Coronary Artery Disease

Left Ventricular Wall Segments

• The most basal third of the left ventricle extends from
the atrioventricular groove to the tip of the papillary
muscles.
• The middle third is identified as that portion of the left
ventricle containing the papillary muscles,
• and the apical third begins at the base of the papillary
muscle and extends to the apex.
• the left ventricular outflow tract as the area extending
from the free edge of the anterior mitral leaflet to the
aortic valve annulus.
• The basal and mid thirds are customarily divided into six
segments each, and the apical region is divided into four
segments, The result is the creation of 16 segments that
comprise the left ventricle.
To define the left ventricular segments, it is first necessary to divide the
left ventricle into apical, mid, and basal thirds, as shown in the
schematic.
Regional LV Function
• In 1989, the ASE recommended a 16-segment model for
LV segmentation.
• This model consists of 6 segments at both basal and
midventricular levels and 4 segments at the apex .
• The attachment of the RV wall to the LV defines the
septum, which is divided at basal and mid-LV levels into
anteroseptum and inferoseptum.
• Continuing counterclockwise, the remaining segments at
both basal and midventricular levels are labeled as
inferior, inferolateral, anterolateral, and anterior.
• The apex includes septal, inferior, lateral, and anterior
segments.
• In 2002, the American Heart Association Writing Group on
Myocardial Segmentation and Registration for Cardiac
Imaging, in an attempt to establish segmentation standards
applicable to all types of imaging, recommended a 17-
segment model This differs from the previous 16-segment
model predominantly by the addition of a 17th segment,
the apical cap.
• The apical cap is the segment beyond the end of the LV
cavity.
Segmental analysis of LV walls based on schematic views, in a parasternal short- and
long-axis orientation, at 3 different levels. The “apex segments” are usually visualized
from apical 4-chamber, apical 2 and 3-chamber views. The apical cap can only be
appreciated on some contrast studies. A 16-segment model can be used, without the
apical cap, as described in an ASE 1989 document.
Typical distributions of the right coronary artery (RCA), the left anterior descending
(LAD), and the circumflex (CX) coronary arteries. The arterial distribution varies between
patients. Some segments have variable coronary perfusion.
Either model is practical for clinical application yet sufficiently
detailed for semiquantitative analysis. The 17-segment model
should be predominantly used for myocardial perfusion
studies or any time efforts are made to compare between
imaging modalities. The 16-segment model is appropriate for
studies assessing wall-motion abnormalities, as the tip of the
normal apex (segment 17) does not move.
It is recommended that each segment be analyzed individually
and scored on the basis of its motion and systolic thickening.
Ideally, the function of each segment should be confirmed in
multiple views.

Segment scores are as follows:

• normal or hyperkinesis 1,
• hypokinesis 2,
• akinesis (negligible thickening) 3,
• dyskinesis (paradoxical systolic motion) 4,
• And aneurysmal (diastolic deformation) 5.

Wall-motion score index can be derived as a sum of all scores

divided by the number of segments visualized.
Pathophysiology of Coronary Syndromes
Normal left ventricular wall motion consists of simultaneous wall thickening and
endocardial excursion so that the cavity decreases in size in a relatively symmetric
Manner.
Interruption of contraction, due to ischemia, infarction, or other process, results in
regional abnormalities of motion.
FIGURE 15.1. Anatomic rendering of a short-axis view of the left ventricle in
diastole (top) and systole (bottom). Note the circular geometry of the left ventricle
in both diastole and systole and the crescent-shaped geometry of the right
ventricle. In the real-time image, note the symmetric wall thickening and inward
endocardial excursion. The location of the major epicardial coronary arteries is also
shown.
FIGURE 15.2. Parasternal short-axis view of the left ventricle (LV) at the papillary
muscle level. As with the accompanying schematic (Fig. 15.1), note the circular
geometry of the left ventricle and the symmetric endocardial inward motion and
wall thickening from diastole (A) to systole (B). RV, right ventricle.
FIGURE 15.4. Demonstration of the ischemic cascade outlining the sequence of
events as the magnitude of ischemia or coronary flow reduction progresses from
none to severe. ECG, electrocardiographic; DTI, Doppler tissue imaging.
