Eur J Echocardiography (2007) 8, 4e14

INVITED PAPER

Echocardiography in heart failure: Beyond

diagnosis
J.K. Oh*
Mayo Clinic College of Medicine, Division of Cardiovascular Diseases, 200 First Street SW,
Rochester, MN 55905-0001, USA
Received 11 September 2006; accepted 13 September 2006
Available online 1 November 2006

* Tel.: 1 507 284 3685; fax: 1 507 284 3968.

E-mail address: oh.jae@mayo.edu

diagnosis of heart failure.1,2 It is important to demonstrate an objective evidence of structural or

functional abnormalities to explain patients
symptoms of heart failure since symptoms of heart
failure are not specific and more than a third of patients with a clinical diagnosis of heart failure may
not actually have heart failure. It is also interesting to note from the SHAPE study that only 3% of
more than 7000 subjects surveyed from nine European countries recognized breathlessness, fatigue,
and edema as symptoms of heart failure.3 Moreover, even when someone presents with typical
symptoms of heart failure, a diagnostic test,
most frequently an echocardiography examination, is required to establish the underlying etiology for an optimal management strategy. In this
lecture, I like to review with you how echocardiography is used for detection of structural abnormality, diagnosis and management of systolic heart
failure, and evaluation of diastolic function in
patients with symptoms of heart failure.
When a cardiac structural abnormality is responsible for patients heart failure, it is usually obvious
on 2-dimensional echocardiogram. Fig. 1 illustrates
an echocardiographic image of a middle age woman
with increasing dyspnea. Parasternal long axis view
demonstrated an enlarged right ventricle consistent
with right ventricular volume or pressure overload
which provides a list of differential diagnoses such

1525-2167/$32 2006 Published by Elsevier Ltd on behalf of The European Society of Cardiology.
doi:10.1016/j.euje.2006.09.002

Downloaded from by guest on April 19, 2016

It is a great honor for me to deliver this years

Euro Echo Lecture in this beautiful city of Florence
and I appreciate the European Association of
Echocardiography for the invitation and this
opportunity to discuss the role of echocardiography
in systolic and diastolic heart failure as the single
most useful test, not only in diagnosis, but also as
a tool to provide insights into the pathophysiological mechanism of various etiologies of heart
failure, as a tool to monitor patients response to
various treatment options, and as a tool to help us
develop innovative new therapies for heart failure.
According to the ESC guidelines published in
2005, heart failure is defined as a complex
clinical syndrome that can result from any structural or functional cardiac disorder that impairs
the ability of ventricles to fill with or eject blood
which includes diastolic as well as systolic heart
failure.1 ACC/AHA guidelines as well as ESC guidelines state that echocardiography is the single
most useful test in the diagnosis of heart failure
since structural abnormality, systolic dysfunction,
diastolic dysfunction, or a combination of these
abnormalities needs to be documented in patients
who present with resting or/and exertional symptoms of heart failure to establish a definitive

Echocardiography in heart failure

Figure 1 Parasternal long axis view from 54-year-old

woman with increasing shortness of breath. The right ventricle (RV) is enlarged. In real time 2-D echocardiographic
image, the left ventricle (LV) was of normal size and function. Subsequent views from subcostal window showed
a large secundum atrial septal defect with left-to-right
shunt resulting in right ventricular volume overload.
Ao Aorta, LA left atrium.

example of identifying an uncommon but clinically

important structural abnormality responsible for
patients heart failure. I believe it would have been
difficult for other diagnostic imaging tests to be able
to identify such an uncommon abnormality so readily.
Heart failure due to systolic dysfunction is
relatively easy to diagnose by echocardiography
which demonstrates a dilated left ventricle with
a reduced ejection fraction. In systolic heart
failure, however, echocardiography has many
other roles beyond the recognition of systolic heart
failure since dilatation of the LV results in alteration of intracardiac geometry and hemodynamics
leading to increased morbidity and mortality. New
medication strategies, devices, and surgical therapies are being developed to manage systolic heart
failure. Echocardiography has been essential in
identifying structural and hemodynamic abnormalities associated with systolic heart failure and to
monitor patients response to new and novel
therapies. It has been well documented for the
last 20 years that the left ventricular volume is one
of the most important prognostic indicators for the
patients with ischemic or dilated cardiomyopathy.4,5 White and his associates demonstrated
that worsening of patients survival was associated
with increased end systolic volume after an acute
myocardial infarction. With LV remodeling and
a progressive dilatation of the heart, although initially an adaptive process to the myocardial damage, the left ventricle becomes more spherical,
and the mitral annulus is dilated with apical displacement of the mitral leaflets causing functional
mitral valve regurgitation.6e8 A combination of LV
dilatation and mitral valve regurgitation results
in increased filling pressure, symptoms of heart
failure, and death. Grayburn and his collaborators
in the BEST trial demonstrated that among various
echocardiography parameters, LV end-diastolic
volume, deceleration time of early diastolic mitral
inflow velocity which is a surrogate for pulmonary
capillary wedge pressure, and severity of mitral
valve regurgitation were the strongest predictors
of survival in patients with ejection fraction of
35% or less5 (Fig. 2). Since a smaller LV with less
amount of mitral regurgitation is associated with
a better functional capacity and survival, there
are many management attempts to reduce the
left ventricular volume and MR with the use of
surgical, pacing, and other percutaneous devices,
as well as medications and surgical revascularization. In this context, echocardiography is a valuable tool since it can measure or assess LV
dimensions, volumes, sphericity index, severity of
mitral regurgitation, diastolic filling parameters,
and pulmonary artery systolic pressure.

