fig. 17.38: Aortic narrowing at the sinotubular junction associated with
valvular stenosis.
Fig. 17.40: Parasternal short-axis view for judging the size of ductus.
main pulmonary artery near the origin of the left branch
pulmonary artery (Fig. 17.39). In the normal heart with a
left-sided aortic arch, the ductus arteriosus connects the
left pulmonary artery near its origin to the descending
aorta just distal to the left subclavian artery.12
The physiological impact and clinical significance of
the ductus depend largely on its size and the underlying
cardiovascular status of the patient. The ductus may be
silent (not evident clinically but diagnosed incidentally
by echocardiography done for a different reason), small,
moderate or large.
The hemodynamic impact of ductus in an otherwise
normal cardiovascular system is determined by the
magnitude of shunting, which depends largely on the
flow resistance of the ductus arteriosus. The length,
Aorta: Congenital and Acquired Disorders 331
Fig. 17.39: Parasternal short-axis view showing patent ductus
arteriosus by color flow mapping (arrow).
the narrowest diameter, and the overall shape and
configuration of the ductus arteriosus determine
resistance.
Increased flow returning to the left heart results in
increased left atrial and left ventricular end-diastolic
pressures. The left ventricle compensates by increasing
stroke volume and eventually may hypertrophy to
normalize wall stress.
Two-dimensional imaging demonstrates the geometry
of the ductus. Color Doppler is a very sensitive modality
in detecting the presence of a ductus and is frequently
used to estimate the degree of ductal shunting (Fig. 17.40).
Even an extremely tiny patent ductus can be detected
by a color flow signal entering the pulmonary artery near
the origin of the left pulmonary artery. In patients with
high pulmonary vascular resistance and ductus, with low
velocity or right-to-left flow, the ductus arteriosus may be
very difficult to demonstrate with color flow Doppler, even
if it is large. Findings such as septal flattening, unexplained
right ventricular hypertrophy and high-velocity pulmonary
regurgitation should prompt a thorough investigation for a
ductus.
Following device closure of the ductus, flow obliteration
can be seen by echocardiography (Fig. 17.41).
ACQUIRED AORTOPATHIES
Marfan Syndrome
Marfan syndrome is a multisystemic connective tissue
disorder of autosomal dominant inheritance that is
characterized by skeletal, cardiovascular and ocular
abnormalities.13,14
332 Section 5: CHD, Aorta and Pericardium
Fig. 17.41: Ductus closure device (arrow) shown as projection in
pulmonary artery.
In the 2010 revised Ghent nosology, aortic root
aneurysm and ectopia lentis are cardinal features.
In the absence of any family history, the presence
of these two manifestations is sufficient for the
unequivocal diagnosis of the syndrome.
In the absence of any of these two, the presence of
bonafide FBN1 mutation or a combination of systemic
features is required.
Minor criteria consist of dilatation or dissection of
the descending or abdominal aorta before the age
of 50 years, dilatation of the main pulmonary artery
before the age of 40 years, mitral valve prolapse and
calcification of the mitral annulus before the age of 40
years.
Aortic root dilatation with Z score > 2 is a major criterion
(Figs 17.42 to 17.47). Cardiovascular major criteria include
dilatation of the ascending aorta (involving at least the
sinuses of Valsalva) with or without aortic regurgitation, as
well as dissection of the descending aorta.
Marfan syndrome is caused by mutations in the
fibrillin-1 gene (FBN1) on chromosome 15 (more than
135 mutations have been identified). FBN1 encodes for
microfibrils that connect the elastic lamina to adjacent
endothelial cells and smooth muscle cells, contribute to
structural integrity, and coordinate contractile and elastic
tension of the vessel wall. Dysfunction of microfibrils
causes disintegration and elastolysis of the connective
tissue, which ultimately result in aneurysm formation and
dissection. Aortic enlargement 4 cm or an increase in
Fig. 17.42: Annuloaortic dilatation in a 27-year-old female with skel
etal features of Marfan syndrome. Transthoracic echocardiographic
parasternal long-axis view.
aortic root diameter in patients with bicuspid aortic valve
or Marfan syndrome is associated with a dramatic increase
in risk of type A aortic dissection.15
Cardiovascular and valvular disease is seen in the
majority of patients (90%) and is the dominant cause of
mortality. The term annuloaortic ectasia refers to uniform
dilatation of all three sinuses of Valsalva, with extension
into the ascending aorta and obliteration of the normal
sinotubular ridge; it is found in 60% to 80% of adults with
Marfan syndrome (Figs 17.43 and 17.46).
The ectasia finally extends into the annulus, causing
aortic regurgitation, which may progress to root dissection
or rupture.16 With annular ectasia, the aortic valve assumes
triangular shape in diastole (Fig. 17.48).
Aortic aneurysm without annuloaortic ectasia is
not uncommon but is not classic of Marfan syndrome.
In comparison with atherosclerotic aortic aneurysms,
aortic aneurysms in Marfan syndrome commonly
occur in younger patients and enlarge more rapidly. In
addition, there may be a wide range of musculoskeletal
manifestations, including scoliosis, chest wall deformity,
arachnodactyly and acetabular protrusion.
In comparison with atherosclerotic aneurysms, the
aortic aneurysms seen in Marfan syndrome rarely show
intimal calcification or atherosclerotic plaques.
Takayasu Arteritis
Aortitis is caused by several connective tissue disorders
(e.g. Takayasus arteritis, temporal arteritis, ankylosing
 Aorta: Congenital and Acquired Disorders 333

Fig. 17.43: Another pattern of aortic root dilatation in a patient with Fig. 17.44: Tethering of the aortic valve leaflets due to root dilatation
suspected Marfan syndrome. Transesophageal echocardiographic causing severe aortic valve incompetence.
long-axis view.

A B
Figs 17.45A and B: Type I aortic valve regurgitation (right panel) due to annular dilatation.

Fig. 17.46: Normal aortic annulus diameter (22) but dilated aortic root, Fig. 17.47: Suprasternal long-axis view showing dilatation of the aortic
effacement of sinotubular ridge and aneurysmal ascending aorta in a root.
patient with classic Marfan syndrome.
334 Section 5: CHD, Aorta and Pericardium
Fig. 17.48: Aortic sinus dilatation causing triangular aortic valve
opening in diastole.
spondylitis, relapsing polychondritis) and infections
(e.g. bacterial endocarditis, syphilis, Rocky Mountain
spotted fever, fungal infections). It is also a feature of
Cogans syndrome (inflammatory keratitis, vestibular and
auditory dysfunction, and aortitis).
Takayasu arteritis is a primary large-vessel arteritis
of unknown origin that affects the aorta and its main
branches mainly in tropical countries.17
It basically affects young women (8090% of patients
with Takayasu arteritis are female and in the second or
third decade of life).
Echocardiography demonstrates aortic luminal
changes including stenosis, dilatation and aneurysm.
Furthermore, axial images demonstrate circumferential
wall thickening of the aorta and its involved branches,
thus allowing detection of Takayasu arteritis in the early
systemic phase, when inflammation or thickening of the
vessel wall may already be seen in the absence of luminal
abnormalities (Figs 17.49 to 17.51).
Left subclavian artery involvement is a major criterion
especially in females below the age of 40 years.
The Numano classification is based on the involved
anatomy.
Type I: Involvement of only the branches of the aortic
arch (Figs 17.50 and 17.51).
Type IIa: Involvement of the ascending aorta or the
aortic arch with or without branches.
Type IIb: Involvement of the descending thoracic aorta
with or without the ascending aorta or the aortic arch
with its branches.
Fig. 17.49: Circumferential wall thickening with markedly reduced
lumen of left subclavian artery in an 18-year-old young girl with
Takayasu arteritis. Arrow points to the residual lumen.
Type III: Involvement of the entire descending aorta
with or without the renal arteries.
Type IV: Involvement of only the abdominal aorta with
or without the renal arteries.
Type V: Involvement of the entire aorta with branches.
Involvement of the coronary or pulmonary arteries
should be indicated.
Atherosclerosis and Degeneration of Aorta
Echocardiography is commonly used to detect aortic
atheroma. The presence of detectable atherosclerotic
plaques in the aorta indicates the presence of athero
sclerotic disease and is a possible source of embolism.18
Atherosclerosis of the aorta is an independent predictor
of long-term neurological events and mortality.1922
Presence of plaque is defined as visible thickening of
the aortic wall (Figs 17.52 and 17.53). Maximal plaque
thickness and the maximal circumferential extent of
atheroma is measured in each segment.
The type of aortic atheromatous plaque is classified
simple or complex and also calcified or noncalcified. TEE
characterizes the plaque by assessing plaque thickness,
ulceration, calcification and superimposed mobile
thrombi, thereby determining the embolic potential of
each plaque.21,22
The grading of aortic atheroma is as follows:
Normal aorta (no intimal thickening).
Mild atherosclerosis (< 3 mm intimal thickening
without intimal irregularities).
Moderate aortic atherosclerosis (intimal thickening
3 mm, with diffuse irregularities and/or calcification).

Fig. 17.50: Longitudinal view of the right common carotid artery
showing markedly thickened walls (arrows).
Fig. 17.52: Transesophageal echocardiographic short-axis view of
descending thoracic aorta showing mild circumferential diffuse intimal
thickening (Grade II atheroma).
Severe atherosclerosis (> 5 mm intimal thickening
and one or more of the following: large protruding or
mobile atheromatous debris, ulcerated plaques and/
or thrombi).
Some have described mobile atheromas as Grade V
with highest embolic potential.21
Atherosclerotic plaques are defined as complex in the
presence of protruding atheromas of > 4 mm in thickness,
mobile debris or the presence of plaque ulceration
(Figs 17.54 and 17.55).
Aorta: Congenital and Acquired Disorders 335
Fig. 17.51: Duplex scan of the left common carotid artery with color
Doppler. Markedly reduced lumen in the middle with circumferential
diffuse wall thickening (arrows).
Fig. 17.53: Transesophageal echocardiographic longitudinal view of
the ascending aorta showing diffuse intimal thickening.
There is a strong association between aortic stenosis
and aortic atherosclerosis.
Presence of ulcerated plaques in the ascending aorta
and/or the aortic arch is associated with a significantly
greater prevalence of cerebral embolic events than that in
the absence of such plaques (Figs 17.55 and 17.56).
Acute Aortic Syndrome
Diseases of aorta that present with acute severe chest or
back pain with hemodynamic impairment are collectively
labeled as acute aortic syndrome. These include:4,23
336 Section 5: CHD, Aorta and Pericardium
Fig. 17.54: Grade III atheroma in the aortic arch. There is localized
thickening with no calcification.
Fig. 17.56: Grade IV atheroma in the aortic arch with penetrating ulcer.
Note the ulcerated plaque with a crater (arrow).
Aortic dissection.
Intramural hematoma.
Impending rupture of aortic aneurysm.
Penetrating atheromatous ulcers.
Traumatic transection of aorta.
Degenerative Aortic Aneurysms
Disease processes affecting the ascending and arch
aorta include degenerative aneurysms and aneurysms
associated with connective tissue disease, as well as acute
aortic dissection and its variants of intramural hematoma
and penetrating ulcer.
An aortic aneurysm is a general term for any dilation
of the aorta to > 1.5-times normal, usually representing
Fig. 17.55: Calcified atheromatous ulcer in anterior wall of the
ascending aorta close to sinotubular junction with protrusion (arrow).
Fig. 17.57: A 12-year-old boy with aneurysm of aortic root. Although
the root diameter is only 3.8 cm, Z score is > 2.
an underlying weakness in the wall of the aorta at that
location (Fig. 17.57).
The most common acquired condition predisposing
patients to dissection is chronic hypertension, which is
present in 75% of cases.24
Elevated arterial pressure leads to intimal thickening,
fibrosis and calcification. This limits blood supply to
the arterial wall. In addition, the extracellular matrix is
modified with enhanced apoptosis and elastolysis.
Atherosclerosis leads to adventitial fibrosis and
compromise of the vasa vasorumthe small vessels that
penetrate into the vessel wall.
All of the above lead to necrosis of the smooth muscle
cells and fibrosis of elastic structures in the media,
resulting in stiffness, weakness and a vulnerability to shear

Fig. 17.58: Transthoracic echocardiographic parasternal long-axis
view showing aneurysm of the descending thoracic aorta behind left
atrium.
Fig. 17.60: Dissecting aneurysm confined to descending thoracic
aorta and below.
forces. With time, this leads to aneurysmal dilation and
dissection.25
Morphologically, aneurysms are classified into three
types.26
1. Fusiform (spindle-shaped), which involve the entire
circumference of the aorta (Fig. 17.58).
2. Sacciform, which are characterized by a pouch-
like protrusion from a narrow opening in the aortic
wall.
3. Dissecting aorta, which is characterized by intramural
separation, usually within the medial layer.
Two commonly used classification for aortic dissection
Aorta: Congenital and Acquired Disorders 337
Fig. 17.59: Aortic dissection confined to ascending aorta.
Fig. 17.61: Dissecting aneurysm spreading down and upward from
the arch of aorta.
are that by DeBakey and by Stanford University.27,28 There
are some differences between the two, which are shown
graphically in Figures 17.59 to 17.61.
In the Stanford system, type A dissections involve the
ascending aorta, while type B dissections involve only the
descending aorta.
In the DeBakey classification system, a type I dissection
involves the entire aorta, while a type II dissection involves
only the ascending aorta and a type III dissection involves
only the descending aorta.
Of all aortic dissections, 50% are type I, 35% are type II
and 15% are type III.
338 Section 5: CHD, Aorta and Pericardium
Fig. 17.62: Graphical representation of aortic dissection.
The importance of aortic diameter in determining risk
for complications has been demonstrated in numerous
studies. The normal ascending aortic diameter is
23 cm depending on patient age, size and sex. The risk
for aortic rupture, dissection or death for the ascending
aorta relative to absolute size has been well characterized
with rupture reaching up to 10% per annum in case the
diameter exceeds 6 cm. An aneurysm 5 cm diameter
warrants intervention.23
Aortic Dissection
Aortic dissection occurs when a tear in the inner wall of the
aorta causes blood to flow between the layers of the wall of
the aorta, forcing the layers apart. The dissection typically
extends anterograde, but can extend retrograde from the
site of the intimal tear.
Because mechanical stress in the aortic wall is
proportional to blood pressure and vessel diameter,
hypertension and aortic dilation are known risk factors for
dissections.
Most aortic dissections occur with a transverse tear
along the greater curvature of the aorta a few centimeters
above the aortic valve (Fig. 17.62).
Type A aortic dissection, defined here as the presence
of dissection proximal to the left subclavian artery,
represents a true cardiac surgical emergency (Figs 17.63
and 17.64). Its mortality if left untreated has been estimated
from classical studies at 1% per hour for the first 48 hours
and can result in a mortality rate exceeding 80% in the first
month. Pericardial tamponade is the most common cause
of death from aortic dissection.
Fig. 17.63: Apical three-chamber view showing intimal flap in
ascending aorta.
As blood flows down the false lumen, it may cause
secondary tears in the intima. Through these secondary
tears, the blood can re-enter the true lumen (Fig. 17.64).
Entry tear size is of major prognostic significance since
it causes greater inflow volume into the false lumen, which
may increase its diastolic pressure and lead to an increase
in wall stress and, consequently, a greater risk of aortic
dilatation or rupture.
Classic aortic dissection is a longitudinal split or
partition in the media of the aorta. An intimal tear connects
the media with the aortic lumen, and an exit tear creates a
true and a false lumen. The smaller true lumen is lined by
intima, and the false lumen is lined by media. Typically,
flow in the false lumen is slower than in the true lumen,
and the false lumen often becomes aneurysmal when
subjected to systemic pressure (Figs 17.65A and B).
Characters of the True Lumen
Usually smaller than the false lumen.
Shows systolic expansion (false lumen shows systolic
compression).
Systolic antegrade flow by Doppler.
No thrombus.
Brisk contrast flow.
Flow from true to false lumen in systole through the
communication.
The TEE is an excellent test in the diagnosis of aortic
dissection, with a sensitivity of up to 98% and a specificity of
up to 97%.29 It has become the preferred imaging modality
for suspected aortic dissection. It is especially good in
 Aorta: Congenital and Acquired Disorders 339

Fig. 17.64: Transesophageal echocardiographic view showing waving intimal tear in ascending aorta with a hole.

A B
Figs 17.65A and B: Transesophageal echocardiographic midesophageal short-axis view showing true lumen (TL) and the false lumen (FL).
(B)shows flow in the true lumen.

the evaluation of aorta in the setting of ascending aortic
dissection, and to determine whether the ostia (origins) of
the coronary arteries are involved.
In addition, TEE has also an important role in the
follow-up of patients with aortic dissection as it shows the
structure of the dissection, surgical repair, healing of the
dissection and obliteration of the false lumen, or blood flow
dynamics in true and false lumina (Figs 17.66 and 17.67).
Three-dimensional TTE/TEE provides additional
information to 2D TTE/TEE in aortic dissection assessment,
particularly in entry tear size quantification. Agreement
between entry tear area defined by 3D TEE and computed
tomography is excellent. Three-dimensional TEE permits
better morphological and dynamic understanding of aortic
dissection when the flap is spiroidal. This technique may
be particularly useful in the indication and monitoring of
surgical or endovascular treatment of aortic dissection.
In the ascending aorta, particularly when dilated,
linear reverberation images are very common, being
observed in 4455% of studies and must not be confused
with dissection flaps. Three-dimensional TEE helps to
identify these artifacts (Fig. 17.68).
Intramural Hematoma
In approximately 13% of aortic dissections, there is no
evidence of an intimal tear. It is believed that in these
cases, the inciting event is an intramural hematoma
(caused by hemorrhage within the media). Since there
340 Section 5: CHD, Aorta and Pericardium
Fig. 17.66: High transesophageal echocardiographic view showing
dissection in ascending aorta.
(FL: False lumen; TL: True lumen).
Fig. 17.68: Full volume three-dimensional transthoracic echocardio
graphic imaging of the ascending aorta.
is no direct connection between the true lumen and the
false lumen in these cases, it is difficult to diagnose an
aortic dissection. An aortic dissection secondary to an
intramural hematoma should be treated the same as one
caused by an intimal tear.30
Intramural hematoma is characterized by circular or
crescentic thickening of the aortic wall > 5 mm (Fig. 17.69).
Inner margin of intramural hematoma is smooth,
and aortic thickening occurs beneath the bright
echo-dense intima, whereas an irregular margin with
dilated aorta is commonly observed in patients with
aneurysmal dilatation and mural thrombi. Intramural
hematoma is quite easily differentiated from classical
aortic dissection with flow in two lumina.30
Fig. 17.67: High transesophageal echocardiographic view showing
dissection in ascending aorta. Flow moving into false lumen during
systole. (FL: False lumen; TL: True lumen).
Fig. 17.69: Intramural hematoma (IMH) in the arch of aorta.
Penetrating aortic ulcer presents as an image of crater-
like outpouching with jagged edges in the aortic wall,
generally associated with extensive aortic atheromas31
(Fig. 17.70).
True Versus False Aneurysms of Aorta
Thoracic aortic aneurysms can be broadly divided
into true aneurysms and false aneurysms (pseudo
aneurysms). True aneurysms contain all three layers of
the aortic wall (intima, media and adventitia), whereas
false aneurysms have fewer than three layers and are
contained by the adventitia or periadventitial tissues
(Figs 17.71 to 17.73).