Experimentally, immediately
after coronary artery occlusion,
abnormalities in diastolic
function occur and can be
detected with echocardiographic
and Doppler techniques. The
easiest and most commonly
identified abnormality is
abnormal mitral valve inflow,
with reduction in E-wave velocity
and an increase in A-wave
velocity occurring within seconds
of total coronary occlusion

FIGURE 15.5. Pulsed Doppler recording of mitral inflow in an experimental model of

myocardial ischemia. Top: Note the normal E/A ratio and the reversal of the E/A ratio
within seconds of coronary occlusion in the bottom panel.
FIGURE 15.6. Anatomic rendering in diastole
(top) and systole (bottom) of ischemia or
myocardial infarction in the distribution of the
left anterior descending coronary artery.
When comparing diastole and systole, note
the lack of thickening in the anterior wall and
anterior septum compared with normal
hyperdynamic motion in the uninvolved
segments. (Graphics by Amanda Almon and
Travis Vermile)
Detailed analysis methods such as strain or strain rate imaging have
demonstrated that, in many instances, this abnormality is the result of
postsystolic contraction.

This is followed almost immediately by loss of systolic wall thickening and

decreased endocardial excursion in the region perfused by the
obstructed coronary artery

If the coronary artery obstruction persists for a threshold period

(typically defined as ≥4 hours), myocardial necrosis ensues and a
persistent wall motion abnormality will develop.
FIGURE 15.7. Parasternal short-axis view recorded in diastole (A) and in systole
(B) in a patient with acute left anterior descending coronary artery occlusion and
myocardial infarction. B: Note the lack of wall thickening and the dyskinesis of the
anterior septum (outward-pointing arrows) and the normal motion of the
posterior wall (inward-pointing arrows). LV, left ventricle; RV, right ventricle.
FIGURE 15.8. Anatomic rendering in the four-chamber view depicts a left
ventricular apical aneurysm. Left: Diastole. Right: Systole. Note in diastole the
abnormal geometry of the apex with localized apical and septal dilation and the
relative thinning of the wall compared with the thickness in the proximal walls.
Right: The preserved thickening of the proximal walls and a lack of thickening in
the aneurysmal segment in all segments distal to the arrows are shown. This
abnormal geometry in both diastole and systole with wall thinning is the hallmark
of true ventricular aneurysm. LA, left atrium; RA, right atrium. (Graphics by
Amanda Almon and Travis Vermile)
FIGURE 15.14.Apical four-chamber views recorded in a normal ventricle in diastole
(A) and systole (B). Note the normal bullet-shaped geometry of the left ventricle
that tapers at the apex and the symmetric contraction of all visualized walls. Note
also the stable position of the apex in the real-time image, indicating that the
transducer is at the true apex. LA, left atrium; LV, left ventricle; RA, right atrium; RV,
right ventricle.
FIGURE 15.20. Parasternal long-axis echocardiogram recorded in a patient with
extensive anteroapical and anterior wall myocardial infarction. Figures 15.20
through 15.23 are recorded in the same patient. A: In the parasternal long-axis view,
note the normal geometry of the left ventricle (LV) in diastole. B: In systole, note
the normal motion of the proximal inferior wall and a lack of thickening and akinesis
of the entire anterior septum (arrows). Incidental note is made of a pleural effusion
(Pleff). Ao, aorta; LA, left atrium; LV, left ventricle.
FIGURE 15.21. Parasternal short-axis view recorded in the same patient depicted in
Figure 15.20. Note preserved circular geometry of the left ventricle (LV) in diastole (A)
and the normal myocardial thickening and endocardial excursion of the posterior
wall. B: Recorded in systole, the anterior and mid septum are both full thickness but
dyskinetic (arrows). RV, right ventricle.
FIGURE 15.22. Apical two-
chamber view recorded in
diastole (A) and systole (B) in
the patient previously
presented with extensive left
anterior descending coronary
artery territory myocardial
infarction. In the two-
chamber view, note the
preserved function of the
proximal 50% of the inferior
wall and the akinesis or
dyskinesis of the distal
inferior wall, apex, and
anterior wall (arrows). In this
example, the involvement of
the distal inferior wall is due
to a wraparound left anterior
descending coronary artery
and not the result of
concurrent ischemia in the
right coronary artery. LA, left
atrium; LV, left ventricle.