Downloaded from by guest on April 19, 2016

as severe tricuspid regurgitation, pulmonary hypertension, or intracardiac shunt to be investigated. A

subcostal view subsequently showed a large secundum atrial septal defect. Echocardiographic detection of most structural abnormalities responsible for
heart failure is straight forward, but some structural
abnormalities demands a more detective work and
echocardiographers knowledge as illustrated in
a 55-year-old woman with increasing shortness of
breath and history of radiation to the chest. Because
of her radiation history, restrictive myopathy, pericardial disease, coronary disease, and valvular
heart disease are considered and evaluated.4 However, echocardiography showed an unusual flow directed to the right atrium and the tricuspid valve
which was initially thought of as an atrial septal defect, but there was no evidence of right ventricular
enlargement or volume overload. Further investigation with color-flow imaging and Doppler echocardiography demonstrates that the flow was originated
from the coronary sinus with a peak velocity of
greater than 2 m/sec. Because of a concern for
coronary sinus stenosis, transesophageal echocardiography was performed and it confirmed the presence of high velocity jet originating from the
stenotic coronary sinus ostium. That was followed
by the cardiac catheterization, and coronary sinus
venography demonstrated a tight ostium which
was stented successfully. Her LV end-diastolic pressure was increased (29 mmHg) due to the coronary
sinus stenosis. Three months after the stent, the patients symptoms markedly improved. This is a good

SAVE trial was one of the first studies where

echocardiography was used in a systolic heart
failure trial to show that adverse cardiac events
were associated with increased left ventricular
size after acute myocardial infarction.8 Biventricular pacing has been found to improve functional
status and survival of patients with reduced LVEF
and ventricular conduction delay.9e11 Echocardiography has been used to assess the success of
the device therapy by documenting smaller LV volume, increased LVEF, increased dP/dT, and less
amount of mitral regurgitation which are all signs
of reverse remodeling. Another potentially critical
role of echocardiography in biventricular pacing is
to identify the patients who respond positively to
the therapy since 30e50% of patients who receive
biventricular pacing may not improve. Currently,
mechanical dyssnchrony measures obtained by
tissue Doppler imaging velocities are considered to
be best in that role. Time intervals from the onset
of QRS to the time of peak systolic velocity of 2 to
12 segments of LV are used to determine the
maximum or standard deviation interval.12,13 The
maximum interval of 100 msec or standard

deviation interval of 34 msec were found to have

the highest predictive power for identifying positive
responder. However, we have found that such
intervals by TDI are present in normal subjects and
patients without reduced ejection fraction or
conduction delay.14 Instead, time intervals from
the QRS to the peak negative strain from 12 segments correlated best with LV remodeling parameters and hemodynamic improvement after cardiac
resynchronization therapy.15 It is, however, time
consuming and challenging to obtain tissue Doppler
or strain imaging from 12 segments. Further clinical
experience and simplification of current strain imaging procedure are required to use echocardiography in identification of positive responders to CRT
routinely in clinical practice.
Another innovative device for reducing LV volume or achieving reverse LV remodeling is a passive
constraint device called ACORN.16 Mayo Clinic
Echocardiography Core Lab has been working for
the US clinical trial of this device which was recently completed. I would like also to acknowledge
that many European centers were the initial clinical sites for development and testing the safety of
this device. There was a progressive and significant
reduction in left ventricular volume measured by
echocardiography in patients treated with this
device compared to a control group. The left
ventricular volume reduction was associated with
significant reduction in major cardiac procedures
including cardiac transplantation.
Surgical Ventricular Restoration or Reconstruction (SVR) procedure which was pioneered by
Dr. Dor in 1984 is a surgical attempt to restore LV
size and shape by excluding the scarred and akinetic
apical segments.17 The results from SVR procedure
in more than 1000 patients were reported with an
overall 30 day mortality of 5.3%.18 LVEF improved
from 29% to 39% and LV end-systolic volume index
decreased from 80 mL/m2 to 56 mL/m2. Patients
with a larger ventricle and worse functional class
preoperatively had worse outcome after SVR. However, this report did not come from a randomized
trial, and there is no way to compare this result
with the intensive medical therapy, other device
therapy, or revascularization therapy alone in
patients with reduced ejection fraction and akinetic apex. If SVR procedure has an incremental
beneficial effect, echocardiography should be
helpful in identifying ideal patients with the large
left ventricle, akinetic scared apex, reduced LVEF
as well as normally functioning inferior-lateral
wall. Structural and hemodynamic response to
the SVR can be readily assessed by comprehensive
echocardiogram. However, the long-term structural and functional result of SVR procedure is not

Downloaded from by guest on April 19, 2016

Figure 2 Survival curve of patients with reduced left

ventricular ejection fraction in the Best Trial. LVEDVI
left ventricular end diastolic volume index, DT deceleration time, and VCW vena contracta width (Reproduced with permission from Ref. 5).