Fig. 17.70: Penetrating ulcer in the arch.
Fig. 17.72: Pseudoaneurysm containing thrombus and no apparent
communication with the thoracic aorta.
In summary, aorta needs greater attention by those
performing echocardiography. It is therapeutically and
prognostically important in a large number of conditions.
Aortic degenerative diseases are likely to increase with
increased longevity and ever-increasing diabetes and
hypertension. TTE remains an initial screening technique
and TEE should be performed with reasonable suspicion of
aortic dissection or penetrating ulcer. Both techniques can
be used for imaging surveillance as well as for follow-up
of patients after endovascular repair and surgery.
Aorta: Congenital and Acquired Disorders 341
Fig. 17.71: Pseudoaneurysm (A) of descending thoracic aorta with a
narrow neck (arrow). Note the presence of thrombus in the pseudo
aneurysm.
Fig. 17.73: To-and-fro flow across the neck of the pseudoaneurysm.
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 Chapter

18 Pericardial Diseases

Introduction
Pericardium is a double-layered sac with minimal fluid
which covers the heart and the base of great vessels. It fixes
the heart to the mediastinum, acts as a protective barrier
against infections, prevents excessive dilatation and offers
lubrication during movements. The common disorders
that affect pericardium are its partial absence, acute
pericarditis, pericardial effusion (PE), cardiac tamponade,
constrictive pericarditis (CP), pericardial tumors and so
on. Echocardiography provides a useful tool to detect,
treat and monitor the progress of pericardial diseases.

ECHOCARDIOGRAPHIC
ANATOMY OF PERICARDIUM
Pericardium is a double layered membrane which
covers the heart. It is placed behind the sternum
and the cartilages of the third, fourth, fifth, sixth and
seventh ribs of the left side, in the mediastinal cavity.1
The space between the two layers of it is filled with a
pericardial fluid (1550 mL) that protects the heart
from any kind of external jerk or shock (Figs 18.1
and 18.2).
There are two layers to the pericardial sac: the
outermost fibrous pericardium and the inner serous
pericardium.
The serous pericardium, in turn, is divided into two
layers, the parietal pericardium, which is fused to and
Fig. 18.1: Graphic representation of the conical fibroserous sac of
pericardium (white solid line) and the structure contained by it
besides the heart. (SVC: Superior vena cava; IVC: Inferior vena cava;
AO: Aorta; PT: Pulmonary trunk).
inseparable from the fibrous pericardium, and the
visceral pericardium, which is part of the epicardium
(Fig. 18.3).
The epicardium is the layer immediately outside of the
myocardium.
The visceral layer extends to the beginning of the great
vessels, becoming one with the parietal layer of the
serous pericardium. This happens at two areas; where
the aorta and pulmonary trunk leave the heart and
where the superior vena cava, inferior vena cava (IVC)
and pulmonary veins enter the heart.
344 Section 5: CHD, Aorta and Pericardium

Fig. 18.2: Frontal View: Outline of the pericardial space by injecting Fig. 18.3: Separation of two layers of pericardium in a subject with
a small amount of contrast in a normal person. White arrow shows fluid collection in the pericardial space.
posterior interventricular groove. (AV: Atrioventricular; RV: Right ventricular; LV: Left ventricular;
AO: Aorta; LA: Left atrium).

Fig. 18.4: Pericardium outlined by its calcification in left anterior Fig. 18.5: Chest Skiagram in lateral view of thorax showing
oblique view. It rests on diaphragm below and is separated from the relationship of the pericardium. The arrows point toward pericardial
spine by the oesophagus and the descending thoracic aorta. calcification that posteriorly ends in atrioventricular groove.

In between the parietal and visceral pericardial layers the phrenic nerve, with its accompanying vessels,
there is a potential space called the pericardial cavity. descends between the pericardium and pleura on
It is normally lubricated by a film of pericardial fluid either side.
(Fig. 18.2).
Anteriorly, it is separated from the anterior wall of the PERICARDIAL DISORDERS
thorax, in the greater part of its extent, by the lungs and
pleurae. The principal manifestations of pericardial disease are:
Posteriorly, it rests upon the bronchi, the oesophagus, Acute pericarditis.
the descending thoracic aorta and the posterior part Pericardial effusion.
of the mediastinal surface of each lung (Figs 18.4 Cardiac tamponade.
and 18.5). Transient or irreversible CP.
Laterally, it is covered by the pleurae, and is in Pericardial calcification.
relation with the mediastinal surfaces of the lungs; Invasion by neoplastic diseases.

Fig. 18.6: Transthoracic apical 4-CV showing apical dyskinesis with
thrombus, T (acute anterior myocardial infarction). Yellow arrow points
toward pericardial effusion.
Fig. 18.8: Pericardial effusion (arrows) with typical clinical picture of
acute pericarditis in an elderly female with hypothyroidism.
Pericardial cysts.
Pericardial hematoma (e.g. in cardiac rupture, aortic
dissection, etc.)
Acute pericarditis and PE are two distinctly different
clinical entities, which on occasion may be present
simultaneously. In some cases, the clinical presentation
of acute pericardial inflammation predominates, and
the presence of excess pericardial fluid is clinically
unimportant. In other cases, the effusion and its clinical
consequences (cardiac tamponade) are of primary
importance.
The major causes of pericardial diseases include:
Viral infection.
Pyogenic pericarditis.
Tuberculosis.
Pericardial Diseases 345
Fig. 18.7: Parasternal short-axis view showing site of left ventricular
rupture (arrow) with localized pericardial hematoma (PE).
Myocardial infarction (Figs 18.6 and 18.7).
Cardiac surgery.
Recent or remote sharp or blunt chest trauma.
Cardiac diagnostic or interventional procedure.
Drugs and toxins.
Metabolic disorders, especially uraemia, dialysis and
hypothyroidism.
Malignancy, especially lung and breast cancer,
Hodgkin lymphoma and mesothelioma.
Mediastinal radiation, recent or remote.
Collagen vascular diseases.
Idiopathic.
Rheumatic fever.
Pericardial disease may also be a feature of other
disorders, including inflammatory bowel disease and
familial Mediterranean fever. Aortic dissection or free
wall rupture should also be considered in patients with
unstable hemodynamics and PE.
ACUTE PERICARDITIS AND
PERICARDIAL EFFUSION
Acute pericarditis refers to inflammation of the pericardial
sac. Acute pericarditis is a common disorder caused by
inflammation of the pericardium and can occur as an
isolated entity or as a manifestation of an underlying
systemic disease (Fig. 18.8).
Acute pericarditis is diagnosed in approximately 0.1%
of hospitalized patients and in 5% of patients admitted
to the emergency department with noncardiac chest
pain (Fig. 18.8).
346 Section 5: CHD, Aorta and Pericardium
Fig. 18.9: Transthoracic echocardiographic parasternal long-axis view
showing mild pericardial effusion (PE) in a patient on maintenance
hemodialysis. Typical signs of pericarditis were present.
Initial evaluation includes a clinical history and
physical examination, electrocardiographic (ECG),
echocardiography, chest radiography and lab studies.
At least two of the following four criteria should be
present to diagnose pericarditis:2
Characteristic chest pain
Pericardial friction rub
Suggestive ECG changes
New or worsening PE
In most patients, the cause of acute pericarditis is
thought to be idiopathic because the yield of diagnostic
tests to confirm aetiology has been relatively low.
The term myopericarditis, or perimyocarditis, is used
for cases of acute pericarditis that also demonstrate
myocardial inflammation. The term myopericarditis
indicates a primarily pericardial syndrome with
minor myocardial involvement, which describes the
majority of combined pericarditis and myocarditis
cases encountered in clinical practice. On the other
hand, the term perimyocarditis indicates a primarily
myocardial syndrome.34 However, these two terms
are often used interchangeably without regard to the
predominant type of cardiac involvement (Fig. 18.9).
Myocarditis is common in acute pericarditis especially
with viral etiology but also in other inflammatory and
systemic disorders (Fig. 18.10).
Echocardiography aids in the detection, localization
and quantification of PE.
The appearance of the normal pericardium in M-mode
or two-dimensional echocardiography is that of a bright,
Fig. 18.10: Transthoracic parasternal short-axis view. Pericardial
effusion (arrows) in a 44-year old female with endomyocardial fibrosis.
dense layer of echoes inseparable from the epicardial echo
with a thickness of about 2 mm.
The sensitivity of echocardiography in detecting
pericardial fluid is very high and even 20 mL of fluid
inside the pericardium may be visualized.5 Since even
healthy individuals occasionally may have up to 50 mL
of pericardial fluid, echocardiographic visualization
of a very small amount of pericardial fluid (in an
otherwise healthy individual) should not be cause for
concern (Fig. 18.11).
The size of the effusion may be graded as:5-7
Small (echo-free space in diastole < 10 mm,
corresponding approximately to 300 mL).
Moderate (1020 mm, corresponding to 500 mL).
Large (> 20 mm, > 700 mL) (Fig. 18.12).
Alternatively, Horowitz et al.8 classified PE as:
Type A: No effusion.
Type B: Systolic separation of epicardium and pericar
dium (316 mL).
Type C1: Systolic and diastolic separation of epicardium
and pericardium (> 16 mL).
Type C2: Systolic and diastolic separation of pericar
dium with attenuated pericardial motion.
Type D: Pronounced separation of epicardium and
pericardium with large echo-free space.
Type E: Pericardial thickening (> 4 mm).
Important points for estimating PE are:
Even in diffused and circumferential effusion
dimensions of the echo-free space may be different

Fig. 18.11: M-mode cross-section of a healthy 19-year old boy show-
ing separation of two layers of pericardium with some fluid (arrow).
Fig. 18.13: Localized pericardial effusion (PE) (arrow) adjacent to the
lateral wall.
in the examined views and therefore it is more correct
and easy to measure and annotate the dimension of
the effusion and to report where it has been.
This methodology not only facilitates the definition of
effusion size, but it allows follow-up studies, detecting
changes in the amount of pericardial fluid after therapy.
Most PEs are circumferential, and therefore moderate
and large effusions in particular result in echo-free
spaces along the entire heart profile in the different
views.
Small or loculated effusion (Fig. 18.13) may be observed
only in the posterior regions or (particularly iatrogenic
and postsurgical effusion) along one or more heart
Pericardial Diseases 347
Fig. 18.12: Comparing mild versus large pericardial effusion.
Fig. 18.14: Pericardial fluid reflecting at posterior atrioventricular
groove (arrow) in parasternal long-axis view.
(PE: Pericardial effusion).
regions (more frequently along the right side of the
heart).
With regard to technical rules it is important to visualize
the pericardium from as many planes as possible,
including off-axis views, and to utilize the gray scale
and gain settings correctly.
A small PE may be more precisely defined by setting
the gain low so that only the posterior pericardium is
seen.
In the parasternal long-axis view pericardial fluid
reflects at the posterior atrioventricular groove
(Fig. 18.14), while pleural fluid continues under the left
atrium, posterior to the descending aorta.
348 Section 5: CHD, Aorta and Pericardium

Fig. 18.15: Paradoxical motion of interventricular septum (IVS) in a Fig. 18.16: M-mode section of the ventricles showing swinging heart
large pericardial effusion (PE) seen in M-mode section. with all walls moving forward in diastole and backward in systole.
(PW: Posterior wall). (PE: Pericardial effusion).

Fig. 18.17: Arrows point to intrapericardial bands in a patient with Fig. 18.18: Apical 4-CV showing large pericardial effusion (PE) with a
tubercular pericardial effusion in apical 4-CV. band (arrow) in a 19-year old boy with fever of 2 weeks duration.
(RV: Right ventricular; LV: Left ventricular; RA: Right atrial; LA: Left
atrial)

In large PEs, the heart may move freely within the Echocardiographic Masqueraders of PE:
pericardial cavity (swinging heart) inducing pseudo Hematoma (Fig. 18.7).
prolapse and pseudosystolic anterior motion of the Cysts.
mitral valve, paradoxical motion of the interventricular Foramen of Morgagni hernia.
septum and midsystolic aortic valve closure (Figs 18.15 Hiatus hernia.
and 18.16). Lipodystrophia with paracardial fat.
Large effusions generally indicate more serious disease. Left pleural effusion (Fig. 18.20).
Intrapericardial bands, combined with a thick visceral or Mitral annulus calcification.
parietal pericardium are often found after radiation of the Giant left atrium.
chest, tubercular or pyogenic PE (Figs 18.17 and 18.18). Epicardial fat best differentiated in computerized
Rarely granulomatous masses are found within the tomography (CT).
pericardium and may masquerade as tumors (Fig. 18.19). Left ventricular pseudoaneurysm (Fig. 18.21).

Fig. 18.19: Cresentic intrapericardial mass (arrow) with pericardial
effusion (PE).
Fig. 18.21: Left ventricular pseudoaneurysm (arrow) masquerading
as a pericardial effusion in a surgically proven case. The neck of
the pseudoaneurysm was serpigenous at the junction of apical and
mid-lateral wall.
CARDIAC TAMPONADE
Cardiac tamponade is defined as a significant compression
of the heart by accumulating pericardial contents (effusion
fluids, clots, pus and gas), alone or in combination.9
Normally intrapericardial pressure is zero or slightly
negative and the transmural pressure gradient across the
myocardium during diastole is positive, thus facilitating
ventricular filling. The accumulation of fluids into
the pericardial cavity causes an increase of both the
intrapericardial and intracardiac pressures and impedes
diastolic filling.10
Pericardial Diseases 349
Fig. 18.20: Large left-sided pleural effusion, which reflects behind the
left atrium, compared to small pericardial effusion, which reflects in
posterior atrioventricular groove.
Fig. 18.22: Relationship between intrapericardial pressure and
intrapericardial volume depending upon speed of fluid accumulation.
There is dissociation between intrathoracic and intra
cardiac pressures also.
Important points to remember are:
It is not the amount of fluid but the rapidity with which
it accumulates that decides the hemodynamic effects
(Fig. 18.22).
Sudden fluid, blood or pus accumulation in the
pericardial sac can cause rise in intrapericardial and
right and left atrial pressures even if the accumulated
content is less than 50 mL (Fig. 18.23).
Under normal physiologic conditions, the intraperi
cardial pressure is equal to intrapleural pressure and
350 Section 5: CHD, Aorta and Pericardium
Fig. 18.23: M-mode Echocardiogram of a patient with cardiac
tamponade during percutaneous coronary intervention. There is
evidence of right ventricular compression with marked tachycardia and
no respiratory variation even though there is small expansion of the
pericardial space.
Fig. 18.25: Parasternal long-axis view showing pericardial effusion
(PE) and diastolic right ventricular collapse (arrow).
therefore negative. The elevation of the intrapericardial
pressure is the result of rapid or slow accumulation
of fluid, gas or tissue within the pericardial cavity.
As the pericardial contents initially increase, the
pericardial space accommodates the expanding
volume of material without an increase in pressure or
compromise of the cardiac chambers until the limit
of the pericardial reserve volume is reached. Slow or
gradual accumulation of pericardial fluid of up to
1,0001,500 mL can be tolerated without hemodynamic
impairment.
Fig. 18.24: Apical 4-CV showing large pericardial effusion with right
atrial collapse (arrow).
Table 18.1: Echo-Doppler signs of cardiac tamponade
Exaggerated inspiratory variation of the two ventricles with
> 25% variation in early diastolic velocities (inspiratory expansion
of the right ventricle and simultaneous compression of the left
ventricle reciprocal changes in the expiratory phase)
Right atrial collapse
Right ventricular collapse
Left atrial collapse
Left ventricular collapse
Inferior vena cava (IVC) plethora
Aortic flow pulsus paradoxus
Rarely, pulmonary trunk and IVC collapse
An abnormally thickened pericardium may have a
much lower threshold for increases in pressure that lead
to tamponade due to its inability to expand normally to
accommodate an increasing intrapericardial volume.
Right atrial collapse,1113 which occurs in late diastole
or early systole, reflects increased intrapericardial
pressure inverting the right atrial wall inward when the
right atrial pressure is lowest (Fig. 18.24).
This echocardiographic sign of right atrial collapse
has a reported sensitivity of 5560% and specificity of
5068% for tamponade. Right atrial collapse is more
specific if the inward movement lasts for at least 30% of
the cardiac cycle.13
Right ventricular collapse,12 which occurs in early
diastole, is a less sensitive (3848%) but more specific

Fig. 18.26: Transthoracic apical 4-CV showing diastolic left atrial
collapse while there is no collapse of the right atrial free wall.
Fig. 18.28: Spontaneous echo contrast in inferior vena cava (IVC).
(84%100%) finding for cardiac tamponade (Fig. 18.25).
However, it has been considered a late sign.
Collapse of the left atrium,1415 which takes place in late
diastole, may occur in approximately 25% of patients
and is highly specific for tamponade (Fig. 18.26).
Left ventricular collapse16 also has low sensitivity and
usually occurs under specific circumstances such as
localized postsurgical tamponade (Fig. 18.27).
Another echocardiographic sign for tamponade
is a distended IVC or IVC plethora. Normally, the
proximal IVC decreases by more than 50% in diameter
after a deep inspiration or a sniff. In tamponade, by
definition the right atrial pressure is elevated and
the IVC typically is distended and will not decrease
Pericardial Diseases 351
Fig. 18.27: Transthoracic parasternal long-axis view showing left
ventricular (LV) collapse due to localized pericardial effusion (PE).
in diameter with these maneuvers.17 However, IVC
plethora is not a specific finding for tamponade
and may be present in other conditions causing
elevated right atrial pressure. Markedly raised right
atrial pressure in tamponade occasionally results in
spontaneous contrast in IVC (Fig. 18.28).
Abnormal Doppler flow has a good correlation with
clinical features of tamponade, with a higher sensitivity
(7580%) than right ventricular collapse and a much
higher specificity (91%) than right atrial collapse.1820
Marked respiratory variation in Doppler velocities, the
so-called Doppler flow velocity paradoxus, is a pattern
of reciprocal variation in the left-sided and right-sided
transvalvular inflow velocities (Fig. 18.29).
Normally, there is no significant respiratory variation
in early diastolic filling velocities across the tricuspid
and mitral valves (Fig. 18.30).
In tamponade, however, there may be an exaggerated
paradoxical increase in right-sided inflow velocities
with an exaggerated decrease in left-sided inflow
velocities (Fig. 18.31).
Other recently described echocardiographic signs in
tamponade include compression of two intrapericardial
structures, the pulmonary trunk and the thoracic IVC.
The pulmonary trunk is an entirely intrapericardial
short and wide vessel. The short intrathoracic segment
of the IVC is extrapericardial in its posterior aspect
but is covered by pericardium on its anterior aspect.
This is the reason why in PE with tamponade, there is
indentation of the right atrium at the level of the IVC
junction anteriorly but not posteriorly.
352 Section 5: CHD, Aorta and Pericardium
Fig. 18.29: Velocity flow paradoxus across mitral (left) and tricuspid
valve (right) in a patient with cardiac tamponade.
Fig. 18.31: Left panel shows large pericardial effusion (PE) in par-
asternal long-axis view while the right panel shows greater than 25%
respiratory variation with inspiratory decrease in early diastolic mitral
inflow velocities suggesting cardiac tamponade.
Aortic flow frequently exhibits pulsus paradoxus
or significantly decreased inspiratory systolic flow
velocities that is equivalent of clinical pulsus paradoxus
observed (Fig. 18.32). 21
One mechanism of pulsus paradoxus is also visible at
echocardiography when both the ventricular and atrial
septa move sharply to the left with an increase in right
chamber volumes at the expense of the left chambers.
The reverse occurs in expiration. This paradoxical
motion of the septa occurs because each side of the
heart fills at the expense of the other due to the fixed
intrapericardial volume.
Fig. 18.30: Transmitral flow velocities with respiratory signal in a
normal person. There is hardly any respiratory variation of early dias-
tolic velocities.
Fig. 18.32: Continuous Doppler interrogation of the aortic flow in a
patient with cardiac tamponade. Note greater than 40% inspiratory de-
crease in systolic velocities.
As more fluid is added to the cavity, cardiac stroke
volume falls and there is compensatory tachycardia to
maintain cardiac output.22
Even in cases with diffuse circumferential effusion the
hemodynamic effects of tamponade are due primarily
to right heart compression. This is because right heart
filling pressures are lower than that of the left and are
easily overcome by the rising intrapericardial pressure.
Hence, sensitivity of right heart collapse in diagnosing
tamponade is higher.
Duration of the collapse should also be taken into
account. Duration of collapse is directly related to