FIGURE 15.23. Apical four-chamber
view recorded in the same patient
depicted in the three previous
figures. In the four-chamber view,
note the abnormal geometry of the
distal septum (area between the
two arrows) present in diastole (A).
B: In systole, function is preserved
at the base of the heart (inward-
pointing arrows) with akinesis or
dyskinesis in the distal half of the
left ventricle (outward-pointing
arrows). Incidental note is also
made of an atrial septal aneurysm
[arrow in the left atrium (LA)]. Note
the bowing of the atrial septum
from left to right, implying elevated
left atrial pressure, presumably
secondary to left ventricular
dysfunction. LV, left ventricle, RA,
right atrium; RV, right ventricle.
FIGURE 15.24. Parasternal short-axis view recorded in a patient with a classic inferior
wall myocardial infarction. A: Recorded in diastole. Note the normal shape of the left
ventricle (LV) in diastole. In systole (B), the true inferior wall is thin and frankly
dyskinetic (arrows), whereas the remaining walls contract normally. RV< right
ventricle.
FIGURE 15.25. Apical two-chamber view recorded in diastole (A) and systole (B) in a
patient with an inferior myocardial infarction. In systole (B), note the normal motion of
the anterior wall and the frank dyskinesis of the proximal two-thirds of the inferior wall
(arrows). LA, left atrium; LV, left ventricle.
FIGURE 15.26. Apical four-chamber view recorded in the same patient depicted in Figure 15.25 in diastole (A) and
systole (B). Note the dyskinesis of the proximal 25% of the ventricular septum, which in this instance is
attributable to septal involvement by the inferior myocardial infarction. Caution is advised when interpreting a
wall motion abnormality in this location. The proximal ventricular septum in the apical four-chamber view often
has abnormal motion. Only when the abnormality is seen in association with concurrent inferior wall myocardial
infarction should it be presumed to be infarct as well.
FIGURE 15.28A. Echocardiograms recorded in two patients with remote myocardial infarctions.
Left:Apical long-axis views recorded in diastole (A) and systole (B) in a patient with an inferior
myocardial infarction attributed to disease of the left circumflex coronary artery. Note in systole
that the proximal two-thirds of the inferoposterior wall are dyskinetic and there is normal
contraction of the anterior septum and apex.
Right: Parasternal long-axis views recorded in a patient with a remote
inferior/inferolateral myocardial infarction. Image at the top (B) , was recorded in
diastole; note that the proximal one-third of the inferior wall is pathologically thinned
with a dense echo signature consistent with scar. In the image at the bottom (C) , there is
normal contraction of the anterior septum and more distal portions of the
inferoposterior wall with akinesis of the infarct area (downward-pointing arrows). LA, left
atrium; LV, left ventricle.
FIGURE 15.30. Parasternal long-axis echocardiogram recorded in a patient presenting with an
acute myocardial infarction and left bundle branch block. Note from diastole (A) to systole (B),
only the very proximal portion of the anterior septum has moved downward (long arrow) and the
more distal portions of the septum are dyskinetic (upward-pointing arrows). This pattern should
be easily distinguished from the wall motion abnormality seen in left bundle branch block. Ao,
aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.
FIGURE 15.31. Apical four-chamber view recorded in a patient
presenting with a non---ST-segment elevation myocardial
infarction. In this instance, only ST-segment depression with T-
wave inversion was noted on the electrocardiogram, maximally
in the anterior precordium. A was recorded in diastole. B: Note
the fairly extensive area of dyskinesis in the distal septum and
apex (arrows). The wall motion abnormality noted here is
virtually identical to that seen with typical ST-segment elevation
or Q-wave myocardial infarction. LA, left atrium; LV, left
ventricle, RA, right atrium; RV, right ventricle.
FIGURE 15.32AB.
Parasternal long-axis
echocardiogram recorded in
a patient at the time of
presentation with an
impending anterior ST-
segment elevation
myocardial infarction (A, B).