J.K. Oh

Echocardiography in heart failure

endpoints of death and HF hospitalization. Echocardiography data from 2000 patients from all
over the world with ischemic cardiomyopathy will
be analyzed independently and correlated with
clinical and other laboratory data. We are looking
forward to sharing many interesting results from
this rich STICH echocardiographic data.
Now, I like to turn my discussion to assessment
of diastolic function in patients who present with
symptoms of heart failure. It has been well
established that about 50% of patients with new
onset of heart failure do have a normal ejection
fraction.19,20 Some have suggested that this condition be called heart failure with preserved ejection fraction (HFPEF) since intrinsic diastolic
dysfunction may not be a unifying underlying
mechanism for heart failure.21,22 However, the terminology is also troublesome since there are many
conditions other than a myocardial disease which
can cause heart failure with preserved ejection
fraction such as constrictive pericarditis, severe
valvular heart disease, congenital heart disease,
and intracardiac tumor. Since the most common
etiology for heart failure with preserved ejection
fraction and no other structural abnormalities is
due to diastolic dysfunction, diastolic heart failure
appears to be a better terminology to describe this
disease entity.20 This condition is often difficult to be
diagnosed by 2-D echocardiography alone although
there are diagnostic clues in two-dimensional echocardiography if carefully looked for. Compared
to a normal heart, the heart with diastolic dysfunction has less vigorous mitral annulus motion
during systole and early diastole corresponding to
the period of active myocardial relaxation, the
left ventricular wall tends to be thicker than
normal, and the left atrial size is increased. These
abnormalities suggest that the patients diastolic
dysfunction is abnormal and a more detailed
Doppler assessment is required. Doppler evaluation of diastolic function requires the following:
Early (E) and late (A) diastolic velocities of the
mitral inflow, Deceleration time (DT) of mitral E
velocity, early diastolic mitral annulus velocity
(Ea), pulmonary vein velocities, hepatic vein
velocities, and mitral inflow propagation velocity
obtained by color M-mode (Fig. 3). It usually begins
with recording of mitral inflow velocities which reflect the relationship between LA and LV pressures. This relationship, hence the configuration
of mitral inflow velocities, alters predictably with
impaired myocardial relaxation and increased filling pressure. Mitral inflow velocity pattern of normal subjects is characterized by predominant
early diastolic filling with DT of 200  40 msec.
Impaired myocardial relaxation which is usually an

Downloaded from by guest on April 19, 2016

yet clearly understood and further clinical trial is

required to demonstrate beneficial effects of SVR
compared to other device and medical/surgical
therapy. Also, the long axis dimension becomes
shorter by SVR, but the short axis dimension and
mitral annulus may continue to dilate in some patients which may lead to more severe mitral valve
regurgitation and higher diastolic filling pressure.
Hence, echocardiography should be able to provide
an insight and understanding of the long-term
structural and hemodynamic outcome of the SVR.
In patients with severe coronary artery disease,
reduced LVEF, and heart failure, there has not
been a clinical trial data to guide our treatment. Is
surgical revascularization better than medical
therapy? What if the patient has akinetic apex?
Does additional SVR procedure improve functional
class and survival of the patients with ischemic
cardiomyopathy? These important clinical questions are being investigated by STICH (Surgical
Treatment In patients with Coronary artery disease
and Heart failure) trial in which patients with
ischemic cardiomyopathy and revascularizable
coronary disease are randomized to intensive
medical therapy, coronary artery bypass surgery,
and bypass plus SVR. The first phase of STICH trial
of comparing two surgical strategies was completed in the early 2006 with 1000 patients
enrolled. The comparison of medical therapy
versus surgical therapy will be completed in early
2007. STICH trial is truly an international trial with
many European clinical centers participating. In
fact, STICH investigators in Poland has enrolled the
largest number of patients in the study and should
be congratulated on their fantastic effort. This
study will provide a very rich imaging data since all
patients in the trial have baseline, four month, and
two year follow-up echocardiograms and selected
patients will have cardiac magnetic resonance
imaging and nuclear studies. Mayo Clinic Echo
Core Lab is analyzing all echocardiography data
for the STCIH to address the following two aims;
1) To determine if the use of echocardiography at
baseline to assess LV systolic and diastolic dysfunction, cardiac hemodynamics, and valvular regurgitation in the STICH Trial population can
identify a subgroup that derives a substantial
benefit or incurs a significant harm from surgical
intervention as determined by all-cause mortality.
2) To assess the effects of the different randomized treatment strategies on echocardiographically-derived parameters of cardiac systolic and
diastolic dysfunction, hemodynamics, and the
severity of valvular regurgitation at 4 months and
2 years as compared to baseline as they relate to
changes in HF functional class and the clinical

Figure 3 Schematic of pulse-wave Doppler of mitral

inflow, color M-mode demonstrating mitral inflow propagation velocity, and tissue Doppler of the septal mitral
annulus in normal diastolic function and various stages
of diastolic dysfunction. (Reproduced with permission
from reference 28.)