Fig. 18.33: Apical 4-CV in a patient with chronic constriction and
calcification (arrow). The right panel is the graphic representation of
the constriction.
severity of tamponade and improves the specificity
and predictive value of these diagnostic signs. With
increasing severity, right atrial (RA) collapse tends
to begin earlier and right ventricular (RV) collapse to
extend later in diastole. Even though these two signs are
too sensitive, the presence of both RA and RV collapses
always indicates that the effusion is hemodynamically
significant.
From a technical point of view, it is important to
control the positioning of the sample volume during
the examination trying to exclude differences in
location during respiration and to utilize the electro
cardiography and respiratory signals.
Occurrences of tamponade can be acute, subacute,
regional or characterized by low pressure. Acute
tamponade is sudden, life-threatening if not treated
promptly and often associated with hypotension as
well as chest pain and dyspnea.
PERICARDIAL CYSTS AND MASSES
Pericardial cysts can be congenital or inflammatory.
Congenital cysts are uncommon, mostly unilocular
and located at the right cardiodiaphragmatic angle,
with a diameter from 1 cm to 5 cm, and clinically silent.
However, sometimes they are associated with chest pain,
dyspnea, cough and/or significant arrhythmias, due to
the compression of the heart. Inflammatory cysts can
be caused by rheumatic pericarditis, bacterial infection,
particularly tuberculosis, trauma and cardiac surgery.
Pericardial Diseases 353
Fig. 18.34: M-mode echocardiogram showing rapid expansion of the
left ventricular posterior wall in early diastole (arrow) in a patient with
constrictive pericarditis.
Most cysts are discovered accidentally on chest X-ray,
or at echocardiography [particularly at transesophageal
echocardiography (TEE)]. Usually, CT and magnetic
resonance imaging (MRI) are diagnostic. Pericardial cysts
are seen as an echolucent unilocular cavity that can cause
extrinsic compression of the atrium. Sometimes, they may
have a grossly heterogeneous echodense appearance on
TEE, due to the collection of mucilaginous material or
embryonic residua (bronchogenic cyst). Echinococcal
cysts, usually originated from ruptured cysts in the liver
and lungs, are the typical hydatid and multiseptate.
PERICARDIAL CONSTRICTION
When an inelastic pericardium impedes cardiac filling
during diastole with exaggerated ventricular interdepen
dence and dissociation between intrathoracic and
intrapericardial pressures, it is labeled CP (Fig. 18.33).2325
The types of constriction can be:
Acute CP.
Subacute constriction.
Effusive CP.
Chronic CP.
Pericardial calcification with constriction.
Both CP and restrictive cardiomyopathy limit diastolic
filling and result in diastolic heart failure, with relatively
preserved global systolic function.26 In CP, diastolic filling
is restricted by an inelastic pericardium after an initial
expansion of the myocardium (Fig. 18.34). The upper
limit of ventricular volume is constrained by an inflamed,
354 Section 5: CHD, Aorta and Pericardium

Fig. 18.36: Intrinsic reduced myocardial compliance in restrictive

Fig. 18.35: Calcified pericardium restricting the transverse expansion
cardiomyopathy (left panel) contrasted with reduced compliance in
of the heart with dilated left atrium.
late diastole due to inelastic pericardium in constrictive pericarditis
(right panel).

annulus motion were identified. Left ventricular systolic

function as judged by the ejection fraction is typically
normal but may be impaired in mixed constrictive-
restrictive disease. Following are the echocardiographic
observations in CP:
Increased pericardial thickness measured with greater
sensitivity by transesophageal echocardiography
and cardiac CT than transthoracic echocardiography
(Fig. 18.37).27
However, CP can occur without increased
pericardial thickness in about 20% cases more so after
surgery or radiation therapy.28
Abnormal ventricular septal motion (Figs 18.38 to
Fig. 18.37: Thickness of the posterior pericardium (arrows) at lowest 18.40).
possible gain by transthoracic echo may still be an overestimate. Dilatation and absent or diminished collapse of the
IVC and hepatic veins
scarred or calcified pericardium (Fig. 18.35) that is usually, Restrictive mitral and tricuspid inflow velocities,
but not always, thicker than normal. typically (but not always) with respiratory variation
Restrictive cardiomyopathy (Fig. 18.36) is defined by a (Figs 18.41 and 18.42).2931
nondilated ventricle with a rigid myocardium that causes There may be no or insignificant respiratory
a major decrease in the effective operative compliance of variation of the early diastolic velocities in about 20% of
the heart muscle itself. This decrease distinguishes it from CP because of markedly increased filling pressures
CP, in which no such decrease in myocardial compliance due to greater severity of constriction.32 In such
is usually seen. cases, preload manipulation can unmask respiratory
Echocardiography is usually the initial diagnostic variation (Fig. 18.44A).
imaging and hemodynamic study in patients with Marked respiratory change in pulmonary vein flow
suspected CP. Its diagnostic accuracy for CP has increased is observed in CP. The S2 and D velocities increase,
since characteristic hemodynamic changes and mitral especially the D velocity, during expiration, and

Fig. 18.38: Diastolic fluttering of the interventricular septum (IVS) with
exaggerated respiratory motion and septal bulging toward left ventricle
(LV) during inspiration.
Fig. 18.40: Prominent early diastolic motion of the interventricular
septum (IVS; arrow) with increased tissue velocity observed during
expiration.
decrease during inspiration. This is explained by
incomplete transmission of the inspiratory fall of
intrathoracic pressure to the LA. These changes are
more prominent compared with changes in mitral
inflow velocities. The combination of the S2/D ratio
> 0.65 in inspiration and a respiratory variation of D
velocity > 40% correctly classifies 8085% of patients
with CP (Fig. 18.44B).
Preserved or increased medial mitral annulus early
diastolic (e) velocity (Fig. 18.45), which is an important
distinction from restrictive cardiomyopathy in which
the e is diminished with a cut-off value of 8 cm/s.
Pericardial Diseases 355
Fig. 18.39: Prominent early diastolic notch in interventricular septum
(IVS) with concavity toward left ventricular in constrictive pericarditis.
Normally, early diastolic notch in IVS is concave toward the right
ventricular (RV) cavity due to beginning of RV filling after a delay in
opening of the tricuspid valve compared to mitral valve.
(LVPW: Left ventricular posterior wall).
Fig. 18.41: Restrictive transmitral flow pattern on pulsed wave Doppler
interrogation with marked respiratory variation.
Sensitivity of e 8 cm/sec in detecting CP is 89% while
the specificity is 95%.3335
However, e may be reduced in CP in presence
of myocardial disease, patchy fibrosis or extensive
calcification.
Increased hepatic vein flow reversal with expiration,
reflecting the ventricular interaction and the disso
ciation of the intracardiac and intrathoracic pressures
(Fig. 18.46).36
Annulus paradoxus: Normally, mitral flow early
diastolic velocity (E) to tissue early diastolic velocity
(e) ratio is a good index of pulmonary capillary wedge
356 Section 5: CHD, Aorta and Pericardium

Fig. 18.42: Decreasing mitral flow early diastolic velocities during Fig. 18.43: Dissociation between intrapericardial (intracardiac)
inspiration with corresponding increase during expiration. versus intrathoracic pressures explaining the respiratory variation inflow
velocities of mitral valve and pulmonary veins. (PCW: Pulmonary
capillary wedge pressure; IP: Intrapericardial pressure).

A B
Figs 18.44A and B: Transmitral early diastolic velocities during quiet respiration in left lateral position (left panel) and after standing (right panel).
Standing induces preload reduction and sometimes may restore respiratory variation in constriction; (B) Respiratory variation in right upper
pulmonary vein flow in constrictive pericarditis.

pressure. E/e increases with increasing LV filling

Fig. 18.45: Surgically proven CP with mitral tissue e velocity of
20 cm/sec due to enhanced longitudinal LV expansion.
pressure (Fig. 18.47). This relationship gets reversed in
CP and has been labeled as annulus paradoxus.37
This is because e remains normal or is enhanced
with increasing severity of constriction due to
unidirectional (longitudinal) diastolic expansion of the
LV in early diastole (Fig. 18.48).
Annulus reversus: In CP, mitral medial early diastolic
(e) velocity is preserved or even increased because of
the limitation of lateral expansion by the constricting
pericardium, and mitral lateral e velocity tends to be
lower than medial e velocity, which is a reversal of
their normal relationship.38 The mitral lateral/medial
e ratio is reversed in three fourths of patients with CP
(Figs 18.49 and 18.50). After pericardiectomy, there is

reduction of all annular velocities and normalization of
the mitral lateral/medial e ratio.
Tissue velocity diastolic waves have been studied in
CP in short-axis or in parasternal long-axis view using
color Doppler myocardial imaging. Polyphasic tissue
waves are common during early diastole. Diastolic
velocities > 9 cm/sec are highly specific for CP.
(Fig. 18.51).39
Majority of patients with CP have some degree of
pulmonary regurgitation (PR). CW Doppler spectrum
of PR has been studied in a variety of conditions. In
CP, the duration of PR Doppler signal varies with
respiration pan-diastolic during expiration and only
Fig. 18.46: Augmented expiratory flow reversal in hepatic vein in a
patient with constrictive pericarditis.
Fig. 18.48: Effusive-constrictive pericarditis in a young female. Note
E/e in early expiration is 6 while in first beat during inspiration, it is 4.5.
Pericardial Diseases 357
early and mid-diastolic during inspiration due to
increased RV end-diastolic pressure (Fig. 18.52). This
sign has about 70% sensitivity and specificity.
Torsion and rotational characteristics of the LV have
been studied in CP and found to be different compared
to restrictive cardiomyopathy.
Constrictive pericarditis may have involvement
of subepicardial muscle fibers either by fibrosis and
calcification or tethering.40 This can result in hypo-rotation
and reduced twist (Fig. 18.53).
In summary, echocardiographic diagnosis of CP needs
a multiparametric approach because different echocar
diographic signs have variable sensitivity and specificity.
Fig. 18.47: Schematic diagram showing relationship between E/e and
LV filling pressure in heart failure versus constrictive pericarditis.
Fig. 18.49: Medial mitral versus lateral mitral e in a normal subject.
Lateral e is higher due to greater free wall motion.
358 Section 5: CHD, Aorta and Pericardium

Fig. 18.50: Reduced lateral e compared to medial e in a patient with constrictive pericarditis (annulus reversus).

Fig. 18.51: Large Diastolic tissue velocity waves (arrow) seen in Fig. 18.52: Temporal variation in pulmonary regurgitation (PR)
early diastole in constrictive pericarditis. The waves are much more continuous wave Doppler spectrum produced by phases of respiration
prominent during early expiration. in a patient with constrictive pericarditis.

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2. Imazio M, Trinchero R. The spectrum of inflammatory
myopericardial diseases. Int J Cardiol. 2010;144(1):134.
3. Spodick DH. Myopericarditis/Perimyocarditis. In: The Peri-
cardium: A comprehensive Textbook. Marcel Dekker, Inc.:
New York; 2001. p.114.
4. Imazio M, Cecchi E, Demichelis B, et al. Myopericardi-
tis versus viral or idiopathic acute pericarditis. Heart.
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5. Parameswaran R, Goldberg H. Echocardiographic quanti-
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6. Vazquez de Prada J, Jiang L, Handschumacher M, et al.
Fig. 18.53: Surgically proven case of constrictive pericarditis. Quantification of pericardial effusions by three dimension-
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7. DCruz IA, Hoffman PK. A new cross sectional echocardio-
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dial effusions. Br Heart J. 1991;66(6):448-51.
8. Horowitz MS, Schultz CS, Stinson EB, et al. Sensitivity and
specificity of echocardiographic diagnosis of pericardial
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9. Shabetai R. Changing concepts of cardiac tamponade. J Am
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10. Singh S, Wann LS, Schuchard GH, et al. Right ventricular
and right atrial collapse in patients with cardiac tampon-
adea combined echocardiographic and hemodynamic
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11. Armstrong WF, Schilt BF, Helper DJ, et al. Diastolic collapse
of the right ventricle with cardiac tamponade: an echocar-
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13. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic com
pression of the right atrium: a new echocardiographic sign
of cardiac tamponade. Circulation. 1983;68(2):294-301.
14. Torelli J, Marwick TH, Salcedo EE. Left atrial tamponade:
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15. Fusman B, Schwinger ME, Charney R, et al. Isolated
collapse of left-sided heart chambers in cardiac tampon-
ade: demonstration by two-dimensional echocardiogra-
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16. Chuttani K, Pandian NG, Mohanty PK, et al. Left ventricular
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cardiac tamponade. Circulation. 1991;83(6):1999-2006.
17. Himelman RB, Kircher B, Rockey DC, et al. Inferior vena
cava plethora with blunted respiratory response: a sensitive
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18. Fowler NO. The significance of echocardiographic-Doppler
studies in cardiac tamponade. J Am Coll Cardiol. 1988;11(5):
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19. Appleton CP, Hatle LK, Popp RL. Cardiac tamponade and
pericardial effusion: respiratory variation in transvalvular
flow velocities studied by Doppler echocardiography. J Am
Coll Cardiol. 1988;11(5):1020-30.
20. Schutzman JJ, Obarski TP, Pearce GL, et al. Comparison
of Doppler and two-dimensional echocardiography for
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21. Curtiss EI, Reddy PS, Uretsky BF, et al. Pulsus paradoxus:
definition and relation to the severity of cardiac tampon-
ade. Am Heart J. 1988;115(2):391-8.
22. Levine MJ, Lorell BH, Diver DJ, et al. Implications of echo-
cardiographically assisted diagnosis of pericardial tam-
ponade in contemporary medical patients: detection be-
fore hemodynamic embarrassment. J Am Coll Cardiol.
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23. Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in
the modern era: evolving clinical spectrum and impact on
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24. Myers RB, Spodick DH. Constrictive pericarditis:
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28. Talreja DR, Edwards WD, Danielson GK, et al. Constric-
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29. Rajagopalan N, Garcia MJ, Rodriguez L, et al. Comparison
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30. Oh JK, Hatle LK, Seward JB, et al. Diagnostic role of Dop-
pler echocardiography in constrictive pericarditis. J Am
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31. Hatle LK, Appleton CP, Popp RL. Differentiation of constric-
tive pericarditis and restrictive cardiomyopathy by Doppler
echocardiography. Circulation. 1989;79(2):357-70.
32. Oh JK, Tajik AJ, Appleton CP, et al. Preload reduction to
unmask the characteristic Doppler features of constric-
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95(4):796-9.
33. Sengupta PP, Mohan JC, Mehta V, et al. Accuracy and
pitfalls of early diastolic motion of the mitral annulus for di-
agnosing constrictive pericarditis by tissue Doppler imag-
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34. Ha JW, Ommen SR, Tajik AJ, et al. Differentiation of
constrictive pericarditis from restrictive cardiomyopathy
using mitral annular velocity by tissue Doppler echocardi-
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35. Garcia MJ, Rodriguez L, Ares M, et al. Differentiation of
constrictive pericarditis from restrictive cardiomyopathy:
assessment of left ventricular diastolic velocities in longi-
tudinal axis by Doppler tissue imaging. J Am Coll Cardiol.
1996;27(1):108-14.
36. von Bibra H, Schober K, Jenni R, et al. Diagnosis of constric-
tive pericarditis by pulsed Doppler echocardiography of the
hepatic vein. Am J Cardiol. 1989;63(7):483-8.
37. Ha JW, Oh JK, Ling LH, et al. Annulus paradoxus: trans-
mitral flow velocity to mitral annular velocity ratio is
inversely proportional to pulmonary capillary wedge pres-
sure in patients with constrictive pericarditis. Circulation.
2001;104(9):976-8.
38. Reuss CS, Wilansky SM, Lester SJ, et al. Using mitral
annulus reversus to diagnose constrictive pericarditis. Eur
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39. Sengupta PP, Mohan JC, Mehta V, et al. Doppler tissue
imaging improves assessment of abnormal interventricular
septal and posterior wall motion in constrictive pericar
ditis. J Am Soc Echocardiogr. 2005;18(3):226-30.
40. Sengupta PP, Krishnamoorthy VK, Abhayaratna WP, et al.
Disparate patterns of left ventricular mechanics differentiate
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JACC Cardiovasc Imaging. 2008;1(1):29-38.
 SEction 6
Structural Heart Disease

Chapters

Ischemic Heart Disease Cardiomyopathies

Tumors, Masses and Infection
 Chapter
19 Ischemic Heart Disease
Introduction
One of the commonest indications for the echocar
diographic examinations is ischemic heart disease
(IHD) because of its prevalence, indication for function
assessment, occurrence of heart failure, mitral regur
gitation and the mechanical complications. The purpose
of echocardiography in IHD is detection of ischemia,
extent of ischemia and its consequences. Efforts to quan
titate segmental wall-motion abnormality, area at risk
of inducible ischemia, precise degree of stress-related
hemodynamic alteration and quantitative change in
pattern of regional contraction started along with the
advent of the technique. Currently stress echocardio
graphy (SE) is routinely used in detection of myocardial
ischemia and viability. A 16- or 17-segment model of
wall-motion scoring provides semiquantitation and has
been extensively used and polar maps can be generated
with the help of software.
MYOCARDIAL SEGMENT NOMENCLATURE
AND CORONARY VASCULAR TERRITORY
Myocardium gets nutritive flow from the coronary arteries
(Table 19.1). The nutritive flow sustains its systolic
contractile and diastolic relaxation behavior. Coronary
tree supplies specific segments (Fig. 19.1). Myocardial
flow has a reserve, which is called upon to participate
Table 19.1: Myocardium and its blood supply
Segments Blood Supply
Anterior septum Left anterior descending (LAD)-septal
perforating branches
Anterior wall LAD-diagonal branches
Lateral wall Circumflex-obtuse marginal branches
Posterior wall Right coronary artery-extension branches
Circumflex-obtuse marginal branches
Inferior Septum Posterior desceding (PD) artery
Interior wall PD artery
Apex LAD and or PD arteries
in its activities during physiological stress. Anatomical
obstruction reduces the flow reserve and produces
ischemia that can be detected by echocardiographic
examination.
For convenience, myocardium has been converted into
a 17-segment model1,2 to supersede earlier 16-segment
nomenclature (Fig. 19.2). Various views of 2D echocardio
graphic examination depict these segments (Figs 19.3
to 19.7).
RIGHT VENTRICULAR SEGMENTATION
The right ventricle is divided into three walls: anterior,
lateral (also called right ventricular free wall) and posterior
wall and shares the septal wall with the left ventricle (LV).
Each wall is divided into a basal, mid and apical segment.3
364 Section 6: Structural Heart Disease

Fig. 19.1: Diagram of the coronary arterial tree. Fig. 19.2: Schematic depiction of the 17 segments of the myocardium.
(RCA: Right coronary artery, PDA: Posterior descending artery, LAD: Entire myocardium is divided into 16 segments in apical and short-axis
Left anterior descending artery, D1 and D2-diagonal arteries, Cx: views. True apex as a cap represents 17th segment.
Circumflex artery, OM1 and OM2: Obtuse marginal arteries).