C,D: The same patient on a follow-up
echocardiogram recorded several days
after successful reperfusion therapy. For
each set of images, the end-diastolic
frames are on the left and end-systolic
on the right. At the time of acute
presentation, note preserved motion of
the proximal anterior septum
(downward-pointing arrow) with
dyskinesis of the distal septum
(upward-pointing arrows). D: Recorded
in systole after reperfusion therapy and
recovery of function; note the normal
motion of both the anterior septum and
inferoposterior walls.
FIGURE 15.33AB. Apical
four-chamber views
recorded in a patient
presenting with extensive
LAD distribution myocardial
infarction. A, B: Recorded at
the time of presentation; C,
D: recorded approximately
3 months later after
successful reperfusion
therapy. For each set of
images, diastole is on the
left and systole on the right.
Note the extensive wall
motion abnormalities at the
time of presentation with
the acute event and near
complete recovery of
function 3 months later,
with only a limited residual
apical wall motion
abnormality
FIGURE 15.33AB. Apical four-
chamber views recorded in a
patient presenting with extensive
LAD distribution myocardial
infarction. A, B: Recorded at the
time of presentation; C, D:
recorded approximately 3 months
later after successful reperfusion
therapy. For each set of images,
diastole is on the left and systole
on the right. Note the extensive
wall motion abnormalities at the
time of presentation with the
acute event and near complete
recovery of function 3 months
later, with only a limited residual
apical wall motion abnormality
FIGURE 15.38. Apical four-chamber view recorded 36 hours after presentation with
an extensive anteroapical ST-segment elevation myocardial infarction. A: Note in the
image recorded in diastole that there is already abnormal left ventricular geometry
with regional dilation of the distal septum (begins at arrow). This is more apparent in
the image recorded in systole (B) where there is akinesis and dyskinesis of the distal
septum and lateral walls (distal to the arrows). Because of the regional dilation, there
is an obligatory thinning of the necrotic myocardium due to infarct expansion.
FIGURE 15.39. Apical four-chamber view recorded in a patient with an acute anterior
apical myocardial infarction and early thrombus formation. Note the regional dilation of
the left ventricle at the apex and the pedunculated, multilobulated mass protruding into
the cavity of the left ventricle (LV) (arrows). RV, right ventricle.
FIGURE 15.40. Subcostal view recorded in a patient with a limited inferior
myocardial infarction and concurrent right ventricular infarction. A: Recorded in
diastole. Note the dilated right ventricular cavity with relatively preserved right
ventricular shape. B: Recorded in systole. Note the normal inward motion of the
proximal right ventricular wall (downward-pointing arrows) and the dyskinesis of
the apical portion of the right ventricular wall (upward-pointing arrow). LV, left
ventricle; RV, right ventricle.
FIGURE 15.41. Off-axis four-chamber view recorded in a patient with an inferior
myocardial infarction and right ventricular infarction. Note the dilation of the right
ventricular cavity and the marked reduction in systolic function in the real-time
image. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.42A. Apical four-chamber view recorded in the same patient depicted
in Figure 15.41 with an inferior myocardial infarction complicated by right
ventricular infarction. In this instance, marked arterial desaturation was noted. A:
Note the marked dilation of the right ventricle (RV) and right atrium (RA). B: Image
recorded after injection of intravenous saline shows marked opacification of the
right ventricle with a substantial contrast effect in the left ventricle (LV) and left
atrium (LA), indicative of a pathologic right to left shunt, subsequently
documented to be due to a large patent foramen ovale.
FIGURE 15.42A. Apical four-chamber view recorded in the same patient depicted
in Figure 15.41 with an inferior myocardial infarction complicated by right
ventricular infarction. In this instance, marked arterial desaturation was noted. A:
Note the marked dilation of the right ventricle (RV) and right atrium (RA). B: Image
recorded after injection of intravenous saline shows marked opacification of the
right ventricle with a substantial contrast effect in the left ventricle (LV) and left
atrium (LA), indicative of a pathologic right to left shunt, subsequently
documented to be due to a large patent foramen ovale.