relaxation.23,24 Ea is lower at the septal annulus

(normal  10 cm/sec) compared to the lateral annulus (normal  15 cm/sec) and at our institution
we use the septal annulus in all patients except
when there is regional wall motion abnormality in
the basal inferior septum. Pulmonary vein, hepatic
vein, and the color M-mode of mitral inflow may be
beneficial in certain cases to evaluate diastolic
function and estimated filling pressures. Pulmonary venous flow velocity shows progressive reduction of systolic forward flow velocity compared to
the diastolic flow velocity with increased filling
pressure (Fig. 4). In all phases of diastolic dysfunction, early diastolic velocity of the mitral annulus
(Ea) is reduced and it does not increase with high
filling pressure. Since mitral E velocity increases
with a higher filling pressure and tissue Doppler
Ea remains reduced, the ratio of the mitral E velocity and the mitral annulus velocity of Ea (E/
Ea) has a good correlation with the pulmonary capillary wedge pressure or left ventricular filling
pressure.25,26 E/Ea ratio >15 usually indicates pulmonary capillary wedge pressure of greater than
20 mmHg when septal Ea is used; and if the ratio
<8, the filling pressure is usually normal and for
the ratio between 8 and 15, we may require further diastolic parameters to estimate diastolic filling pressures.25 As mentioned earlier, motion or
velocity of the mitral annulus can also be appreciated from parasternal long axis and apical four
chamber views of 2-dimensional echocardiography. Assessment of filling pressure by 2-dimensional and Doppler echocardiography is useful in
patients with systolic dysfunction as well as in patients with normal LVEF. Numerous studies have
demonstrated a good prognostic value of Doppler
echocardiographic assessment of filling pressures.
We also have demonstrated that E/Ea >15 was one
of the strongest predictors for survival after acute
myocardial infarction whether LVEF was normal or
abnormal.27,28 This work of retrospective review
was carried out by G. Hillis who was a research fellow from the United Kingdom, and he has led a prospective study upon return to his University of
assessing prognostic power of clinical, laboratory,
and echocardiographic parameters in patients
with acute myocardial infarction. His group presented at the last AHA meeting that Plasma BNP,
LVEF, and septal E/Ea were strong independent predictors of morbidity following acute myocardial infarction. Of them, septal E/Ea ratio was found to
be the single most powerful predictor of death.29
In our retrospective review, LA volume was found
to be also prognostic for death after acute MI.30
Therefore, estimation of filling pressure should
also be an integral part of echocardiographic

Downloaded from by guest on April 19, 2016

initial diastolic abnormality decreases E velocity,

increases A velocity, and lengthens DT. On the
other hand, increased filling pressure has an
opposite effects on these Doppler parameters.
Therefore, during an early stage of diastolic
dysfunction with impaired myocardial relaxation
and normal filling pressure, mitral inflow velocity
recording alone is usually sufficient for diastolic
function assessment. As filling pressure increases
with worsening of diastolic function, mitral E velocity increases with shorten DT and A velocity decreases with shorter flow duration. When diastolic
dysfunction is far advanced and/or filling pressure
is markedly elevated, mitral inflow velocity is
again sufficient. However, mitral inflow velocity
pattern may appear normal (so called pseudonormalized mitral inflow) in patients with moderate
elevation of filling pressure. Even in this situation,
a careful attention to isovolumic relaxation time
and atrial flow duration is helpful in distinguishing
pseudonormalized from truly normal mitral inflow
velocities. It is important to keep in mind that
pseudonormalized mitral inflow is a product of impaired myocardial relaxation and moderate elevation of filling pressure. In this context, Doppler
parameter to evaluate myocardial relaxation is
critical in our evaluation of diastolic function. Tissue Doppler Imaging allows recording of myocardial tissue velocities and it turned out that early
diastolic velocity of the mitral annulus (Ea) correlates well with tau or the status of LV myocardial

J.K. Oh

Echocardiography in heart failure

Downloaded from by guest on April 19, 2016

Figure 4 A: Parasternal long axis view from a middle-aged man with heart failure. It shows normal left ventricular
cavity dimension with increased wall thickness and enlarged left atrium. The left ventricular systolic function was
well preserved. There was a small amount of pericardial effusion (*) circumferentially and large pleural effusion
(PL). LA left atrium, RV right ventricle, VS ventricular septum. B: A composite of mitral inflow (left upper), pulmonary vein (right upper), tissue Doppler velocity of the mitral annulus (left lower), and color M-mode of mitral inflow
demonstrating flow propagation velocity (right lower). Mitral inflow velocity shows E/A ratio of 2 and deceleration
time of 160 msec which is in the low normal range. Pulmonary venous flow velocity, however, shows marked reduction
in systolic forward flow velocity (S) and decreased deceleration time of diastolic forward flow (D) velocity consistent
with increased filling pressure. Mitral annulus velocity shows reduction in early diastolic velocity (E0 ) to 6 cm/sec
which represents marked impairment of myocardial relaxation. Flow propagation is slightly reduced (slope in white
color of the highest velocity in the center of mitral inflow shown).

evaluation in patients with reduced LVEF. Let me

then share with you how echocardiographic evaluation of diastolic function should be used in patients
with symptoms of heart failure and normal LVEF. I
will start with an example of a 70-year-old man
who presented with sudden onset of dyspnea to

the emergency room. Chest X-ray suggested pulmonary edema, but serum BNP was within normal
limits, and the echocardiography showed normal
ejection fraction and mild increase in LV wall thickness. Because of the normal BNP and ejection fraction, the patients clinical and chest X-ray findings