Fig. 19.3: Apical views to show 17-segment model. In long-axis view, only four segments are counted. 17th segment is the true apical cap.
 Ischemic Heart Disease 365

A B
Figs 19.4A and B: Biplane view showing six midwall segments in short axis and four basal and mid segments in long-axis view.

Fig. 19.5: Parasternal short-axis view at the level of mitral valve leaf- Fig. 19.6: Basal and mid left ventricle (LV) short-axis views showing
lets showing six basal segments with nomenclature. the blood supply by the artery involved.

The right coronary artery is the primary coronary supply to

the right ventricle via acute marginal branches.

Fig. 19.7: Apical views showing coronary arteries supplying various
segments.
ISCHEMIA AND
ECHOCARDIOGRAPHIC IMAGING
Transient or reversible ischemia can be detected by
echocardiography. Most often, ischemia is due to
reduced or absent flow or flow reserve due to anatomical
obstruction as seen in coronary artery disease (CAD).
Following is the cascade of ischemia (Fig. 19.8).
Two-dimensional (2D) echocardiography is widely
used for the evaluation of regional left ventricular function
because of its ability to depict endocardial excursion
and wall thickening in real time.4 Normally, myocardial
366 Section 6: Structural Heart Disease
Fig. 19.8: Ischemic cascade. Flow abnormality precedes wall-motion
abnormality.
Fig. 19.10: Apical four-chamber view in systole. Lateral wall shows
dyskinesis in basal and mid segments compared to apicolateral
segment.
segments show radial thickening and longitudinal
and circumferential shortening during systole. Radial
thickening is most readily appreciated and conventionally
used to detect wall-motion abnormality.5,6 Following
terms describe the thickening behavior of the normal
myocardium:7
Normokinesisnormal radial thickening compared to
the adjacent segments
Hyperkinesisincreased radial thickening compared
to the other segments with local cavity obliteration
The earliest change provoked by ischemia is delayed
contraction, and the eye has insufficient temporal
resolution to identify this in real-time, although the
Fig. 19.9: Radial thickening behavior of an ischemic segment (red)
compared to an ischemic segment (blue).
(IVC: Isovolumic contractions; ET: Ejection time; IVRT: Isovolumic
relaxation time)
Fig. 19.11: Apical long-axis view showing diastolic thinning with
reduced thickening of the mid anterior ventricular septum during
systole (arrow). This is called hypokinesis.
ability to freeze and step through the image is a
means of identifying changes that are not visible in
real-time (Fig. 19.9).
One of the least contested observation during ischemia
is systolic thinning called dyskinesis (Fig. 19.10).
Reduction in systolic wall thickening is more often
seen during ischemia (LV asynergy). This is labeled as:
Hypokinesis-reduced wall thickening (Fig. 19.11).
Akinesis-absent wall thickening (Fig. 19.12).
Tardokinesis-delayed wall thickening.
Dyskinesis-systolic wall thinning.
Wall motion abnormalities (asynergy) are best
evaluated by comparison of the diastolic and systolic
 Ischemic Heart Disease 367

Fig. 19.12: Long-axis view showing akinesis of the mid anterior Fig. 19.13: Comparing basal and mid anterior septum and posterior
septum. wall thickness in diastole and systole. Normal thickening is noted in all
the four segments.

A B
Figs 19.14A and B: Increased systolic wall thickening of the inferior septum after revascularization of the right coronary artery.

images (Fig. 19.13). Wall motion is then labeled
as normal, hypokinetic, akinetic, dyskinetic and
aneurysmal in each of the 17 segments and scored
15 respectively.1,2
If images of suitable quality are available, it is possible to
analyze ventricular wall motion on a regional basis and
to apply semiquantitative or quantitative descriptors to
each segment of the myocardium. A number of simple
and complex formats for performing such assessment
have been proposed.
Digitization of a single cardiac cycle and continuous
loop replay (cine loops) is mandatory to assist the
interpreter in detecting wall-motion abnormalities.
Wall-motion score can improve when areas of stunned
myocardium regain contractility.8 Similar recovery
can also occur after revascularisation of hibernating
myocardium (Figs 19.14A and B).
Thin, akinetic/dyskinetic and bright segments are
strongly suggestive of myocardial scar due to old
infarction (Fig. 19.15).
The average of the scores of all LV segments is referred
to as wall motion score index (WMSI) and provides
comparable prognostic information as LV ejection
fraction.
The magnitude of LV asynergy caused by actual
ischemia is related to the location of the culprit lesion
368 Section 6: Structural Heart Disease
Fig. 19.15: Apical dyskinesis and increased echogenicity of the
mid-septum (arrows).
Fig. 19.17: Apical four-chamber view showing normal radial thickening
of the lateral wall but markedly reduced as well as paradoxical longi
tudinal strain (right panel, arrow).
in the ischemia-related artery, presence of collateral
circulation and the extent of CAD.
Apart from subjectivity of the visual assessment of LV
asynergy, interpretation difficulties may also arise from
both poor imaging technique and poor echogenicity.
While the latter problem can be partially overcome by
the use of contrast agents (Fig. 19.16), the first two can
be addressed only by adequate training and experience
of echocardiographers.
Echocardiography can overestimate the amount of
ischemic or infarcted myocardium, as wall motion
of adjacent regions may be affected by tethering,
disturbance of regional loading conditions and
stunning.9 Therefore, wall thickening appears more
precise than motion in order to evaluate the extent of
regional systolic abnormalities.10
Fig. 19.16: Use of contrast agent to define endocardium and wall
motion.
Regional wall-motion abnormalities may occur in the
absence of CAD, for example, in stress cardiomyopathy,
myocarditis and so on.
Ideally, the function of each segment should be
confirmed in multiple views.
In the ischemic cascade, impairment of longitudinal
strain precedes impairment of wall thickening and
motion.11 Hence, longitudinal function assessment is a
better marker of regional function (Fig. 19.17).
A semiautomated method of measuring regional
longitudinal strain to develop segmental scores,
classifying segments as normal, hypokinetic or akinetic
is almost ready for prime-time use.12
There is a graded decrease in longitudinal peak
systolic strain between normal, hypokinetic and
akinetic segments (Fig. 19.18).
It must be kept in mind that the heart moves through
the interrogating plane as it cycles through diastole
and systole. This gross movement, even in normal
individuals causes different regions of the myocardium
to be interrogated in systole and in diastole and may
lead to spurious interpretive errors. 13
Incorrect orientation of the short-axis plane such that
the ventricle appears elliptical rather than circular will
cause any motion of the posteroseptal and lateral walls
to appear exaggerated.
In patients with average image quality where only a
portion of the endocardium is identified, one should
not compare areas of endocardial movement to areas
of movement where only the pericardium is visualized.
This leads to the incorrect interpretation that asynergy
is present in the poorly visualized segment.

Fig. 19.18: 2D longitudinal strain at rest and during stress in dominant
left circumflex artery stenosis. Note longitudinal strain turning positive
in basal and mid lateral segments as well as in inferior basal septum.
Fig. 19.20: Apicoanterior myocardial infarction seven days after the
onset. Note systolic asynergy (arrows) with apical hypertrabeculation.
ECHOCARDIOGRAPHY IN IHD
Echocardiography is used for a variety of reasons in IHD.
These are:
Suspected acute coronary syndrome.
Detection of ischemia in suspected IHD.
Evaluation of myocardial infarction.
Detection of mechanical complications of IHD.
Stress echocardiography for detection of viability.
Myocardial perfusion imaging with contrast.
Tissue Doppler and strain imaging for prognosis.
3DE for LV volumes, function and sphericity, dys
synchrony.
Ischemic Heart Disease 369
Fig. 19.19: Parasternal short-axis view showing increased diastolic
thickness of the basal posterior and inferior segments with enhanced
echogenicity.
EVALUATION OF
MYOCARDIAL INFARCTION
New LV asynergy is the hallmark of acute coronary
syndrome. In patients with acute chest pain of suspected
ischemic origin, echocardiography is used to detect LV
asynergy, which is of diagnostic significance in following
situations:
Patients with normal or nonspecific ECG changes.
Preexisting left bundle branch block.
Patients on pacemakers.
Most often, there is wall-motion abnormality defined
by a specific coronary territory. Usually, there is akinesis
or dyskinesis. However, occasionally, there is increased
wall thickness and increased echogenic texture due to
myocardial edema or hemorrhage (Fig. 19.19).
Apical myocardial infarction initially shows asynergy
and subsequently quite often shows hypertrabeculation
because of loss regional function (Fig. 19.20).
Echocardiography is routinely used during acute
phase of myocardial infarction to assess the extent of wall-
motion abnormalities, remodeling, presence of mitral
regurgitation and grade of diastolic dysfunction.14
The involvement of RV or isolated RV infarction
is easily detected by echocardiographic examination
(Figs 19.21 and 19.22).
After healing of myocardial infarction, the segments
involved become thin and scarred (enhanced echo
genicity). These segments cause tethering of the adjacent
segments (Figs 19.23 to 19.25).
370 Section 6: Structural Heart Disease

Fig. 19.21: Apical four-chamber view showing dilated right atrium (RA)
and right ventricle (RV) (left upper panel) with systolic thinning of the
basal inferoposterior wall (right lower panel). Note systolic lengthening
of the RV free wall by tissue Doppler (arrows).
(LV: Left ventricle; LA: Left atrium).
Fig. 19.22: Cardiogenic shock in a patient with isolated right ventricle
(RV) infarction. Acute phase shows marked right atrium (RA) and RV
dilatation with hinge point (left panel). Right panel shows RA and RV
after recovery following angioplasty of the nondominant right coronary
artery.

Fig. 19.23: Parasternal long-axis view showing diastolic thinning of Fig. 19.24: Scarred basal inferior segment with dyskinesis.
the posterior wall.

MECHANICAL COMPLICATIONS OF myocardial infarction.15 Echocardiography is valuable for

MYOCARDIAL INFARCTION detecting the presence of an effusion and for showing that
any apparent increase in heart size is due to this and not to
Dresslers Syndrome the development of a ventricular aneurysm.
Echocardiography can be of great assistance in the With a large effusion and impaired ventricular filling,
evaluation of a patient who, either in the immediate cardiac tamponade may develop. The provisional
postinfarction period or later during recovery, develops diagnosis is usually made from the clinical signs, but rapid
complications. echocardiographic confirmation of a large effusion in the
The most common complication is Dresslers synd presence of tamponade physiology indicates the need for
rome, a pericarditis typically occurring a few weeks after pericardiocentesis.

Fig. 19.25: Color kinesis in apical four-chamber view showing apical
akinesis.
Fig. 19.27: Rupture of the posterior ventricular septum causing
ventricular septal defect (arrow) following inferior myocardial
infarction.
Ventricular Septal Rupture
Post infarction ventricular septal defect (VSD) most
commonly occurs at the junction of the anterior and
posterior portions of the septum,16,17 usually near the apex
(Figs 19.27 to 19.29).
It is frequently difficult to visualize on any single
view. While visualization of the actual defect may be
difficult, it may strongly be suspected by a severe wall
motion abnormality in the distal septum. With color
Doppler echocardiography and 3DE, the presence of a
postinfarction VSD may be confirmed with certainty.
Ischemic Heart Disease 371
Fig. 19.26: Pericardial effusion (PE) following anterior myocardial
infarction (arrows.)
Fig. 19.28: Modified apical four-chamber view showing ventricular
septal defect (arrow) due to distal septal rupture.
Intramyocardial Hematoma
Intramyocardial hematoma or localized hemorrhagic
area detected by echocardiography is a subacute, partial
rupture of the myocardium.18,19 These hematomas usually
occur after myocardial infarction, chest trauma, surgery
or percutaneous coronary intervention, but they can also
develop spontaneously. Standard transthoracic echocardi
ography usually shows an echo-free or hypoechoic
intramyocardial neocavity (Figs 19.30 to 19.32).
Hemorrhagic myocardial infarction was rarely seen in
autopsy studies in the prereperfusion era, but its reported
372 Section 6: Structural Heart Disease
Fig. 19.29: Mid muscular ventricular septal defect (arrow).
Fig. 19.31: 3DE showing apical hematoma (arrow).
incidence markedly increased after the introduction
of thrombolytic therapy. Recent studies showed that it
occurs frequently after primary percutaneous coronary
intervention and is related to worse remodeling, falling
ejection fraction and larger volumes.
Echocardiographic detection of intramyocardial
hemorrhage is subtle and needs careful evaluation of
zoomed out pictures of the affected segments. Apical
involvement is more frequent but it occurs at other places
as well. Some patients have been seen to develop sudden
cardiac rupture.
There is a clear difference with pseudoaneurysm as this
latter is a total rupture of the myocardial wall contained by
Fig. 19.30: Intramural hematoma (arrow) just after the percutaneous
stent implantation in left anterior descending artery following acute
anterior myocardial infarction.
Fig. 19.32: Dissecting myocardial hematoma in apical myocardium
after delayed angioplasty (arrows).
the pericardium, whereas the dissecting intramyocardial
hematoma is a bloody cavity delimited externally by part
of myocardium and pericardium. Anatomorphologic
examination reveals a bloody cavity externally delimited
by myocardium and pericardium and internally by the
myocardium remaining and endocardium.
Myocardial Dissection Without Hematoma
Occasionally, myocardial dissection occurs with flap
falling into the cavity like in aortic dissection with no blood
collection between layers (Figs 19.33 to 19.38). This may
be associated with true or false aneurysm.
 Ischemic Heart Disease 373

Fig. 19.33: Apical myocardial dissection with hematoma (arrows). Fig. 19.34: Localized pericardial effusion adjacent to intramural
hematoma in the basal posterior wall with dyskinesis of the mid
posterior segment.

Fig. 19.35: Myocardial dissection without definite echolucent delimiting Fig. 19.36: Dissecting flap fluttering in the left ventricle (LV) cavity
cavity. (arrow) in a patient with large anterior myocardial infarction.

Fig. 19.37: Parasternal short-axis view with myocardial flap obliterating Fig. 19.38: Parasternal long-axis view showing dissection of the
the cavity. anterior interventricular septum (arrow) in an old lady.
374 Section 6: Structural Heart Disease
Fig. 19.39: Papillary muscle rupture with head attached to the
posterior leaflet (arrow). Right upper panel shows triangular jet of
mitral regurgitation with low velocities indicating presence of shock.
Fig. 19.41: Longitudinally sliced left ventricular (LV) showing a large
thrombus attached to the apicolateral segment (arrows).
Papillary Muscle Rupture
As with postinfarction VSD, discovery of a new systolic
murmur following infarction suggests rupture of a papillary
muscle leading to mitral regurgitation. Echocardiography,
in combination with Doppler methods, serves as the
principal means for the detection and differentiation of
these two entities.
Rupture of a papillary muscle head also provides
a striking echocardiographic picture (Fig. 19.39). Flail
chordae and the muscle head itself may be seen to be
whirling around in the ventricle with the flail leaflet
moving into the atrium in systole.20
Fig. 19.40: Biplane imaging showing multilobed apical thrombus
(arrows).
Mural Thrombi
Mural thrombi are almost invariably associated with an
underlying wall-motion abnormality.21 Occasionally, chest
wall reverberations make adequate interrogation of the left
ventricular apex quite difficult, and the diagnosis of apical
mural thrombus is best left to experienced observers.
Multilobulated presentation of a mural thrombus,
particularly one with rapidly moving intracavitary compo
nents, has a higher incidence of peripheral embolization
(Fig. 19.40).
While the sensitivity and specificity of the echocardio
graphic diagnosis of ventricular thrombus are not known
precisely, there is a growing abundance of data that this
approach is the most clinically reliable method currently
available. Thrombus can be delineated better with contrast
echocardiography and real-time 3DE (Fig. 19.41).
Free Wall Rupture
Left ventricular free wall rupture (LVFWR) is a dramatic
complication of acute myocardial infarction (AMI) and
is presumably responsible for as much as 2030% of all
infarct related deaths.2224 Mechanical complications of
AMI, including LVFWR, are becoming less frequent in
day-to-day practice, at least in part due to our growing
ability to deliver safe and effective reperfusion therapies
(both pharmacological and mechanical) to a wide range
of AMI patients.