FIGURE 15.44. Apical four-chamber view recorded in the same patient depicted
in Figure 15.43. A: Note the break in the continuity of the posterolateral
papillary muscle with two portions of the papillary muscle head (arrows). B:
Recorded in systole. Note the marked buckling of the mitral valve leaflet into
the left atrium (LA) (upward-pointing arrow) and the ruptured papillary muscle
base in the cavity of the left ventricle (horizontal arrow). LV, ventricle; RA, right
atrium; RV, right ventricle.
FIGURE 15.45. Transesophageal echocardiogram recorded in a longitudinal plane in
a patient with inferior myocardial infarction and acute severe mitral regurgitation.
This frame was recorded in systole, and a large portion of the papillary muscle head
can be seen prolapsing into the left atrium (LA) (arrows). Ao, aorta; LV, left ventricle.
FIGURE 15.46A. Parasternal long-axis view recorded in a patient with functional mitral
regurgitation due to myocardial ischemia and subsequent malcoaptation of the mitral valve. A:
Image recorded in end-systole demonstrates tethering of the mitral valve toward the apex. The
dashed line denotes the plane of the mitral anulus. Note the ``tenting’’ of the mitral leaflets
into the cavity of the left ventricle. B: Image recorded in the same patient with color Doppler
flow imaging reveals severe mitral regurgitation. In this instance, there is no anatomic
disruption of the mitral valve apparatus and mitral regurgitation is due to functional
abnormalities of mitral valve closure rather than an anatomic defect of the valve itself. The
schematics denote normal (A) and abnormal (B) coaptation patterns for comparison.
FIGURE 15.46A. Parasternal long-axis view recorded in a patient with functional mitral
regurgitation due to myocardial ischemia and subsequent malcoaptation of the mitral valve. A:
Image recorded in end-systole demonstrates tethering of the mitral valve toward the apex. The
dashed line denotes the plane of the mitral anulus. Note the ``tenting’’ of the mitral leaflets
into the cavity of the left ventricle. B: Image recorded in the same patient with color Doppler
flow imaging reveals severe mitral regurgitation. In this instance, there is no anatomic
disruption of the mitral valve apparatus and mitral regurgitation is due to functional
abnormalities of mitral valve closure rather than an anatomic defect of the valve itself. The
schematics denote normal (A) and abnormal (B) coaptation patterns for comparison.
FIGURE 15.47A. A: Parasternal short-axis view recorded in a patient with an extensive
inferior and inferoseptal myocardial infarction with a partial rupture of the septum.
Note the very thin-walled aneurysmal tissue extending from the inferior septum
(downward-pointing arrow) and a relatively narrow entrance (leftward-pointing
arrows).B: Note the color flow signal demonstrating marked turbulent flow from the
cavity of the left ventricle (LV) into the pseudoaneurysm and subsequently into the right
ventricular cavity. RA, right atrium.
FIGURE 15.47A. A: Parasternal short-axis view recorded in a patient with an extensive
inferior and inferoseptal myocardial infarction with a partial rupture of the septum.
Note the very thin-walled aneurysmal tissue extending from the inferior septum
(downward-pointing arrow) and a relatively narrow entrance (leftward-pointing
arrows).B: Note the color flow signal demonstrating marked turbulent flow from the
cavity of the left ventricle (LV) into the pseudoaneurysm and subsequently into the right
ventricular cavity. RA, right atrium.
FIGURE 15.48A. Apical four-chamber view recorded in a patient with acute inferoseptal
and inferior myocardial infarction. Note the distinct break in the septal contour (arrow)
(A) and the color flow signal traversing this ventricular septal defect (arrow) (B). LA, left
atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.48A. Apical four-chamber view recorded in a patient with acute inferoseptal
and inferior myocardial infarction. Note the distinct break in the septal contour (arrow)
(A) and the color flow signal traversing this ventricular septal defect (arrow) (B). LA, left
atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.49. Transesophageal echocardiogram recorded in a transverse plane (0
degrees) in a patient with a ventricular septal defect after acute myocardial infarction.
Note the turbulent color flow signal traversing the ventricular septum through the large
ventricular septal defect. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right
ventricle.