10

myocardial diseases is increased in constrictive

pericarditis34,35 (Fig. 5). Other subtle findings
such as ventricular septal motion changes with respiration and septal shudder in constriction can be
appreciated from careful evaluation of 2-D echocardiography. At our institution, more careful attention to these echocardiographic features of
constrictive pericarditis allowed increased detection of this entity in patients with heart failure
which has been partly responsible for higher number of pericardiectomies (from 15 in 1990 to more
than 60 in 2005). More reliable detection of constrictive pericarditis has been a valuable product
of assessing diastolic function by 2-D, Doppler,
and myocardial tissue imaging.
Let me summarize what I have discussed so far
regarding the role of echocardiography in patients
with symptoms of heart failure. When heart failure
is clinically suspected, echocardiography is the
single most important diagnostic imaging technique. In a half of patients with a final diagnosis
of heart failure, transthoracic and/or transesophageal echocardiography demonstrates a major
structural and/or functional abnormality such as
in systolic heart failure, severe valvular heart
disease, congenital heart disease, or cardiomyopathies. It is more difficult to diagnose heart failure
when there are no obvious structural and functional abnormalities in 2-dimensional echocardiography. In the other half of patients with heart
failure, most likely diastolic heart failure, there
may be subtle abnormalities in 2-dimensional
echocardiography, but a firm diagnosis of diastolic
heart failure requires Doppler and myocardial
(or tissue Doppler) imaging. If mitral inflow velocity
demonstrates clearly a restrictive filling pattern
and/or high filling pressure at resting stage, the
diagnosis of diastolic heart failure or constrictive
pericarditis is usually secured. Tissue Doppler
imaging of the septal mitral annulus is helpful in
differentiating pseudonormal from true normal
mitral inflow velocities, and differentiating constrictive pericarditis from myocardial diseases. It is
more problematic when diastolic function evaluation shows relatively normal filling pressure or
predominantly impaired myocardial relaxation at
rest. In this situation, right heart failure, pulmonary process, and non-cardiopulmonary process
should be considered. Another important condition
we need to consider is exercise-induced increased
filling pressure responsible for patients symptoms
of shortness of breath with exertion. Therefore,
we need to assess filling pressure with exercise as
well as at resting stage.
The mitral annulus Ea velocity which reflects the
status of mitral relaxation does actually increases

Downloaded from by guest on April 19, 2016

were thought to be of non-cardiac etiology initially.

However, when his echocardiogram was reviewed
more carefully, it was obvious that LV myocardial relaxation was markedly impaired (mitral annulus motion was reduced) and diastolic evaluation showed
E/Ea ratio was 22, much higher than the 15 cutoff
value. Subsequent evaluation showed a critical
left main coronary artery disease and LV end diastolic pressure of 28 mmHg. When plasma BNP and
mitral E/Ea0 ratio were correlated with pulmonary
capillary wedge pressure, correlation was better
for the mitral E/Ea ratio compared to the BNP.31
BNP has been shown to be helpful in triaging patients with dyspnea in the emergency room, but
we should be mindful that the sensitivity and the
specificity of BNP for increased filling pressure is
less than optimal, and probably lower than echocardiographic estimation of filling pressure. Even when
high filling pressure is detected by BNP in patients
with heart failure, echocardiography will be necessary to establish an etiology and to provide an optimal treatment. In patients with heart failure and
normal LVEF, optimal therapy has not been established although there are several studies demonstrating some benefits in this group of patients. I
anticipate several large clinical trials to identify
the most efficacious management strategy in diastolic heart failure and echocardiography will be
an integral part of those trials for identification of
ideal patients and monitoring the response of various therapies.
Constrictive pericarditis is an elusive entity
which causes heart failure in patients with normal
LVEF and is potentially curable. Its hemodynamic
manifestations are similar to those of myocardial
diseases and it is often challenging to differentiate
constrictive pericarditis from restrictive myopathy
or other myocardial diseases. With comprehensive
echocardiography, we now should be able to
diagnose constrictive pericarditis in almost all
cases non-invasively. There are two unique features of constriction which are not present in
myocardial diseases: 1. Dissociation between intrathoracic and intracardiac pressures; and 2.
Exaggerated interventricular dependence.32 These
two features in constriction result in characteristic
diastolic filling pattern which can be reliably recorded by Doppler echocardiography. Typically,
mitral inflow early diastolic velocity decreases
with inspiration and hepatic vein diastolic reversal
flow increases with expiration. However, the respiratory variation of mitral inflow velocities may not
be present in some patients.33 Tissue Doppler recording of mitral annulus velocity has added an important diagnostic value in constrictive pericarditis
since Ea velocity which is reduced in almost all

J.K. Oh

Echocardiography in heart failure

11

with exercise or increased preload when myocardial relaxation is normal, but Ea velocity does not
augment as much with higher transmitral pressure
gradient or with exercise when relaxation is impaired with increased tau. Therefore, we hypothesized several years ago that in normal subjects
mitral inflow E velocity and mitral annulus Ea
velocity increase proportionately with a result
that E/Ea remains less than 15 at resting stage
and exercise.36,37 However, in patients with diastolic dysfunction and exertional dyspnea, E velocity increases with exercise but the Ea velocity
remains reduced or increases less with exercise.
Therefore, E/Ea ratio increases with exercise compared with the resting stage in patients with

diastolic dysfunction. We used a supine bike or

treadmill exercise test for assessment of filling
pressure with exercise, and we analyzed diastolic
parameters of mitral inflow and mitral annulus velocities which provided E/Ea ratio. Initially we performed diastolic stress test in healthy individuals.
This work was initially carried out by Dr. F. Lulic
from Croatia, and then completed by Dr. J. Ha
from Korea working in our laboratory.36,37 It was
found that in normal subjects, mitral E velocity increased about 25% with exercise from baseline data
and deceleration time decreased an average of
16 msec (from 192 to 176 msec) and Ea velocity increased also about 25%. Therefore, E/Ea ratio remained the same (mean of 6.6) at baseline and