Fig. 19.42: Left ventricle (LV) in short-axis view showing a tear in the
free wall (arrow) with pericardial effusion (PE).
Fig. 19.44: Acute rupture of subendocardial muscle layer with blood
seeping into the outer layer (arrow).
When the acute form of LVFWR occurs, it usually results
in an abrupt hemodynamic collapse with cardiac
tamponade and electromechanical dissociation.
Less frequently, in up to one-third of the cases, the
rupture can be sealed by the epicardium or by a
hematoma on the epicardial surface of the heart,
forming a LV diverticulum or contained myocardial
rupture (Figs 19.42 to 19.45).
This situation represents a subacute pathologic
condition standing somewhere between free rupture
into the pericardial cavity and formation of a pseudo
aneurysm.
Ischemic Heart Disease 375
Fig. 19.43: Apical four-chamber view showing free wall rupture and
pericardial effusion (PE).
Fig. 19.45: 3DE slice showing communication with the pericardial
space (arrow).
Those with sub-acute rupture usually have canalicular
or serpigenous communication, which can be better seen
by 3DE by slicing the data set (Fig. 19.45).
Aneurysm Formation
True aneurysm formation is closely related to infarct
expansion which is defined as acute dilation and thinning
of the area of infarction that cannot be explained by
additional myocardial necrosis.25 On echocardiography,
true aneurysms appear as highly echogenic areas of
thinned, scarred myocardium (Fig. 19.46). True aneurysms
376 Section 6: Structural Heart Disease
Fig. 19.46: True apical aneurysm with wall thinning marked by arrows.
Fig. 19.48: Pseudoaneurysm of the left ventricle (LV) posterior wall
(arrow). Note the narrow neck just below the mitral valve.
Fig. 19.50: Massive pseudoaneurysm (arrows) adjacent to inferolateral
wall of the left ventricle (LV) as a result of small lateral wall infarction.
The communication is not visible in this view.
Fig. 19.47: True aneurysm of the inferoposterior wall.
Fig. 19.49: Color Doppler interrogation of the narrow communication
of pseudoaneurysm (PA).
most commonly involve LV apex but can be seen anywhere
in the LV (Fig. 19.47). Due to the stagnant blood flow, LV
thrombi may frequently be seen within the aneurysms.
Pseudoaneurysms are contained ruptures with
remodelling over time.25 The outer covering is of the
pericardium (Figs 19.48 to 19.50). Some ruptures may
occur over time rather than abruptly and then seal locally
within the pericardium. A left ventricular pseudoaneurysm
is thought to originate following this series of events. Such
pseudoaneurysms are differentiated from true aneurysms
by their very narrow neck and they may frequently contain
clot.
Pseudoaneurysms may occur on any left ventricular
wall segment involved with a severe transmural myocardial
infarction. Table 19.2 differentiates true aneurysm from
the pseudoaneurysm.
 Ischemic Heart Disease 377

Fig. 19.51: Wide-neck pseudoaneurysm of the inferoposterior wall. Fig. 19.52: Spontaneous ischemia (angina at rest) showing dilatation
Note thick walls of the margins. of the cavity and systolic wall thinning compared to recovery image in
systole on the right side.

Table 19.2: True aneurysm pseudoaneurysm Table 19.3: Traditional echocardiographic parameters related to
Orifice (Neck) Wide Narrow prognosis after myocardial infarction
LV wall Uninterrupted with Abrupt interruption Left ventricular volumes
gradual thinning LV ejection fraction
Doppler No flow Bidirectional blood flow Mitral regurgitation
Contrast No extravasation Extravasation into the Wall motion score index
pericardial space
Diastolic function
Left atrial volume
Right ventricular function

Occasionally, pseudoaneurysms may have wide neck Basic purpose of SE is to assess:

(Fig. 19.51).
In summary, echocardiography is useful for evaluation
of LV function, risk stratification and assessment of
prognosis after myocardial infarction (Table 19.3). At
present, 2D echocardiography is frequently used in the
management of patients with AMI. It is a low cost and safe
imaging modality, which can be easily applied at bedside
and is valuable for patient follow-up. Important benefit of
echocardiography has been demonstrated in establishing
the diagnosis, location and extent of myocardial infarction,
and in detection of mechanical complications after
myocardial infarction.
STRESS ECHOCARDIOGRAPHY
Functional abnormalities secondary to diminished
perfusion can cause segmental or global contractile or
relaxation dysfunction and elevation of filling pressures
which can be quantified. This premise forms the basis of
quantitative SE.26
Contractile reserve.
Perfusion reserve.
Stroke volume reserve.
Chamber compliance/stiffness.
Wall motion starts becoming apparent when the
flow reserve falls either spontaneously or during stress
(Fig. 19.52).
However, diameter stenosis by coronary angiography
is an anatomical number and may not always have a
good correlation with flow reserve which in turn may not
correlate with wall-motion score. SE is performed in two
ways (Figs 19.53 and 19.54):
1. Dynamic exercise combined with echocardiography.
2. Pharmacological stress (dobutamine-atropine, dipyri
damole or adenosine).
Dobutamine stress echocardiography is performed in
six stages: resting, 10 mic/kg/min, 20 mic/kg/min, 30 mic/
kg/minute, 40 mic/kg/minute and poststress. Each stage
is of 3 minutes duration. At peak dose, atropine is used if
target heart rate is not achieved.
378 Section 6: Structural Heart Disease
Fig. 19.53: Parasternal long-axis views in systole for comparison
at rest and immediately after exercise. There is decreased wall
thickening of the anterior septum with some dilatation of the left
ventricle cavity after exercise.
Fig. 19.55: Apical four-chamber view postexercise compared to the
rest (right panel). There is decreased wall thickening of the mid and
apical septum (arrows).
For the purpose of viability detection, small dose of
dobutamine is used beginning at 2.5 mic/kg/minute and
going upto 10 mic/kg/min.27
Echocardiographic analysis of regional left ventricular
function is based upon the assessment of radial motion.26
State-of-the-art SE technique is use of quad screen
and capturing only systolic images for simultaneous
comparison as endless cine loops (Figs 19.55 to 19.57).
Advantages of SE over other techniques:
Inexpensive
Radiation-free
Portable
Fig. 19.54: Dobutamine-atropine stress echocardiography to compare
the parasternal long-axis views. There is stress-induced hypokinesis
of the anterior septum with left ventricle cavity dilatation.
Disadvantages are:
Highly operator-dependent.
Dependent upon acquiring good images at peak stress.
Semi-quantitative or qualitative.
Stress echocardiography has nearly 80% sensitivity and
specificity for detecting inducible ischemia.26
Both dynamic exercise and pharmacological stress
provide comparable data although dynamic exercise is
more physiological.
Images in dynamic stress are obtained immediately
after the exercise and there may be some loss of
information from the peak stress.
During dobutamine stress, because of reduced preload
and indifferent afterload, there is quite often reduced
wall stress at rest and peak stress which may mask
ischemia.
End diastolic wall thickness at rest less than 6 mm
is usually associated with nonviability.28 If the wall
thickening is biphasic with initial improvement at
low dose of dobutamine and worsening at high dose,
this is highly suggestive of viability of the segment (s)
concerned.27
Long-axis motion is an important contributor to overall
function, but has been difficult to evaluate clinically
until the recent development of tissue Doppler and 2D
strain techniques. Longitudinal strain in automated
or semiautomated algorithm may be used to detect
inducible ischemia.12

Fig. 19.56: Short-axis images in quad screen in various stages of stress.
False normal interpretations of SE persist despite
improved interpretive guidelines.
Although some false negative results are a result of
stenoses of borderline severity or submaximal stress,
another important cause of false negative could be
subtle wall-motion abnormality due to mild ischemia
or hypertrophied walls or inadequate stress.26
Inducible myocardial ischemia is characterized by
simultaneous changes in systolic velocity, early diastolic
and postsystolic velocity. Impaired augmentation of
systolic, postsystolic and myocardial early diastolic
velocity during dobutamine infusion can identify presence
of underlying CAD (Figs 19.58 and 19.59). The postsystolic
shortening appears to be a new sensitive marker of induced
Ischemic Heart Disease 379
ischemia compared with WMSI. All these parameters are
being further explored before these become available for
prime-time use.
Recent work suggests that longitudinal strain may
provide a quantitative parameter to detect ischemia.
A threshold value of > -5% and > -10% is indicative of
akinesis and hypokinesis respectively (Fig. 19.59).
Strain and strain rate imaging may have its greatest
utility in situations in which suboptimal stress limits
the sensitivity of wall-motion analysis. There may be a
physiologic basis for an enhanced sensitivity of strain
imaging compared with wall-motion analysis in patients
with suboptimal stress because of early involvement of
longitudinal fibers in ischemic process.
380 Section 6: Structural Heart Disease

Fig. 19.57: Quad screen format for analysis of segmental wall motion in parasternal long-axis views.

Fig. 19.58: Peak systolic myocardial velocities at rest (2.56 cm/sec from apex to base) show a 2 to 3 fold increase during dobutamine
infusion (right panel).

Fig. 19.59: Change in 2D longitudinal strain in all the six segments in apical four-chamber view during stress (dobutamine infusion). Only basal
and mid lateral segments show change above a threshold. Overall 2D longitudinal strain of six segments changes from -11.7% to -9.2% (20%
change).
References
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5. Lieberman AN, Weiss JL, Jugdutt BI, et al. Two-dimensional
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infarcts. Am J Cardiol. 1985;55(5):551-5.
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7. Weiss JL, Bulkley BH, Hutchins GM, et al. Two-dimensional
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8. Miller TD, Weissler AM, Christian TF, et al. Quantitative
measures of regional asynergy add independent prog
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9. Blondheim DS, Beeri R, Feinberg MS, et al. Reliability of
visual assessment of global and segmental left ventricular
function: a multicenter study by the Israeli Echocardiogra
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258-64.
10. Moynihan PF, Parisi AF, Feldman CL. Quantitative detec
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11. Liel Cohen N. A new tool for automated assessment of seg
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ticenter study by the Israeli Echocardiography Research
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12. Yip G, Khandheria B, Belohlavek M, et al. Strain echocar
diography tracks dobutamine-induced decrease in regional
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Am Coll Cardiol. 2004;44(8):1664-71.
13. Picano E, Lattanzi F, Orlandini A, et al. Stress echocardi
ography and the human factor: the importance of being
expert. J Am Coll Cardiol. 1991;17(3):666-9.
14. Neskovic AN, Bolognese L, Picard MH. Echocardiography
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FA, Picard MH (Eds) Emergency Echocardiography. 2005;
129-46.
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15. Neskovic AN, Picard MH. Echocardiography in complica
tions of acute myocardial infarction. Neskovic AN, Flach
skampf FA, Picard MH (Eds) Emergency Echocardiogra
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16. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk
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and TPA for Occluded Coronary Arteries) Trial Investiga
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18. Vargas-Barrn J, Romero-Crdenas A, Roldn FJ, et al.
Long-term follow-up of intramyocardial dissecting hema
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19. Jahnke C, Hetzer R, Komoda T, et al. Images in cardiovas
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23. Moreno R, Lpez de S E, Lpez-Sendn JL, et al. Frequen
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complicating acute myocardial infarction in the direct
percutaneous coronary intervention reperfusion era. Chest.
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25. Schattenberg TT, Giuliani ER, Campion BC, et al. Postin
farction ventricular aneurysm. Mayo Clin Proc. 1970;45(1):
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27. Allman KC. Noninvasive assessment myocardial viabil
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28. Cwajg JM, Cwajg E, Nagueh SF, et al. End-diastolic wall
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 Chapter

20
Tumors, Masses and
Infection

Introduction
Cerebral or peripheral embolism is a frequent indication
for echocardiographic study to rule out cardiac masses or
any other source of embolism. Echocardiography is the
method of choice in identifying the presence and extent
of both intracavitary and intramural tumors, masses
and infective vegetations. Masses can cause obstruction,
infiltration, thromboembolism, arrhythmias and even
death. Echocardiography answers key questions like
size, shape, mobility, tissue characteristics, potential for
embolization, hemodynamic consequences and extra
cardiac effects of masses. Echocardiographic contrast
perfusion imaging differentiates the neovascularization
Fig. 20.1: Mitral valve myxoma obstructing mitral inflow as well as the
of malignancies from the avascularity of thrombi and the
left ventricular outflow tract (parasternal long axis view).
sparse vascularity of stromal tumors. Compared with the (RV: Right ventricle; AO: Aorta; LV: Left ventricle; LA: Left atrium).
adjacent myocardium, malignant and vascular tumors
hyper-enhance, whereas stromal tumors and thrombi Two-dimensional (2D) echocardiography has a good
hypo-enhance. sensitivity to detect intracardiac tumors, but a lower
There are a variety of other conditions which can detection rate for pericardial lesions or paracardial
present as cardiac masses like hydatid cysts, blood lesions. It can easily be used to detect pericardial effusion
cysts, thrombi, intramyocardial hematomas. There are due to metastasis in the pericardium. Smaller masses and
characteristic echocardiographic features to differentiate greater details are better seen by transesophageal echocar
these. Perivalvular abscesses due to infective endocarditis diography (TEE).
are another important space-occupying lesions. Mobile
and sessile masses on the valve leaflets in presence of CARDIAC MANIFESTATIONS OF MASSES
fever may represent infective vegetations and these have
typical features. This chapter is more of a descriptive Obstruction of circulation (Fig. 20.1).
and illustrative atlas of the masses rather than a detailed Interference with valve function (Fig. 20.2).
analysis. Direct invasion (Fig. 20.3).
384 Section 6: Structural Heart Disease

Fig. 20.2: Transesophageal echocardiographic (TEE) view. Doughnut Fig. 20.3: Right atrial angiosarcoma producing obstruction at the
shaped mass (arrows) obstructing the mitral orifice (detached orifice of the superior vena cava with peak instantaneous pressure
thrombus). gradients of 20 mm Hg during inspiration (right panel).
(LAA: Left atrial appendage).

Fig. 20.4: Dilated atria with a doughnut thrombus (arrows) in the left Fig. 20.5: 3D echocardiography (3DE) longitudinal slice of the left ven-
atrium with spontaneous contrast. tricle (LV) cavity. Apical dyskinesis with large thrombus (arrows).

Decreased myocardial contractility. Valvular heart disease (Fig. 20.7).

Conduction disturbance (block and arrhythmias). Thrombophilia.
Tamponade. Atrial fibrillation and dilated atria usually have
spontaneous echo contrast (Fig. 20.8). It usually
CARDIAC THROMBI AND SPONTANEOUS represents aggregation of the cellular components of
ECHO CONTRAST blood in conditions of stasis and low flow. It represents a
high risk for thrombus formation (Fig. 20.9). Presence of
Cardiac thrombi are one of the most important causes spontaneous contrast should compel one to look for the
of stroke, peripheral and pulmonary embolism.13 The thrombus. This contrast is best seen in TEE examination.
predisposing factors are: In suspected cardiac thrombi, echocardiography is
Dilated atria (Fig. 20.4). used for:
Atrial fibrillation. Detection of thrombi.
Segmental wall motion abnormality (Fig. 20.5). Location and number.
Severe ventricular hypokinesis (Figs 20.6A and B). Attachment and mobility.
 Tumors, Masses and Infection 385

A B
Figs 20.6A and B: Parasternal long-axis view in dilated cardiomyopathy. (A) Left panel shows large thrombus (arrow) and (B) the right panel
shows dissolution of the thrombus after heparin.

Fig. 20.7: Rheumatic mitral stenosis in apical four-chamber view with Fig. 20.8: Cloud-like spontaneous echo contrast in the right atrium in
large mobile thrombus with narrow stalk (arrows). presence of atrial fibrillation and unguarded tricuspid valve.

Delineation of focal echolucent areas indicative of clot
lysis (Fig. 20.10).
Real-time three-dimensional echocardiography (3DE)
provides a direct view of the left atrial appendage and
hence is superior to 2D transthoracic echocardiography
(TTE) as well as 2D TEE imaging (Figs 20.11 and 20.12)
Real-time 3DE also improves diagnostic yield of
thrombi at other locations (Fig. 20.13).
CARDIAC TUMORS
Echocardiography is now the principle method for the
diagnosis of cardiac tumors. There is, however, nothing
specific about the echocardiographic appearance to
identify the tumor.
Metastatic tumors are most commonly intramyocardial
and may manifest as localized thickening within the
myocardium. Such tumors can affect contractility or they
may impinge upon the various cavities of the heart and
obstruct flow.
Certain extracardiac tumors may affect the heart
and can be noted by echocardiography (Fig. 20.14).
Intrathoracic tumors of any origin can compress the
cardiac chambers from outside the heart.
Renal cell carcinoma may grow into the renal vein and
thus into the inferior vena cava, obstructing venous inflow.
386 Section 6: Structural Heart Disease

Fig. 20.9: Parasternal long-axis view with clockwise tilt of the Fig. 20.10: Echolucency in the center of the apical left ventricle (LV)
transducer to show thrombus in the right atrium (arrow) in presence of thrombus (c)
spontaneous echo contrast.

Fig. 20.11: 3D TEE images of the left atrial appendage. Note the lobular structure on the right side that can hide thrombi.

Fig. 20.12: 3D TEE image of a wall-hugging thrombus in the left Fig. 20.13: 3DE image showing a thrombus at bifurcation of the
atrial appendage (arrows) that was not picked up by 2D TEE. Note the pulmonary artery (PA).
spontaneous echo contrast in the left atrium.