FIGURE 15.50A.A: Apical four-chamber views recorded in a patient with a very large
chronic anteroapical myocardial infarction and apical aneurysm. Note the normal
thickness of the proximal 50% of the left ventricle (LV) with marked aneurysmal
dilation, abnormal geometry, and wall thinning in the distal half of the ventricle. Note
also in the two-chamber view (B) the involvement of the distal inferior wall with a
distinct break in function and wall thickness (arrows). LA, left atrium; RA, right atrium;
RV, right ventricle.
FIGURE 15.50A.A: Apical four-chamber views recorded in a patient with a very large
chronic anteroapical myocardial infarction and apical aneurysm. Note the normal
thickness of the proximal 50% of the left ventricle (LV) with marked aneurysmal
dilation, abnormal geometry, and wall thinning in the distal half of the ventricle. Note
also in the two-chamber view (B) the involvement of the distal inferior wall with a
distinct break in function and wall thickness (arrows). LA, left atrium; RA, right atrium;
RV, right ventricle.
FIGURE 15.51. Apical four-chamber view recorded in
a patient with a smaller apical aneurysm. A: Image
recorded in diastole; note the loss of the normal
tapering of the left ventricular apex. B: Image
recorded in systole in which the abnormal geometry,
and the distinct break between the normally
functioning basal two-thirds of the ventricle and the
aneurysm, is more apparent.
FIGURE 15.52. Three-dimensional reconstruction from a transesophageal
echocardiogram recorded in a patient with a large anteroapical aneurysm. A:
Image recorded in diastole reveals aneurysmal dilation of the distal 50% of the left
ventricle. Note the loss of normal tapering toward the apex and the apical dilation.
B: Image recorded in systole documents preserved function at the base of the
heart with dyskinesis of the apical, aneurysmal segments. LA, left atrium; LV, left
ventricle; MV, mitral valve.
FIGURE 15.53. Apical two-chamber view recorded
in diastole (A) and systole (B) in a patient with a
remote inferior myocardial infarction and inferior
aneurysm at the base of the heart. A: Recorded in
diastole, note the abnormal geometry of the
proximal inferior wall (arrows) (INF). This
abnormality is even more prominent in the image
recorded in systole (B) in which one can appreciate
the preserved contractility of the distal inferior wall
and anterior wall (ANT).
FIGURE 15.54. Apical two-chamber view recorded in a patient with a remote inferior
myocardial infarction and a discrete basal aneurysm. In this instance, the outer wall of
the aneurysm is noted by the upward- pointing arrows. Note the relatively narrow neck
to the aneurysm and a laminar thrombus (downward-pointing arrow). In examples
such as this, it may be difficult to separate a true aneurysm from a pseudoaneurysm.
ANT, anterior wall; INF, inferior wall; LA, left atrium; LV, left ventricle.
FIGURE 15.55A. Apical four-chamber view recorded in a patient with an anteroapical
aneurysm who subsequently underwent a Dor myoplasty for left ventricular remodeling.
A: The preoperative image shows a large anteroapical aneurysm. B: Image recorded after
the Dor myoplasty. Note the position of the patch and the obliterated apex of the left
ventricle. The remaining left ventricular cavity has relatively normal geometry and systolic
function.
FIGURE 15.55A. Apical four-chamber view recorded in a patient with an anteroapical
aneurysm who subsequently underwent a Dor myoplasty for left ventricular remodeling.
A: The preoperative image shows a large anteroapical aneurysm. B: Image recorded after
the Dor myoplasty. Note the position of the patch and the obliterated apex of the left
ventricle. The remaining left ventricular cavity has relatively normal geometry and systolic
function.