Downloaded from by guest on April 19, 2016

Figure 5 Three patients with a similar degree of shortness of breath. Upper panel shows the mitral inflow velocity.
Middle panel shows tissue Doppler velocity from the mitral septal annulus. The bottom row shows color M-mode of the
mitral inflow velocity. The left column is from a normal subject. Middle column from a patient with a myocardial disease (restrictive cardiomyopathy). The right column is from a patient with constrictive pericarditis. The mitral inflow
velocity appeared the same in all three examples with E/A ratio of 2. However, early diastolic velocity of the mitral
annulus is markedly reduced (5 cm/sec) in the patient with myocardial disease (in the center column) whereas early
diastolic velocity (E0 ) of the mitral annulus is normal in normal subject and exaggerated in the patient with constrictive pericarditis (right column, middle row). Color M-mode of mitral inflow demonstrates normal flow propagation in
the normal subject and the patient with pericardial disease. However, it is usually reduced (in the center column,
bottom row, left color M-mode) in patients with myocardial disease but may be falsely normal when LV cavity is relatively small such as in hypertrophic cardiomyopathy for early stage of cardiac amyloid (in the center column, bottom
row, right color M-mode).

12

have also demonstrated a similarly good correlation between E/Ea and PCWP at rest and exercise.39 Several investigators also have explored
use of the duration between the onset of mitral E
velocity and the onset of mitral annulus Ea velocity.
This duration or time interval has been reasonably
well correlated with the filling pressure and also
the status of myocardial relaxation. I had an opportunity to write an editorial to summarize the
current status of using diastolic parameters to estimate diastolic filling pressures, and I concluded in
my editorial from numerous investigations in this
area that now echocardiography is able to estimate left ventricular filling pressure under various
clinical conditions. When I submitted this editorial, the Journal suggested that the phrase, now
echocardiography is able, be changed to echocardiography is now able to which I did not think
was a big issue. I agreed to the change, but when
the paper was published, I was horrified to see
my conclusion. Instead of echocardiography is
now able to estimate left ventricular filling pressures, it read echocardiography is not able to
estimate left ventricular filling pressures which
completely changed the conclusion of my editorial,40 but I hope that some of you who read the
editorial were able to see the obvious error.
Ladies and gentleman, I tried to summarize for
you today in my lecture the current clinical use of
echocardiography in patients with heart failure,
not only systolic but also diastolic heart failure.

Figure 6 (Left) Baseline mitral inflow (top) and tissue Doppler (bottom) demonstrate grade 1 diastolic dysfunction
(E velocity of 50 cm/sec and deceleration time of 250 msec) with impaired myocardial relaxation but normal filling
pressure with E/E0 ratio of 7, and tricuspid regurgitation velocity was also normal indicating normal pulmonary artery
systolic pressure. (Right) With 50 watts of supine bike exercise, E velocity increased to 85 cm/sec and deceleration
time shortened from 250 msec to 140 msec. E0 velocity, however, increased slightly from 7 to 8 cm/sec. Therefore,
E/E0 ratio increased from 7 to 11. TR velocity increased from 2.4 m/sec to 3.8 m/sec (Reproduced with permission
from Ref. 37).

Downloaded from by guest on April 19, 2016

exercise in individuals with normal diastolic function. Subsequently, we performed supine bike diastology stress test in patients with exertional
dyspnea and were able to identify three groups of
patients. The first group of patients was found to
have E/Ea >15 (increased filling pressure) at rest
and the ratio remained elevated with exercise in
all. The second group of patients had relatively
normal filling pressure and impaired myocardial relaxation pattern on mitral inflow velocity at rest
which turned to a restrictive filling pattern with
E/Ea >15 with exercise (Fig. 6). The third group
of patients had normal filling pressure and E/Ea
<15 at rest and with exercise. The patients with increased filling pressure with exercise whether or
not they had normal filling pressure at rest (the first
and second groups), had shorter exercise duration
compared to the patients (the third group) with
normal filling pressure at rest and with exercise.
Subsequently, we have performed simultaneous
cardiac catheterization and Doppler echocardiography in patients who were undergoing exercise
testing in the cardiac catheterization laboratory
for an evaluation of exertional dyspnea.38 In this
patient population, E/Ea >15 correlated well with
pulmonary capillary wedge pressure >20 mmHg,
not only at resting stage but also with exercise.
Therefore, we believe that we now have a very reliable non-invasive diagnostic technique to estimate diastolic filling pressures both at resting
stage, and with exercise. Marwick and his group

J.K. Oh

Echocardiography in heart failure

There are many exciting new technologies and
applications of echocardiography such as 3dimensional echocardiography, strain imaging,
and myocardial perfusion imaging. I am certain
that these new applications will strengthen and
improve the role of echocardiography in general,
but more so in patients with symptoms of heart
failure. Undoubtedly, echocardiography is the
single most useful test in patients with symptoms
of heart failure. It is essential in the diagnosis and
identification of underlying etiology of heart failure. However, we should move beyond the concept of echocardiography as only a diagnostic tool
in patients with heart failure, hence, use this
versatile and easily available technology to gain
pathophysiologic insights of various forms of heart
failure, to help identify or establish an optimal
therapy for the patients with heart failure, to
monitor treatment response, to prognosticate, and
to be an important tool in clinical heart failure
trials.
Thanks again for the invitation to Euro Echo
Lecture 2005 and thank you all for listening.