Fig. 20.14: Extracardiac mass with cystic change compressing the
right ventricular outflow tract (RVOT) and the pulmonary arteries.
(MPA: Main pulmonary artery; RPA: Right pulmonary artery).
Fig. 20.16: Real-time 3DE image in four-chamber view showing
broad-based relatively sessile left atrial myxoma.
Seventy-five percent of the primary cardiac tumors are
benign.46 Amongst, benign tumors, myxomas, fibroela
stomas and lipomas predominate in adults while rhabdo
myoma, fibroma and myxoma are more frequent in
children.5 Primary malignant tumors are mostly sarcomas.7
ECHOCARDIOGRAPHIC FEATURES OF
MYXOMA (FIGs 20.15 to 20.17)
Endocardium-based tumors that do not inflitrate.
Predilection for fossa ovalis.
Mobile in 75%.
Broad-based or pedunculated stalk.
Tumors, Masses and Infection 387
Fig. 20.15: Apical four-chamber view showing a variable shape
myxoma protruding through the mitral orifice and attached to the
limbus of oval fossa.
Fig. 20.17: 2D TEE image. Pedunculated left atrial myxoma protruding
through the mitral orifice (arrows).
Lobular, irregular with variegated echo texture.
Marked fluidity.
Seventy-five percent of the myxomas occur in the left
atrium, 20% in the right atrium and rest 5% at different
places (Figs 20.15 to 20.17).8
Complex cardiac myxomas are those that occur in
families in combination with two or more of the following
conditions: skin myxomas, cutaneous lentiginosis, myxoid
fibroadenomas of the breast, pituitary adenomas, primary
adrenocortical micronodular dysplasia with Cushings
syndrome and testicular tumors. The Carney complex
is a syndrome of myxoma, endocrine hyperfunction
and skin pigmentation. Symptoms in 2550% of patients
388 Section 6: Structural Heart Disease
Fig. 20.18: Parasternal short-axis view showing right atrial myxoma
(T) with attachment to the interatrial septum (arrow).
Fig. 20.20: Papillary fibroelastoma attached to the chords of the
tricuspid valve. Note the papillary fronds on the surface.
are caused by systemic embolization, or inflow or outflow
obstruction. These include transient ischemic attacks,
dyspnea, syncope, sudden death or palpitations (Fig.
20.18).
PAPILLARY FIBROELASTOMA
Papillary fibroelastomas are rare, primary, benign
cardiac tumors most frequently located in the heart
valves. They are a potential cause of systemic emboli,
stroke, myocardial infarction and sudden death.
Even rarer are multiple fibroelastomas, which show
an echocardiographic picture of multiple pedun
culated formations most commonly located in the
atrioventricular valves.
Fig. 20.19: Fibroelastoma of the aortic valve. The right panel is a 3DE
image.
Most common sites are aortic and mitral valves
followed by tricuspid valve, LVOT and interventricular
septum and rarely, the eustachian valve.9,10
Papillary fibroelastoma represents 75% of all valvular
tumors.
Second most common primary cardiac tumor of adults.
Some synonyms:
Giant Lambl excrescence
Papilloma of valves
Myxofibroma
Myxoma of valves
Hyaline fibroma
Fibroma of valves
Pattern of Papillary Fibroelastoma
Attachment to a cardiac valve.
Presence of a pedicle.
Papillariferous surface and papillary fronds detectable
by echocardiography (Figs 20.19 to 20.22).
MALIGNANT TUMORS
The most common primary cardiac malignant tumor
is a cardiac sarcoma.7 Subtypes include angiosarcoma
(most common), undifferentiated sarcoma (second
commonest), malignant fibrous histiocytoma (1124%),
leiomyosarcoma (89%), and osteosarcoma (39%).
An angiosarcoma arises preferentially in the right
atrium of middle-aged men and can be very bulky
(Figs 20.23 and 20.24). Obstruction of the right sides
blood flow may cause right-sided heart failure or may
mimic pericardial tamponade.
 Tumors, Masses and Infection 389

Fig. 20.21: 3DE image in cross-section showing fibroelastoma Fig. 20.22: Complete atrioventricular canal defect with papillary
attached to P2 segment of the mitral valve. fibroelastoma of the mitral valve (arrow).
(AML: Anterior mitral leaflet ).

Fig. 20.23: Angiosarcoma of the right atrium attached to its free wall Fig. 20.24: Mobile mass in the left ventricle (LV) apex with normal wall
and extending into the right ventricle (RV). motion abnormality. Histologically, it was rhabdomyosarcoma.

DIFFERENTIAL DIAGNOSIS OF Hydatid cysts are frequent in certain regions of the

CARDIAC TUMORS world and present with myriad features resembling
tumors.11
Following differential diagnoses need to considered
(Figs 20.25 to 20.33): INFECTIVE ENDOCARDITIS
Thrombi
Anomalous muscle Invasion of endocardium or biofilm of the intravascular
Mural hematoma devices by microbes is called infective endocarditis (IE).
Cysts Microbes produce destruction but local area swells up
Infective masses due to defense mechanisms mounted by host as well as
Abscess organism. These localized swellings produce variable
390 Section 6: Structural Heart Disease

Fig. 20.25: Cardiac masses (arrows) in the left ventricle (LV) that may Fig. 20.26: Anomalous muscle bundle (arrow) in the left ventrical (LV)
be confused with multicentric tumor. Their disappearance (right lower cavity that can be mistaken for a tumor.
panel) after sometimes, suggests these were thrombi.

Fig. 20.27: Abscess between aortic root and the left atrium in a patient Fig. 20.28: Tumor-like infective mass attached to the pacing lead
with infective endocarditis of the aortic valve. (white arrow) in a patient with arrhythmogenic right ventricle (RV)
dysplasia.

Fig. 20.29: Localized pericardial effusion (PE) posterior to the left Fig. 20.30: Caseous degeneration of the calcific mitral annulus
ventricle (LV). mimicking a tumor (arrow). Outer calcified shell with echolucency in
the center is characteristic.
 Tumors, Masses and Infection 391

A B C
Figs 20.31A to C: Myocardial dissection flap (arrow) showing movement during various phases in cardiac cycle (A to C) that can mimic a tumor.

Fig. 20.32: 3DE image. Hydatid cyst (arrows) in the left ventricular free Fig. 20.33: Tumor-like invasion of the left ventricle (LV) free wall due
wall that is abnormally thickened and with distorted cavity. to hydatid cyst (arrow).

Fig. 20.34: 3DE image. Pedunculated mass attached to the Fig. 20.35: Irregular mass along the right ventricular free wall (arrows)
anterior mitral leaflet (arrow) in a patient with fever. Vegetation needs in a patient with prior pacemaker implantation and fever (transeso
differentiation from fibroelastoma. Right lower panel shows gross phageal echocardiographic view).
appearance on surgery.

infective masses called vegetations.12 Predispositions are and intracardiac devices, rheumatic heart disease and
congenital heart disease, degenerated valves, prostheses so on.12
392 Section 6: Structural Heart Disease
Fig. 20.36: Dehiscence of the ventricular septal defect (VSD)
patch due to infective endocarditis (arrow) with vegetations on the
surface.
Fig. 20.38: 3D TEE image. A hole in the anterior mitral leaflet (arrow)
with a mass along margins is seen.
Endocardial involvement is a major criterion amongst
the modified Duke criteria for diagnosis of IE.13,14
Endocardial involvement can be of the following type:
Infective vegetation attached to endocardium
(Fig. 20.34).
Masses attached to the intravascular or intracardiac
devices (Figs 20.35 and 20.36).
Abscess.
Valvular perforation (Figs 20.37 to 20.39).
Aneurysm or Fistula formation due to infection
(Figs 20.40 and 20.41).
Vegetation: An oscillating polypoid mass with
independent motion attached to an endocardial surface in
a patient with clinically suspected IE (Fig. 20.34).
Clinical presentation of IE is showing a change over
time due to graying of the population, greater use of
Fig. 20.37: Perforation in the anterior mitral leaflet seen in transeso
phageal echocardiography 110 view (arrow).
Fig. 20.39: 2D TEE four-chamber view showing flow by color Doppler
through the hole in anterior mitral leaflet.
intracardiac devices, wide spread use of immuno
supressive drugs and changing microbes.15,16
Aneurysm formation is a compelling indication for
surgery17,18
Transesophageal echocardiography is the preferred
imaging technique for the diagnosis and management of
IE in adults with either high risk for IE or moderate to high
clinical suspicion of IE or in patients in whom imaging by
transthoracic echocardiography is difficult.19
Fungal infections produce large masses on the
valves and should be differentiated from the tumors
(Fig. 20.42).
POINTS TO REMEMBER
With amelioration of infection, the vegetations can
become smaller or larger and can disappear as well.
 Tumors, Masses and Infection 393

Fig. 20.40: 3D TEE image showing aneurysm of the anterior mitral Fig. 20.41: Large pseudoaneurysm (P) of sinus of Valsalva obstruct-
leaflet (arrows). A vegetation is seen at the leaflet tip. ing the RV outflow tract secondary to infective endocarditis (IE) of the
aortic valve. Small vegetations are seen on the aortic valve.

Fig. 20.42: Candida ball attached to mitral and aortic valves in an Fig. 20.43: Healed bright echoes on the aortic valve in the parasternal
infant (arrows). long-axis view.

Vegetations that are greater than 10 mm or are

pedunculated have high predilection for embolization.
Healed vegetations may become more echogenic and
still retain their embolic potential (Fig. 20.43).
The infective vegetations require to be differentiated
from:
Lambls excrescences
Fibroma of the valve
Arantius nodules
Degenerated and rheumatic nodules
Ruptured chord (Fig. 20.44)
Lupus vegetations20
Myxomatous valves (Fig. 20.45)
Presence of obstructive vegetations, fistula or abscess
Fig. 20.44: Broken chord attached to the anterior mitral leaflet (arrow).
formation or embolization portend bad prognosis.
394 Section 6: Structural Heart Disease
Fig. 20.45: Myxomatous posterior mitral leaflet with thickening of the
distal half of the cusp (arrow).
Vegetations on the tricuspid valve occur more often
in patients with central venous catheters, intravenous
drug abusers, patients on hemodialysis and those with
pacemakers (Fig. 20.46).
References
1. Egolum UO, Stover DG, Anthony R, et al. Intracardiac
thrombus: diagnosis, complications and management. Am
J Med Sci. 2013;345(5):391-5.
2. Bakalli A, Georgievska-Ismail L, Koinaj D, et al. Prevalence
of left chamber cardiac thrombi in patients with dilated
left ventricle at sinus rhythm: the role of transesophageal
echocardiography. J Clin Ultrasound. 2013;41(1):38-45.
3. Lee JM, Park JJ, Jung HW, et al. Left ventricular throm
bus and subsequent thromboembolism, comparison of
anticoagulation, surgical removal, and antiplatelet agents.
J Atheroscler Thromb. 2013;20(1):73-93.
4. Edwards FH, Hale D, Cohen A, et al. Primary cardiac valve
tumors. Ann Thorac Surg. 1991;52(5):1127-31.
5. Nield LE, Mendelson M, Ahmad N, et al. Clinical
review of obstructive primary cardiac tumors in childhood.
Congenit Heart Dis. 2013.
6. Barreiro M, Renilla A, Jimenez JM, et al. Primary cardiac
tumors: 32 years of experience from a Spanish tertiary
surgical center. Cardiovasc Pathol. 2013.
7. Burnside N, MacGowan SW. Malignant primary cardiac
tumours. Interact Cardiovasc Thorac Surg. 2012;15(6):
1004-6.
8. Ha JW, Kang WC, Chung N, et al. Echocardiographic
and morphologic characteristics of left atrial myxoma
and their relation to systemic embolism. Am J Cardiol.
1999;83(11):157982, A8.
9. Harling L, Athanasiou T, Ashrafian H, et al. Minimal access
excision of aortic valve fibroelastoma: a case report and
review of the literature. J Cardiothorac Surg. 2012;7:80.
Fig. 20.46: Infective vegetations on the tricuspid valve leaflets
(arrows) in a subject with fever and on maintenance hemodialysis.
(IAS: Inter-atrial septum).
10. Klarich KW, Enriquez-Sarano M, Gura GM, et al.
Papillary fibroelastoma: echocardiographic characteristics
for diagnosis and pathologic correlation. J Am Coll Cardiol.
1997;30(3):784-90.
11. Abhishek V, Avinash V. Cardiac hydatid disease: literature
review. Asian Cardiovasc Thorac Ann. 2012;20(6):747-50.
12. Cecchi E, Chirillo F, Faggiano P, et al. For the Italian
Registry on Infective Endocarditis (RIEI) Investigators. The
Diagnostic Utility of Transthoracic Echocardiography for the
Diagnosis of Infective Endocarditis in the Real World of
the Italian Registry on Infective Endocarditis. Echocar
diography. 2013;30(8):871-9.
13. Martos-Perez F, Reguera JM, Colmenero JD. Comparable
sensitivity of the Duke criteria and the modified Beth Israel
criteria for diagnosing infective endocarditis. Clin Infect
Dis. 1996;23(2):410-11.
14. Tissires P, Gervaix A, Beghetti M, et al. Value and limita
tions of the von Reyn, Duke, and modified Duke criteria for
the diagnosis of infective endocarditis in children. Pedi
atrics. 2003;112(6 Pt 1):e467.
15. Nakagawa T, Wada H, Sakakura K, et al. Clinical features of
infective endocarditis: Comparison between the 1990s and
2000s. J Cardiol. 2013;pii:50914-5087.
16. Hoen B, Duval X. Clinical practice. Infective endocarditis.
N Engl J Med. 2013;368(15):1425-33.
17. Silbiger JJ, Krasner A, Chikwe J, et al. Pseudoaneurysm
formation in infective endocarditis. Echocardiography.
2013.
18. Edwards NC, Smith NL, Steeds RP. Beyond the artery and
ventricle-an aneurysm of the mitral valve leaflet. Echocar
diography. 2013;30(8):E258-9.
19. Bruun NE, Habib G, Thuny F, et al. Cardiac imaging in
infectious endocarditis. Eur Heart J. 2013.
20. Contractor T, Bell A, Khasnis A, et al. Antiphospholipid
antibody-associated non-infective mitral valve endocar
ditis successfully treated with medical therapy. J Heart
Valve Dis. 2013;22(1):36-8.
 Index 415

Index
Page numbers followed by f refer to figure and t refer to table.

A Anterior severity of 106

leaflet of tricuspid valve 305 volumetric severity of 104
Abdominal aorta 320 mitral leaflet 48f, 73f, 102, 113, 113f root 318
Acoustic calcification 50f dilatation with suspected Marfan
scattering 7 in transesophageal echocardio- syndrome 333f
shadowing 14 graphy, perforation in 392f sinotubular junction with valvular
speckle tracking 262 type of 74 stenosis 331f
Acquired aortopathies 331
pulmonary leaflet 127f sinus See Sinus of Valsalva
Acute
Anterograde velocity of tricuspid inflow aneurysm of 308
anterior myocardial infarction 345f
122 dilatation triangular aortic valve
aortic syndrome 335
Anterolateral commissure 65f opening in diastole 334f
ischemia 289
Aorta 318 stenosis 286
pericarditis 345
acquired disorders 318 anatomy of 86
rupture of subendocardial muscle
anatomy of 318f etiology of 85
layer with blood seeping into
congenital disorders 318 valve 127f
outer layer 375f
parts of 318 area 83
American Heart Association Classification
properties of 274 for judging severity 90t
of Primary Cardiomyopathies 397t
Aortic cross-section of 83f
Anderson-Fabry disease 402
arch 319 fibroelastoma of 388f
Aneurysm
coarctation 324 guards 83
confined to descending thoracic aorta
cusps 84 opening 177
337f
dilatation of pulmonary artery 132f dimensions, normal values of 329t regurgitation 98
formation 375 disorders, etiopathogenesis of 322 to annular dilatation, type I
spreading down and upward from dissection to ascending aorta 337f 333f
arch of aorta 337f Doppler spectrum, incompletely stenosis 83
Angle formed 91f Aortopulmonary window 329
equal to angle of incidence producing interruption with low-velocity types of 329
less bright echo 6f continuous flow in thoraco- Apical
of incidence 6 abdominal aorta 325f 4-CV large pericardial effusion with
Animal regurgitant volume, concept of 104f right atrial collapse 350f
pericardium 141 regurgitation aneurysm in presence of mid-cavity
vulvar tissue See Animal pericardium anatomical orifice of 36f obstruction 404f
Annular tissue velocities 216 by echo-Doppler dyskinesis and increased echogenicity
from lateral edge of mitral annulus methods 108 of mid-septum 368f
181f, 215f techniques, detection of 102 five-chamber 18f, 19f
Annuloaortic ectasia 332 by vena contracta 105 four-chamber
Annulus 84 concept of 102f apical intramural hematoma 412f
paradoxus 355 functional anatomy of 100 ball thrombus in left atrium 49f
Anomalous muscle bundle in left ventrical of left ventricular outflow tract congenital tricuspid stenosis 120f
cavity 390f height 105f dilated right atrium 370f
416 A Practical Approach to Clinical Echocardiography

free wall Augmented expiratory flow reversal in Biplane

pericardial effusion 375f
rupture 375f
in systole 366f
mitral leaflets 48f
rheumatic tricuspid 116f
with normal left ventricle end-
diastolic volume 406f
long axis 19f
view left ventricle cavity 406f
view with sonovue contrast
injection 412f
muscular ventricular septal defect
303f
myocardial dissection with hematoma
373f
rotation
reduced 289f
values true apex, difference in 285f
two-chamber view with structures 19f
Apicoanterior myocardial infarction
seven days after onset 369f
Applications of strain and strain rate
imaging 276
Arrhythmogenic right ventricular
cardiomyopathy 409
dysplasia 397
Ascending aorta 319
with normal aortic root, dilatation of
324f
Assess severity of MR, methods to 76
Assessing longitudinal function 196
Asymptomatic patient with aortic stenosis,
increased torsion in 286f
Atheroma in aortic arch 336f
with penetrating ulcer 336f
Atherosclerosis 334
Atria with doughnut thrombus in left
atrium, dilated 384f
Atrial
flow reversal of pulmonary vein 220f
kick 209
septal defect 295
types of 295
Atrialized ventricle 306
Atrioventricular septal defect with
large right ventricle in tetralogy of
Fallot 312f
primum defect 301f
Atrium in adult subject with tricuspid
atresia 302f
Attenuation 7
hepatic vein with constrictive area-length method See Biplane
pericarditis 357f ellipsoid formula
Axial versus lateral resolution 11f ellipsoid formula 173
to estimate LV end-diastolic
B volume 173f
multilobed apical thrombus 374f
Ball-in-cage simpson 174f
mechanical prosthesis 139f Both mitral and aortic valves 99f
in aortic position 139f Bowditch effect 170
valve 138 Broad bandwidth transducer with wide
Basal range of resonant frequency 9f
chordae 47, 66 Bulky leaflets of MV in Barlows syndrome
left ventricle 365f 71f
right ventricular radial strain with left Bulls eye 269f
ventricular basal radial strain, Bullet
comparison of 191f formula 173
rotation versus apical rotation 283f method to estimate left ventricle
Base-to-apex from end diastole to end volume 173f
systole, rotation of 282f
Bernoullis C
equation 28
Calcific mitral annulus mimicking tumor,
principle 28
Best lateral resolution in parasternal long caseous degeneration of 390f
axis view 78f Calcified
Bicuspid aortic valve 85 atheromatous ulcer in anterior wall of
in three-dimensional echocardio- ascending aorta 336f
grapic 87f pericardium restricting transverse
with conjoined leaflet to fusion of left expansion of heart with dilated
and noncoronary cusps 86f left atrium 354f
with proximal aortic dilatation in Cardiac
parasternal long-axis 323f cycle of
with stenosis 87f left heart, phases of 206f
Bifurcation of pulmonary artery 20f LV, phases of 168f
Bileaflet manifestations of masses 383
mitral prosthesis in masses in left ventricle 390f
diastole 142f, 143f movement, vectors of 259t
systole three physiological resynchronization therapy See
regurgitant jets 145f Torsion resynchronization
prostheses, types of 33 therapy
prosthetic valves 140 tamponade 349, 384
Bimodal deceleration slope in third beat tumors 385, 389
of transmitral flow 55f Cardiogenic shock with isolated right
Bioprosthesis 141 ventricle infarction 370f
Bioprosthetic Cardiomyopathies 395
degeneration 152 dilated 397
heart valves 141 Carpentiers functional classification 67
valves 141 Carpentier-Edwards
Biphasic bioprosthesis in mitral position
longitudinal expansion of left ventricle stenosis of orifice in diastole 153f
diastole 210f mitral bioprosthesis severe trans-
mitral flow with tips of mitral leaflets prosthetic mitral regurgitation
212f 155f

Causing left ventricle volume overload 99f
Caveats for Bernoullis equation 28
Cavity without walls in diastole and
systole 261f
Central processing unit 8
Chemla equation 41
Chordae tendineae 47, 66
Chords, types of 66f
Chronic ischemia 289
Circumferential
fiber shortening
estimation of 177f
velocity of 177f
flow around ball in Starr-Edwards
ball-in-cage prosthesis in
mitral position 139f
radial shear strain apex 262f
strain 263
of ascending aorta with
hypertension 276f
wall thickening with reduced lumen of
left subclavian artery 334f
Circumflex artery 364f
Cleft anterior mitral leaflet 314f
Clinical utility of TDI 239
Color Doppler
flow reversal in descending thoracic
aorta 107f
interrogation
in mid-cavity obstruction 405f
of narrow communication of
pseudoaneurysm 376f
jet of aortic regurgitation 36f
myocardial
from interventricular septum 233f of functional MR 73f
imaging 231
velocities from basal septum to
basal lateral wall 234f
velocity pattern of septum 400f
of right ventricular outflow tract 129f
Color flow
Doppler
evaluation of aortic regurgitation
104
of mitral regurgitation proximal
isovelocity surface area 35f
jet area in LA 76
mapping 121
Color kinesis in apical four-chamber view
apical akinesis 371f
Color-flow map-adjusted wave Doppler to
obtain transpulmonary gradients
132f
Combined mitral valve stenosis 62f
Commissures 85
Common atrium 300
Comparing mild
aortic regurgitation with severe aortic
regurgitation 108f
versus large pericardial effusion 347f
Congenital
aortic sinus aneurysm 309
bicuspid aortic valve in diastole
regurgitant orifice 99f
disorders of aorta 322
heart disease in adults 295
parachute tricuspid valve causing TS
121f
Conical fibroserous sac of pericardium
343f
Constrictive pericarditis 287
case of 358f
Continuity equation, limitations of 29
Continuous wave Doppler interrogation
155f
Coronary
artery disease 365
sinus 295
vascular territory 363
Cresentic intrapericardial mass with
pericardial effusion 349f
Curved anatomical M-mode TVI 231
Cushings syndrome 387
CW Doppler
interrogation in MR 81
signal alternans of TR 124f
spectrum
in acute aortic regurgitation 108f
of acute MR 81f
of mild versus severe aortic valve
stenosis, comparison of 91f
CW profiles of varying degree of aortic
valve stenosis 91f
D angioplasty 372f
Deceleration time of mitral early filling
wave 208f
Decreasing mitral flow early diastolic
velocities 356f
Degeneration of aorta 334
Degenerative
aortic aneurysms 336
MV disease 68
tricuspid valve disease 118
Dehiscence of
Starr-Edwards mitral prosthesis 156f
ventricular septal defect 392f
Dense continuous wave 76
Index 417
Depth of presumably severe MR 76f
Descending aorta 319
Diaphragm-like aortic valve orifice 92f
Diastole, physiology of 204
Diastolic
dysfunction 210
and twist, grades of 290
in clinical sense 205f
flow
fraction 221f
reversal in descending aorta 106
fluttering of interventricular septum
with exaggerated respiratory
motion 355f
function 204, 210, 239
function See Tissue motion
significance of 205
MR with functional systolic MR 76f
pulmonary artery pressures from PR
jet velocity, estimation of 41f
right ventricular collapse 350f
stress test 224
in normal person 224f
tricuspid indicating elevated right
ventricle diastolic pressures
with dilated cardio -
myopathy 194f
wave 219f
Dilated
cardiomyopathy 397
pulmonary artery, absent pulmonary
valve with 131f
Dimensionless index for tilting-disc aortic
prosthesis, measurement of 151f
Disk summation method See Modified
Simpsons rule
Dissecting
flap fluttering in left ventricle 373f
myocardial hematoma in apical
myocardium after delayed
Dominant medial commissure fusion,
asymmetric commissural fusion
with 59f
Doppler
echo, types of 25
equation 25f
interrogation
left ventricle outflow and inflow
207f
of aortic flow, continuous 352f
of mitral orifice from apical view
velocity profile 52f
measure of contractility 183
principle for estimating velocity 25
418 A Practical Approach to Clinical Echocardiography
signal from left ventricular inflow 206f
spectrum suggests nonobstructed
valve 147f
tissue imaging 224
Double-chambered right ventricle 307,
307f
with aneurysm of membranous
ventricular septal defect 308f
with pulmonary valve stenosis 308f
Double-outlet right ventricle
variant of tetralogy of Fallot 312f
with absent pulmonary valve 313f
with pulmonary stenosis 132f
Dresslers syndrome 370
Ductus closure device projection in
pulmonary artery 332f
Duplex scan of left common carotid artery
with color Doppler 335f
Dysfunctions of prosthetic heart valves
152t
Dysplastic pulmonary valve
filling right ventricular outflow tract
and causing obstruction 130f
with redundant distal parts 131f
E Endocardial
Early
amyloid infiltration with mild
thickening of left ventricle walls
403f
systolic
functional MR 80f
longitudinal lengthening 269
measures 259
Ebsteins anomaly 119, 119f, 304, 306f
carpentier classification of 306
in parasternal long-axis 305f
type
C 306f
D 307f
Eccentric
aortic regurgitation jet to perforation
104f
jet of severe aortic regurgitation with
bicuspid aortic valve 105f
Eccentrically placed medtronic-hall valve
in aortic position 34f
Echo, concept of 5f
Echocardiographic
examination, sequence of 16
imaging 365
methods of studying twist 284
parameters related to prognosis after
myocardial infarction 377t
Echocardiography Doppler alternans of tricuspid
basic principles 3 regurgitation with normal right
display 3 ventricular systolic
in IHD 369 pressure 195f
interpretation 3 regurgitation from membrane in
technique 3 diastole 315f
Echo-Doppler types of 25
for assessing mitral stenosis, Foramen ovale membrane, aneurysm of
comparison of various 53f 300f
signs of cardiac tamponade 350t Force developed and heart rate,
Effective orifice area 30 relationship between 171f
Effusive-constrictive pericarditis in young Four cardiac valves, anatomical position
female 357f of 128f
Ehlers-Danlos syndrome 309 Free wall rupture 374
Elongated MV leaflets in fibroelastic Full volume
data set recorded from apical view
degeneration 69f
179f
EMF echocardiographic features 406
three-dimensional transthoracic
En face
echocardiography of ascending
mitral leaflets with free margin 47f
aorta 340f
of atrioventricular septal defect from
Functional
right side 305f
PR with structurally normal pulmo-
of interventricular septum 302f
nary valve 135f
End-diastolic
tricuspid regurgitation 114
pressure See End-diastolic volume
types of MR 67
volume 171f
Functioning medtronic-hall tilting-disk
prosthesis aortic position 147f
border delineation 174 Functions of aorta 320
shortening fraction level of chordae Fundamental
tendinae 178f basis of TDI 236
End-systolic points, greater dispersion of of torsion 280
regional 181f
Energy loss using simple formula,
G
coefficient of 34f
Estimating Global
energy loss index, method of 92f diastolic performance 248
pulmonary pressures from TR and PR longitudinal strain and strain rate 183
jets 40f systolic performance 248
European classification of
cardiomyopathies 397 H
Hagen-Poiseuille equation See Ohms
F law of fluids
Fabrys disease 402 Heart
Factors contributing to diastole 205 failure 287
False tendons in left ventricle cavity 412f with normal ejection fraction 240
Fibro-muscular strand extending muscle 257
between anterior interventicular Helical orientation of myocardial fibers
septum and posterior wall with figure of 8 166f
of left ventricle 167f Hemispheric proximal isovelocity surface
Flail anterior mitral leaflet coapting 67f area 132f
Flow Hemodynamic
abnormality precedes wall-motion assessment of prosthetic valves 141
abnormality 366f evaluation 24
continuity of 28 by echo-Doppler techniques 24
 Index 419

introduction 24 on regional deformation metrics, heart circulation 26f

of aortic effects of 268 panel
regurgitation 98 Ischemic large pericardial effusion in
valve stenosis 88 heart disease 363 parasternal long-axis view
of mitral stenosis 50 MR 71 352f
of MR 74 Isovolumic parasternal long-axis view 245f
Hepatic vein flow in assessment of TR 123 acceleration 200f tissue velocities of medial mitral
High transesophageal echocardiographic contraction 205 annulus 243f
view dissection in ascending aorta time 168 pulmonary artery 107, 319
340f relaxation 205 ventricle 319
Holodiastolic flow reversal in abdominal time 206 apex by velocity vector, rotation of
aorta 107f 283f
Holosystolic longitudinal stretch with L base in normal, rotation of 283f
post-systolic shortening 272f
Labeling of tissue velocity waveforms 229 cavity by 3D echo, conical shape of
Hyperkinesis 366
Laminar flow 167f
Hypertension cardiomyopathy 286
cylinder 25f ejection fraction with shape of left
Hypertensive functional tricuspid
versus turbulent flow 25f ventricle, relationship of
regurgitaion 115f
Laplaces law 171 170f
in mitral stenosis 115f
Hypertrophic cardiomyopathy 286, 397 Large color jet area 76f in short-axis view 375f
asymmetric septal hypertrophy in Large morphology of 165
401f diastolic tissue velocity waves 358f physiology of 167
types of 404f left-sided pleural effusion f 349 ventricular
mitral E velocity and velocity 76f ejection fraction 174
muscular ventricular septal defect in filling pressure 239
I
posterior septum 303f free wall rupture 374
Idiopathic functional tricuspid perimembranous ventricular septal outflow tract 83, 139f, 142, 165, 319
regurgitaion 115f defect with transventricular in calculation of mitral valve
Image acquisition, technique of 12 peak gradient 304f 57f
Infective endocarditis 389 vena contracta 78f peak velocity 26f
Inferior cava ventricular septal defect 305f velocity time integral 183
cava 295 Lateral pressure-volume loop 168f, 205f
indicates elevated right atrial pressure, edge mitral annular velocities 216f pseudoaneurysm 349f
dilated 194f leaflets to la appendage 65f systolic function 165, 241
Innominate artery 319 mitral annular velocities 241f tension-time sequence 169f
Inter-atrial septum 84 Leaflets Leteral commissure 48f
Interior tricuspid leaflet 153 coaptation 65f
Localized pericardial effusion adjacent to
Intermediate chordae 66 of mitral bioprosthesis in open
lateral wall 347f
Intermittent transprosthetic mitral position 144f
Loeys-Dietz syndrome 309
regurgitation 148f of pulmonary valve without any
Long axis
Internal dependency of velocities 235 definite fibrous annulus 127f
akinesis of mid anterior septum 367f
Interventicular septum 166 with narrow orifice, thickening of 49f
greater septal hypertrophy 402f
part of 168f Left
LV function 171
structure of 166f anterior descending artery 364f
Intimal hyperplasia and medial atrial Longitudinal
hypertrophy 51 appendage 384 oscillations 4
Intramural hematoma 339, 372f function by deformation imaging strain rate analysis, advantages of 185
in arch of aorta 340f 273 Low systolic tissue velocities 248
Intramyocardial hematoma 371 longitudinal strain ventricular Lower panel depicts annular velocities
Intrinsic reduced myocardial compliance systole 276f 215f
in restrictive cardiomyopathy 354f volume 210 Low-gradient low-flow severe aortic valve
Irregular mass right ventricular free wall common carotid artery 107f stenosis, types of 93
391f coronary sinus and left atrium aortic Low-velocity biphasic inflow across mitral
Ischemia valve replacement, communi- valve 26f
imaging 365 cation between 330f Lunula, thicker free margin of cusp 85f
420 A Practical Approach to Clinical Echocardiography

LV Midesophageal valve apparatus

ejection time from box-like opening of bicaval view components of 64f
aortic valve, measurement of inferior vena cavae and interatrial in mitral stenosis, morphology of
176f septum 22f 58
systolic function, determinants of 170 superior vena cavae and interatrial valve
volume estimation by Simpson septum 22f anatomy of 45
method, technical tips for 178 long axis view area 53
volumetry 172 calculation of 56
aorta 22f
L-wave, importance of 209 consists 46
left
leaflets 46
atrium 22f
M ventricle 22f
opening 177
prolapse 69
Main pulmonary artery 387f mitral valve 22f regurgitation introduction 64
Malignant tumors 388 transverse short axis view left atrial to measure size of annular
Mapse estimation, method for 172 appendage 22f caseoma 13f
Marfan syndrome 309, 331 Mid-septal left atrial longitudinal strain M-mode
Marginal chordae 66 275f color
Massive Midwall fiber shortening 178f Doppler myocardial in apical four-
pseudoaneurysm adjacent to Mild chamber view of left
inferolateral wall of left leaflet thickening only tips of leaflets ventricle 234f
ventricle 376f 59f flow
pulmonary artery dilatation with MR by color jet area 76f map across left ventricle long
vestigial pulmonary valve Mitral axis 405f
tissue 131f propagation velocity 108
annular velocities 214
Mauve color versus apex 413f depiction of color-coded tissue
from medial edge 240f
Mean velocities of left ventricular
annulus 46, 66
pulmonary artery pressures from PR short axis 236f
plane systolic excursion 172f
jet velocity, estimation of 41f description of strain rate of
velocity gradient over segment of fixed apparatus in relation to
interventricular septum 239f
length 237f aortic annulus 45f echocardiogram
Medial left level of aortic valve 15f
commissure 48f atrium 45f rapid expansion of left ventricular
calcification 50f ventricle 45f posterior wall in early
mitral bioprosthesis causing mitral valve diastole 353f
annular tissue velocities 240f obstruction 49f echocardiography 14, 102, 175
versus lateral mitral 357f E- and pulmonary D-waves 207 in LV systolic function, current use
Medtronic-hall valve in aortic position E preceding tissue 219f of 177
145f flow propagation by color M-mode limitations of 177
Membranous subaortic stenosis 96f 221 image of
Metallic aortic prosthesis, acoustic inflow aortic valve 177f
shadow to 14f acquisition 213 mitral valve 177f
Microbubble formation 152 feasibility 213 of aortic root 10f
Mid of left atrium 10f
measurements 213
and late systolic MR in presence of MV section of
velocities 212
prolapse 81f inferior vena cava with reduced
orifice secondary to mitral annular
anterior septum and posterior inspiratory collapse 194f
calcification 48f
wall thickness in diastole and ventricles 348f
systole, comparing basal regurgitation 64 Modified
and 367f stenosis 45, 60 continuity equation for estimating
left ventricle 365f criteria for 51t aortic valve area 93f
muscular ventricular septal defect left panel 116f quinones method 174, 174f
372f pathoanatomy of 48 Simpsons rule 173
portion of descending thoracic aorta stroke volume Mono-disk
in parasternal long-axis, aortic stroke volume, ratio of 74f mechanical prosthesis 140f
visualization of 322f ratio of 74f valve See Tilting -disk valve
 Index 421

Morphological variants of ToF 312 Nodule of arantius 85f low-flow with preserved ejection
Morphology of Noncompaction fraction 95
MR, functional 64 cardiomyopathy 410 motion of interventricular septum in
VSD 302 left ventricle cardiomyopathy 288f large pericardial effusion 348
Motion of heart, vectors of 280 Noncoronary strain patterns 272
MR aortic sinus communicating with right Parallel processing of reflected beam 11
etiology of 67 atrium, aneurysm of 311f Paraprosthetic regurgitation 153, 154
severity vena contracta 78 sinus, aneurysm of 309f Parasternal
Multiple Non-holodiastolic severe PR judged by long axis view 17
anomalous bundles in left ventricle rapid deceleration 135f aortic
cavity with regional flow Normal root 17f
obstruction 404f aortic annulus diameter 333f valve 17f
transesophageal echocardiographic cusp retraction with calcification
circumferential strain in presence of
views 298f 101f
advanced diastolic dysfunction
Mural thrombi 374 diastolic thinning of posterior wall
223f
MVA planimetry 53
measurements of aorta 321f 370f
Myo-architecture of left ventricle from
MV competence 66 dilated aortic root with stretched
base to apex 237f
values of left ventricular peak systolic out annulus causing malco-
Myocardial
strains and strain rates 262t aptation of aortic
deformation 257
Normokinesis 366 leaflets 101f
dissection
dissection of anterior inter-
flap 391f
without definite echolucent O ventricular septum 373f
delimiting cavity 373f flail aortic cusps with excessive
Obtuse marginal arteries 364f mobility 101f
without hematoma 372
Ohms law of fluids 27 in dilated cardiomyopathy 385f
Doppler imaging of interventricular
Organic tricuspid in patient with
septum 244f
fibers in systole and in diastole 260f regurgitation, causes of 134 bileaflet valve in mitral position
infarction 370 valve disorders 115 152f
complications of 370 Orifice of regurgitation to loss of leaflet mitral stenosis and aortic
evaluation of 369 tissue in anterolateral commissure regurgitation 104f
muscle mechanics 169 67f large subaortic ventricular septal
performance index 199 Orthogonal strain 263 defect 311f
from combined right ventricle in short-axis direction, vectors of 264f left
inflow and outflow Doppler Ostium atrium 17f
spectra 199f primum 295 ventricle 17f
segment nomenclature 363 atrial septal defect 299 mitral valve 17f
tissue velocities from posterior wall in secundum 295 pericardial effusion 350f
short axis 236f Override of aortic root to anterior right ventricle 17f
twist 260f deviation of infundibular septum subaortic membrane 314f
velocities in short axis 234 311f thoracic aorta 17f
wall thickness 165f whole cusp prolapse of posterior
Myocardium P leaflet 101f
blood supply 363t short axis view 17
deformation 257 Papillary
fibroelastoma 388 for judging size of ductus 331f
Myxoma, echocardiographic of 387
pattern of 388 level of
muscle 73f aortic valve 18f
N and left ventricular wall 48 mitral valve 18f
Narrow ascending aorta 92f rupture 374 mid-LV level 18f
Natural acoustic reflector in different with head attached to posterior three-layered interventicular
planes single cardiac cycle, leaflet 374f septum with increased
complex motion of 262f Paradoxical echogenic texture 166f
Nodular constriction ventriculoarterial longitudinal systolic strain See Early with myocardial flap obliterating
junction 131f systolic longitudinal lengthening cavity 373f
422 A Practical Approach to Clinical Echocardiography