13

9.

10.
11.

12.

13.

14.

15.

1. Swedberg K, Cleland J, Dargie H, Drexler H, Follath F,

Komajola M, et al. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update
2005). Eur Heart J 2005;26:1115e40.
2. Hunt S, Baker D, Chin M, Cinquegrani M, Feldmanmd A,
Francis G, et al. ACC/AHA guidelines for the evaluation
and management of chronic heart failure in the adult: executive summary a report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation 2001;104:2996.
3. Remme W, McMurray J, Rauch B, Zannad F, Keukelaar K,
Cohen-Solal A, et al. Public awareness of heart failure in
Europe: first results from SHAPE. Eur Heart J 2005;26:
2413e21.
4. Wong S, French J, Lydon A, Manda SO, Gao W, Ashton NG,
et al. Relation of left ventricular sphericity to 10-year survival after acute myocardial infarction. Am J Cardiol
2004;94:1270e5.
5. Grayburn P, Appleton C, DeMaria A, Greenberg B, Lowes B,
Oh J, et al. Echocardiographic predictors of morbidity and
mortality in patients with advanced heart failure. The
Beta-blocker Evaluation of Survival Trial (BEST). J Am Coll
Cardiol 2005;45:1064e71.
6. Yiu S, Sarano M, Tribouilloy C, Seward J, Tajik A. Determinants of the degree of functional mitral regurgitation in
patients with systolic left ventricular dysfunction. A quantitative clinical study. Circulation 2000;102:1400e6.
7. Lamas G, Mitchell G, Flaker G, Smith Jr SC, Gersh BJ,
Basta L, et al. Clinical significance of mitral regurgitation
after acute myocardial infarction. Circulation 1997;96:
827e33.
8. Sutton M, Pfeller M, Palppert T, Rouleau JL, Moye LA,
Dagenais GR, et al. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse
cardiovascular events after acute myocardial infarction.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

Downloaded from by guest on April 19, 2016

References

The protective effects of Captopril. Circulation 1994;89:

68e75.
Yu C, Chau E, Sanderson J, Fan K, Tang M, Fung W, et al. Tissue
Doppler echocardiographic evidence of reverse remodeling
and improved synchronicity by simultaneously delaying
regional contraction after biventricular pacing therapy in
heart failure. Circulation 2002;105:438e45.
Abraham W, Hayes D. Cardiac resynchronization therapy for
heart failure. Circulation 2003;108:2596e603.
Bristow M, Saxon L, Boehmer J, Krueger S, Kass DA,
DeMarco T, et al. Cardiac-resynchronization therapy with
or without an implantable defibrillator in advanced chronic
heart failure. N Engl J Med 2004;350:2140e50.
Yu C, Wing-Hong Fung J, Zhang Q, Chan C, Chan Y, Lin H,
et al. Tissue Doppler imaging is superior to strain rate imaging and postsystolic shortening on the prediction of reverse
remodeling in both ischemic and non-ischemic heart failure
after cardiac resynchronization therapy. Circulation 2004;
110:66e73.
Gorscan J, Kanzaki H, Bazaz R, Dohi K, Schwartzman D.
Usefulness of echocardiographic tissue synchronization imaging to predict acute response to cardiac resynchronization therapy. Am J Cardiol 2004;93:1178e81.
Miyazaki C, Miller F, Karon B, Espinosa R, Khandheria B,
Oh J. Measurement of intraventricular mechanical dyssynchrony by tissue Doppler imaging: is it time to peak velocity
the best parameter for dyssynchrony? J Am Coll Cardiol
2005;45:1001e58.
Miyazaki C, Cha Y, Espinosa R, et al. Correlation between
acute effect of cardiac resynchronization therapy and mechanical dyssynchrony measured by tissue velocity and
strain parameters. J Am Coll Cardiol 2006;47:95A.
Mann D, Acker M, Jessup M, Sabbah H, Starling R, Kubo S.
Rationale, design, and methods for a pivotal randomized
clinical trial for the assessment of a cardiac support device
in patients with New York Health Association class IIIeIV
heart failure. J Cardiac Failure 2004;10:185e92.
Dor V, Di Donato M, Sabatier M, Montiglio F, Civaia F. Left
ventricular reconstruction by endoventricular circular
patch plasty repair: a 17-year experience. Semin Thorac
Cardiovasc Surg 2001;13:435e47.
Athanasuleas C, Buckberg G, Stanley A, Siler W, Dor V,
Donato M, et al. Surgical ventricular restoration in the
treatment of congestive heart failure due to post-infarction
ventricular dilation. J Am Coll Cardiol 2004;44:1439e45.
Senni M, Rodeheffer R, Tribouilloy C, Evans J, Jacobsen S,
Bailey K, et al. Use of echocardiography in the management
of congestive heart failure in the community. J Am Coll Cardiol 1999;33:164e70.
Oh J, Hatle L, Tajik A, Little W. Diastolic heart failure can
be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol 2006;47:500e6.
Mauer M, Spevack D, Burkhoff D, Kronzon I. Diastolic dysfunction: can it be diagnosed by Doppler echocardiography?
J Am Coll Cardiol 2004;44:1543e9.
Burkhoff D, Mauer M, Packer M. Heart failure with a normal
ejection fraction: Is it really a disorder of diastolic function?
Circulation 2003;107:656e8.
Sohn D, Chai I, Lee D, Kim HC, Kim HS, Oh BH, et al. Assessment of mitral annulus velocity by Doppler tissue imaging in
the evaluation of left ventricular diastolic function. J Am
Coll Cardiol 1997;30:474e80.
Nagueh S, Sun H, Kopelen H, Middleton K, Khoury D. Hemodynamic determinants of the mitral annulus diastolic velocities by tissue Doppler. J Am Coll Cardiol 2001;37:278e85.
Ommen S, Nishimura R, Appleton C, Miller FA, Oh JK,
Redfield MM, et al. Clinical utility of Doppler