Parietal pericardium 343 mitral leaflet 48f, 66f, 73f flow convergence method 105
Partial rupture of myocardium 371 tricuspid leaflet 153 for calculating mitral regurgitant
Patent ventricular septum causing ventri- orifice area 36f
ductus arteriosus 330 cular septral defect inferior method 57, 122, 135
foramen ovale 299 myocardial infarction, volumetric measurements for
Peak rupture of 371f severity of MR 78
systolic myocardial velocities 380f Postoperative stentless prosthesis in with hemispheric appearance 106f
tricuspid annular systolic velocity 244f aortic position in diastole 150f Pseudoaneurysm 376
Pedunculated left atrial myxoma Postsystolic containing thrombus 341f
protruding mitral orifice 387f annular tissue wave masking 218f of left ventricle posterior wall 376f
Penetrating ulcer in arch 341f longitudinal shortening 270 Pseudonormal pattern with l-wave at end
Perform two-dimensional strain imaging Predominant of Valsalva maneuver 215f
266 left ventricle type of endomyocardial Pulmonary
Pericardial fibrosis 408f artery 40
constriction 353 right ventricle 408f mean pressure, distribution of
cysts and masses 353 Pressure 190f
diseases 343 drop in prosthesis with eccentric systolic pressure, distribution of
disorders 344 opening 148f 190f
effusion 345 gradients in mitral stenosis, depiction flow acceleration time, estimation of
adjacent to intramural hematoma of 51f 41f
in basal posterior wall with half-time regurgitation 39
dyskinesis of mid method for MVA 55 assessment of 134
posterior seg- of aortic regurgitation signal 107 consequences of 136
ment 373f recovery 33 jet with end-diastolic antegrade
posterior to left ventricle 390f volume loop of right ventricle with flow across pulmonary valve
Pericardium 343 that of left ventricle, comparison 195f
echocardiographic anatomy of 343 of 190f vena contracta 134
Perimembranous Pre-stenotic flow velocity 30 stenosis 127
ventricular septal defect 303f Primary chordae See Marginal chordae associations of 134
versus subarterial ventricular septal Prognostic value of TDI in diverse cardiac severity 128
defect 303f disorders 250 systolic wave 219f
Physiological Prominent valve 126
hypertrophy in athlete 403f early diastolic anatomy of 126
principles governing LV systolic motion of interventricular septum disorders 127
function 170 355f in operated tetralogy of Fallot 135f
versus pathological left ventricular notch in interventricular septum stenosis 131f
hypertrophy 245 with concavity toward left vascular resistance 40
Piezoelectric element ventricular in cons- vein flow
encased in housing assembly to trictive pericarditis and diastolic function 218
function transducer 9f 355f parameters 221
in matrix tansducer 16f trabeculations projecting into cavity pattern 219f
Pisa method, limitations of 35, 79 in dilated cardiomyopathy 400f signals, acquisition of 220
Planimetry of Prosthetic venous systolic 221f
aortic valve area in heart valves Pulse repetition frequency 26
aortic stenosis 87 evaluation of 138 Pulsed
transthoracic short-axis view in implantation, number of 138 Doppler 135
mid-systole 88f types of 138t lateral edge mitral annular
mitral valve area in mid-diastole 54f regurgitation 153 velocities 240f
Point-and-click method to extract valve ultrasound 4
longitudinal strain curves 267f dysfunction 152 wave
Posterior stenosis 155 Doppler velocity for assessing
atrioventricular groove in parasternal Proximal isovelocity surface 34 severity of MR 80
long-axis 347f area 57, 79f, 122 mitral flow Doppler 240f
descending artery 364f and volumetric measurements 34 tissue Doppler velocities 244f
 Index 423

Q Right function 189

Quadricuspid aortic valve 86
R with peak instanta-
Radial
strain 263
thickening behavior of ischemic
segment 366f
Rapid filling phase 207
Real-time 3D
right atrial view with atrial septal
defect 298f
TEE examination 299f
transesophageal echocardiographic
view from left atrium 299f
Red blood cells 25
Regurgitant
orifice 75t
area to assess severity of functional
mitral valve regurgitation 75t
volume 75t
Relationship between effective orifice and
anatomical area 30f
geometric area 30f
Relaxation aids in filling during diastole
204
Remodelling in tricuspid regurgitation
114
Resolution and penetration of transducer
probes, relationship between 9f
Restrictive
cardiomyopathy 242, 397, 404
muscular ventricular septal defect
304f
with left-to-right shunt 303f
transmitral flow 222f
trans-tricuspid pulsed wave Doppler
flow velocities 195f
Reverse sabre-shaped CW Doppler
spectrum of acute MR 75f
Rheumatic
mitral stenosis
in apical four-chamber view with
large mobile thrombus with
narrow stalk 385f
with leaflet thickening and
commissural fusion viewed
from left atrium 48f
MR 71
MV thickening and restriction of
leaflets 71f
atrial
angiosarcoma obstruction
orifice of superior vena cava
neous pressure 384f
appendage 112
atrium free wall, angiosarcoma of 389
common carotid artery thickened
walls, longitudinal view of 335f
coronary artery 364f
heart circulation low velocity inflow
26f
panel pathological specimen 398f
pulmonary artery 84, 319, 387f
sided layer inner layer of right
ventricular oblique fibers 166f
sinus of Valsalva
aneurysm of 309f
in short-axis view, aneurysm of
326f
upper pulmonary vein
atrial flow 220f
diastolic flow velocity 220f
flow with atrial fibrillation 208f
ventricle
apical circumferential strain
compared to left ventricle
198f
diastolic function and pressures
193
Doppler myocardial imaging,
parameters of 200
extending into 389f
free wall
aneurysm of 409f
longitudinal shortening of 197f
longitudinal strain 273f
strain in case of pulmonary
embolism 274f
tissue velocity 193f
function by optimizing trans-
thoracic echocardiography
four-chamber 192f
introduction 189
outflow tract 99f
peculiarities of 189
short-axis dimension 196f
strain 200
ventricular
basal circumferential strain 191f
chamber, complex geometry of
192f
deformation 273
outflow tract 26, 126, 192f
pressure-volume loop 190f
segmentation 363
volumetric function 195
Rudimentary
pulmonary valve 130f
tricuspid valve leaflets with normal
annular 120f
Ruptured aneurysm of noncoronary sinus
communicating with right atrium
328f
S
Saddle-shaped mitral annulus and
systolic contraction 66f
Schema of echocardiograph 8f
Septal
annular pulsed wave Doppler tissue
velocity pattern 236f
mitral leaflet, attachment of 113f
tricuspid leaflet 153
Severe
aortic valve regurgitation with
pressure 39f
pulmonary regurgitation causing
over-estimation of forward flow
velocities 133f
thickening of leaflets in parasternal
long-axis 59f
Severity of
mitral stenosis
assessment of 51
miscellaneous parameters of 58
TR, assessment of 121
Shelf-like obstruction proximal to
pulmonary valve 307f
Short axis
images in quad screen stages of stress
379f
levels to extract radial strain 265f
view narrow turbulent color Doppler
jet 129f
view relationship of pulmonary valve
leaflets 126f
view with color flow Doppler flow in
intertrabecular recesses 412f
Shortened tricuspid valve leaflets in
carcinoid heart 118f
Side lobe artifacts 14
Simultaneous long axis and short axis of
aortic root 322f
Single atrium See Common atrium
Single-plane ellipsoid 173
formula to estimate volume 173f
424 A Practical Approach to Clinical Echocardiography

Sinus with time to obtain strain of right filling fraction 220f

of Valsalva 84, 127 ventricular free wall, inte- longitudinal strain 183
aneurysm of 325 gration of 239f rotation of base versus apex 413f
venosus 296 spectrum from mid-septum 238f thinning of basal inferoposterior wall
atrial septal defect 300, 301f types of 262t 370f
Sinutubular junction 127 Stress echocardiography 248, 377 velocities of mitral annulus 181
Sliced left ventricular, longitudinally 374f Stroke distance 26 velocity 235
Slight nodularity in center of free margin Structural heart disease 361
85f Structure of aorta 318 T
Small paraprosthetic mitral regurgitation Subaortic
with clear delineation of membrane very close to aortic valve Takayasu arteritis 332
dehiscence 155f with aortic regurgitation 315f Takotsubo cardiomyopathy 409
Smaller beam 12 membranous stenosis 314 TDI in
Solid body rotation in patient with left stenosis 95 concept of 229
ventricle noncompaction cardio- with eccentric orifice in child 34f constrictive pericarditis 242
myopathy 287f with subaortic ventricular septal coronary artery disease 248
Sound 3 defect 315f detection of intraventricular
beam 12 Subarterial ventricular septal defect in dyssynchrony 246
oscillating wave of mechanical energy transthoracic echocardiography inherited cardiomyopathies 246
4f short-axis 304f limitations of 251
waves, behavior of 3f Subcostal right ventricular function, significance
Spatial resolution 11 four-chamber view of 243
Speckle biventricular origin of aortic root Technical details of TDI 231
derived strain values 263 to aortic override 312f TEE
tracking method to assess torsion, rims of secundum atrial septal probe manipulation 21
limitations of 285 defect 297f RV inflow view tricuspid valve 22f
Spectral pulsed wave tissue velocities long-axis view 297f Temporal
from medial edge of mitral annulus short axis view entire right heart resolution, improving 13
232f structures 20f variation in pulmonary regurgitation
Specular reflection 7, 7f Subpulmonic stenosis with vestigial 358f
Spherical shape in diastole in dilated pulmonary valve and annular Terms used in tissue Doppler imaging 231
cardiomyopathy 398f stenosis 131f Tertiary chordae See Basal chordae
Spongiform heart muscle disease See Superior vena cava 112, 295 Testicular tumors 387
Noncompaction cardiomyopathy Suprasternal Tethering
Spontaneous long axis view and closing forces acting upon leaflets
echo contrast 384 aorta 20f 73f
in inferior vena cava 351f dilatation of aortic root 333f of aortic valve leaflets to root dilatation
ischemia 377f end of arch origin of left subclavian causing severe aortic valve 333f
Starlings law 170 artery 320f Tetralogy of Fallot 311
of heart 170 right and left aortic sinuses 308f with atretic outflow tract 312f
Starr-Edwards ball-in-cage valve ball tubular narrowing of descending with narrow right ventricular outflow
variance to lipid absorption 159f thoracic aorta 324f tract 131f
Strain view 20 Thoracoabdominal aorta 319
estimation in Supravalvular aortic stenosis 330 in subcostal long-axis 320f
apical four-chamber, longitudinal in child with eccentric jet 34f viewed in subcostal long-axis 320f
263f Syndrome Three
four-chamber, longitudinal 266f Ehlers-Danlos 309 arbitrary parts of left ventricle 165f
rate Eisenmenger 295 co-ordinates of deformation 258f
analysis 200 Loeys-Dietz 309 dimensional
advantages of 185 Marfan 309, 331 cross-sectional image of mid-LV
over fixed segment derived from Williams 132f 167f
tissue Doppler method 261f System of mitral valve complex 64 E cross-section three aortic sinuses
spectrum derived from basal Systolic 308f
lateral wall 239f elastance, degree of 204 echo, advantages of 180

echocardiographic
en face 112f
en face view of mitral valve 46f prosthesis in aortic position in
four-chamber 49f
four-chamber view 111 f
of left ventricle 167f
short-axis 327f
short-axis image 130f
short-axis view collapsed
aneurysm of aortic sinus
329f
view of aneurysm of right aortic
sinus 328f
echocardiography 10
for LV systolic function 179
limitations of 181
shape of tricuspid annulus 113f
short-axis view sinuses of
Valsalva 326f
strain by acoustic speckle
tracking 268f
TEE of wall-hugging thrombus in edge of mitral annulus 235f
left 386f
transesophageal 141f
transesophageal echocardio-
graphic view from top of
bileaflet mitral valve
circumferential
nodular pannus or blood 7
157f
mitral bioprosthesis in diastole To-and-fro flow across neck of
153f
tilting-disk mitral prosthesis
158f
pannus with tilting disk aortic resynchronization therapy 288
valve prosthesis 158f
transesophageal image of bileaflet
143f
transthoracic echocardiographic
atrioventricular septal defect
303f
color flow jet area of aortic
regurgitation narrowest
orifice 106f
planimetry of mild aortic
stenosis 88f
view of aortic valve with dias-
tolic regurgitant area
99f
volumetry, method of 179
Thrombus bifurcation of pulmonary
artery 386f
Index 425
Tilting ball-in-cage valve in systole
disk 139f
flow jet across mitral
diastole 140f bioprosthesis 159f
valve 139 tilting- disk mitral valve with
mono-disk prosthesis in aortic thrombus 158f
position 140f long axis view
Time gain compensation 13 aortic regurgitation jet eccentric
Time integral suggestive of severe MR 76f orifice 106f
Tissue communication of left aortic
Doppler sinus 310f
data for deformation 238 eccentric paraprosthetic aortic
derived strain regurgitation 156f
basal right ventricle free wall, with rightward probe deflection
comparison of 275f 296f
spectrum from basal septum midesophageal short axis 329f
238f of ball-in-cage valve in mitral
echocardiography 229
position 156f
concept of 229f of mitral bioprosthesis in young
of lateral edge of mitral annulus
female 154f
235f, 242f
picture with continuous wave
of medial
Doppler flow 330f
short-axis view quadricuspid
mitral annulus 234f
aortic valve 87f
interface right angle, reflection from
view 20
6f
of bileaflet mitral valve large
interfaces with variable acoustic
thrombus 158f
impedance 5f
of mitral bioprosthesis 159f
motion 209
echocardiography 133
in pulmonary stenosis 133
texture 13
long-axis 303f
long-axis view 140f
pseudoaneurysm 341f
Torsion 286 Transmitral
flow velocities with respiratory signal
applications of 285
in normal person 352f
strain See Radial strain
Total stroke volume in left ventricular
outflow tract 104f Transposition of great vessels 315
Transprosthetic
Transducer 8
flow velocity profile 147f
artifact near apex to back reflects from
valve gradients with indexed effective
probe 10f
orifice 146f
in subxiphoid position 18
Transthoracic
probe 8
pulse controls 8 apical 4-CV
shapes of 8f apical dyskinesis with thrombus
Transesophageal 345f
echocardiographic 126f, 384f diastolic left atrial collapse 351f
anatomic secundum atrial septal echocardiographic 149
defect with left-to-right four-chamber view 153f
shunt 296f torn leaflet of mitral
four-chamber view 141f, 152f, 157f bioprosthesis 153f
arrested disk causing high modified apical short-axis image
transprosthetic gradients ventricular septal defect 130f
160f off-axis 149f
426 A Practical Approach to Clinical Echocardiography
parasternal long-axis 150f, 337f,
346f
view eccentric paraprosthetic
mitral regurgitation 155f
short-axis view of right ventricular
outflow tract 129f
echocardiography 10
four-chamber view end-diastole
194f
parasternal long-axis 152f, 158f
short-axis 191f
parasternal long-axis 330f, 351f
view aneurysm of right sinus of
Valsalva 326f
parasternal short-axis 346f
short-axis view commissural fusion
with calcification 87f
Transvalvular velocities, relationship of
90t
Transverse midesophageal four-chamber
view 21f
Transverse oscillations 4
Tricuspid
and pulmonary prosthetic valves 160
annular
peak systolic velocity 198, 199f
plane systolic excursion 198
displayed in M-mode 198f, 199f
tissue velocity 245f
annulus with leaflets and posterior
relationships 111f
regurgitation 116f
jet with peak velocity 193f
stenosis 39
valve 110, 113
apparatus laid open longitudinally
111f
disorders 110
functional morphology of 110
stenosis 62f, 120
Trileaflet
aortic valve, anatomy of 83
bioprosthesis in pulmonary valve
position in case of operated
tetralogy of Fallot 160f
True aneurysm
of inferoposterior wall 376f
pseudoaneurysm 377t
True apical aneurysm with wall thinning
marked by arrows 376f
True lumen, characters of 338
Truncus arteriosus 329
Tumor-like Unusual biphasic rotation in heart failure
infective mass attached to pacing lead with reduced ejection fraction 288f
390f Upper panel
invasion of left ventricle free wall to lower panel 221f, 222f
hydatid cyst 391f middle panel 221f
TVI-based strain of right ventricle free mitral
wall 201f flow 220f, 221f
Two contractile chambers of right inflow pattern 215f
ventricle with distinct pulmonary
morphologies 191f
flow 221f
Two-D echocardiographic
vein flow 222f
ejection fraction 178
restrictive transmitral flow and lower
long axis view 15f
panel 215f
minor axis shortening 177
septal annular velocities 221f
of valvular pulmonary stenosis 129f
tissue velocities of medial mitral
parasternal long axis 178f
annulus 243f
unicuspid pulmonary valve 130f
transmitral flow 222f
Two-D echocardiography 102
and LV systolic function 177
for LV volume estimation, limitations V
of 179
Two-D longitudinal strain Valsalva
in modified apical long axis 263f effect of 215f
of right ventricle 270f maneuver 214
Two-D transesophageal echocardio- changing restrictive flow pattern
graphic 214f
caval 301f Valve apparatus, components of 46
four-chamber view with Starr- Valvular
Edwards mitral prosthesis 160f heart disease 43
view 153f, 154f leaflets 64
arrested lateral disk of bileaflet PS, types of 128
valve 157f pulmonary stenosis with continuous
of bileaflet mitral prosthesis 159f wave Doppler interrogation in
of Starr-Edwards mitral prosthesis right panel 130f
157f Vegetation on
severe transprosthetic regurgi- aortic leaflets with incomplete
tation across mitral coaptation in infective
bioprosthesis 154f endocarditis 100f
tricuspid valve in presence of central
U intravenous line 118f
Velocity
Ultrasound beam 7
flaked by side lobe beams 9f flow paradoxus across mitral 352f
Ultrasound interaction with tissue 4 ratio 30
Unicuspid time integral 26
and bicuspid aortic valve and vector
aortopathy 322 end-diastole in apical four-
aortic valve 85, 86f, 323f chamber 267f
in diastole 85f imaging 264
pulmonary valve with single leaflet in short axis of left ventricle 267f
and single commissure 130f Vena contracta 31, 121
Unresolved issues in noncompaction 413 advantages of 32, 78
Unruptured aneurysm of right sinus of just beyond narrow orifice 32f
Valsalva 328f limitations of 32

measurement with aortic regurgi-
tation by color flow Doppler in
parasternal long-axis
view 32f
of mitral regurgitation jet, width of 32f
of PR in transthoracic echocardio-
graphic short-axis 136f
width 77
limitations of 78
Ventricles with dilated cardiomyopathy,
cross-sectional view of 398f
Ventricular septal
defect 300
site-specific classification of 302f
rupture 371
Ventriculoarterial junction 127
Ventriculovalvular impedance 34
Visceral pericardium 343
Viscoelastic 261
VSD, pathophysiology of 302
W continuous 136f
Wall
motion score index 367
stress, method of measuring 171f
Wave Doppler
and pulmonary regurgitation severity,
continuous 136
envelope of valvular PS, continuous
133f
interrogation for TR signal, continuous
123
interrogation of
coarct segment, continuous 325f
Index 427
pulmonary regurgitation jet 195f
pattern of dynamic infundibular
obstruction, continuous 133f
spectrum of mild versus severe PR,
Wavelength after refraction in second
medium, decreasing 6f
Wide-neck pseudoaneurysm of
inferoposterior wall 377f
Width of vena contracta 78
Williams syndrome 132f
Windkessel phenomenon in
proximal aorta 321f
Z
Zone of apposition 65f