14

26.

27.

28.

29.

30.

31.

echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures. Circulation 2000;
102:1788e94.
Nagueh S, Middleton K, Kopelen H, Zoghbi W, Quinones M.
Doppler tissue imaging: a non-invasive technique for evaluation of left ventricular relaxation and estimation of filling
pressures. J Am Coll Cardiol 1997;30:1527e33.
Hillis G, Moller J, Pellikka P, Gersh B, Wright R, Ommen S,
et al. Non-invasive estimation of left ventricular filling pressure by E/e0 is a powerful predictor of survival after acute
myocardial infarction. J Am Coll Cardiol 2004;43:360e7.
Moller J, Pellikka P, Hillis G, Oh J. Prognostic importance of
diastolic function and filling pressure in patients with acute
myocardial infarction. Circulation 2006;114:438e44.
Kruszewski K, Barclay J, Scott A, Croal B, Oh J, Hillis G.
Non-invasive assessment of left ventricular filling pressure
following acute myocardial infarction: a prospective study
of the relative prognostic utility of clinical, biochemical,
and echocardiographic parameters. Circulation 2005;112:
II-499.
Moller J, Hillis G, Oh J, Seward JB, Reeder GS, Wright RS,
et al. Left atrial volume. A powerful predictor of survival
after acute myocardial infarction. Circulation 2003;107:
2207e12.
Dokainish H, Zoghbi W, Lakkis N, Al-bakshy F, Dhir M,
Quinones M, et al. Optimal non-invasive assessment of left
ventricular filling pressures. A comparison of tissue Doppler
echocardiography and B-type natriuretic peptide in patients
with pulmonary artery catheters. Circulation 2004;109:
2432e9.
Hatle L, Appleton C, Popp R. Differentiation of constrictive
pericarditis and restrictive cardiomyopathy by Doppler
echocardiography. Circulation 1989;79:357e70.

33. Ha J, Oh J, Ommen S, Ling L, Tajik A. Diagnostic value of

mitral annular velocity for constrictive pericarditis in the
absence of respiratory variation in mitral inflow velocity.
J Am Soc Echocardiogr 2002;15:1468e71.
34. Garcia M, Rodriguez L, Ares M, Griffin B, Thomas J, Klein A.
Differentiation of constrictive pericarditis from restrictive
cardiomyopathy: assessment of left ventricular diastolic
velocities in longitudinal axis by Doppler tissue imaging.
J Am Coll Cardiol 1996;27:108e14.
35. Ha J, Ommen S, Tajik A, Barnes M, Ammash N, Gertz M,
et al. Differentiation of constrictive pericarditis from
restrictive cardiomyopathy using mitral annular velocity
by tissue Doppler echocardiography. Am J Cardiol 2004;
94:316e9.
36. Ha J, Lulic F, Bailey K, Pellikka Pa, Seward JB, Tajik AJ,
et al. Effects of treadmill exercise on mitral inflow and
annular velocities in healthy adults. Am J Cardiol 2003;
91:114e5.
37. Ha J, Oh J, Pellikka P, Ommen S, Stussy V, Bailey K, et al.
Diastolic stress echocardiography: a novel invasive diagnostic test for diastolic dysfunction using supine bicycle
exercise Doppler echocardiography. J Am Soc Echocardiogr
2005;18:63e8.
38. Talreja D, Nishimura R, Oh J. Non-invasive parameters of diastolic function reflect invasively measured filling pressures
during exercise. Circulation 2004;110:II-474.
39. Burgess M, Jenkins C, Sharman J, Marwick T. Diastolic
stress echocardiography: hemodynamic validation and
clinical significance of estimation of ventricular filling
pressure with exercise. J Am Coll Cardiol 2006;47:1891e
900.
40. Oh J. Echocardiography as a non-invasive swan-ganz catheter. Circulation 2005;111:3192e4.

Downloaded from by guest on April 19, 2016

32.

J.K. Oh