FIGURE 15.57A. Off-axis transthoracic apical view (A) and transesophageal
echocardiographic view (B) recorded in a patient with an inferior pseudoaneurysm. A:
Note the proximal inferior wall aneurysm that appears to have a communication between
the left ventricle (LV) and aneurysmal cavity that is relatively narrow (arrows). B: In the
transesophageal echocardiogram, note the true extent of the pseudoaneurysm (large
arrow) compared with the communication to the left ventricle (small arrows), which
allows documentation that this is a pseudoaneurysm rather than a true aneurysm. LA, left
atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.57A. Off-axis transthoracic apical view (A) and transesophageal
echocardiographic view (B) recorded in a patient with an inferior pseudoaneurysm. A:
Note the proximal inferior wall aneurysm that appears to have a communication between
the left ventricle (LV) and aneurysmal cavity that is relatively narrow (arrows). B: In the
transesophageal echocardiogram, note the true extent of the pseudoaneurysm (large
arrow) compared with the communication to the left ventricle (small arrows), which
allows documentation that this is a pseudoaneurysm rather than a true aneurysm. LA, left
atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.58. Transesophageal echocardiogram recorded in a patient with an inferior
myocardial infarction and a very large pseudoaneurysm. In this example, the outer
boundary of the pseudoaneurysm is as marked by the outer vertical lines (O) and the
communication with the left ventricle (LV) by the inner vertical lines (I). In this example,
the maximal dimension of the pseudoaneurysm actually exceeds the size of the left
ventricle. The opening to the pseudoaneurysm is noted by the smaller arrows. LA, left
atrium; MV, mitral valve.
FIGURE 15.59A. Apical view recorded in a patient with a chronic small apical
pseudoaneurysm. A: An off-axis four-chamber view. B: A two-chamber view. In each
instance, note the very discrete, nearly spherical pseudoaneurysm cavity bounded
by a fairly echodense border, suggesting calcification in the rim. The
pseudoaneurysm has a very narrow neck communicating with the cavity of the left
ventricle near the apex. In this case, the pseudoaneurysm is the result of apical
infarction noted to have occurred 5 years before recording this echocardiogram. LA,
left atrium; LV, left ventricle; RV, right ventricle.
FIGURE 15.59A. Apical view recorded in a patient with a chronic small apical
pseudoaneurysm. A: An off-axis four-chamber view. B: A two-chamber view. In each
instance, note the very discrete, nearly spherical pseudoaneurysm cavity bounded
by a fairly echodense border, suggesting calcification in the rim. The
pseudoaneurysm has a very narrow neck communicating with the cavity of the left
ventricle near the apex. In this case, the pseudoaneurysm is the result of apical
infarction noted to have occurred 5 years before recording this echocardiogram. LA,
left atrium; LV, left ventricle; RV, right ventricle.
FIGURE 15.60A. Apical four-chamber view recorded in a patient with a large
pseudoaneurysm after lateral wall myocardial infarction. A: Note the very large
pseudoaneurysm cavity communicating with the left ventricle by a relatively narrow
neck (arrows). B: Image recorded with color flow Doppler imaging confirms the
communication between the left ventricular cavity and the pseudoaneurysm. LA,
left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.60A. Apical four-chamber view recorded in a patient with a large
pseudoaneurysm after lateral wall myocardial infarction. A: Note the very large
pseudoaneurysm cavity communicating with the left ventricle by a relatively narrow
neck (arrows). B: Image recorded with color flow Doppler imaging confirms the
communication between the left ventricular cavity and the pseudoaneurysm. LA,
left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 15.63A. Apical long-axis (A) and four chamber (B) views recorded in a patient
with an anteroapical myocardial infarction and a laminar apical thrombus. In each
instance, note the laminar filling defect (upward-pointing arrows) in the apex of the
left ventricle (LV), which is akinetic and dilated. B: Note the multiple laminar lines
(downward-pointing arrow) with variable consistency of the thrombus suggesting
chronicity. LA, left atrium; RV, right ventricle.
FIGURE 15.63A. Apical long-axis (A) and four chamber (B) views recorded in a patient
with an anteroapical myocardial infarction and a laminar apical thrombus. In each
instance, note the laminar filling defect (upward-pointing arrows) in the apex of the
left ventricle (LV), which is akinetic and dilated. B: Note the multiple laminar lines
(downward-pointing arrow) with variable consistency of the thrombus suggesting
chronicity. LA, left atrium; RV, right ventricle.
FIGURE 15.64. Apical four-chamber view recorded in a patient with an acute
anteroapical myocardial infarction and a pedunculated, slightly mobile apical
thrombus.
FIGURE 15.65. Apical two-chamber view recorded in a patient with an anteroapical
myocardial infarction and multiple large pedunculated and mobile thrombi. Note the
multiple masses protruding into the cavity of the left ventricular apex and the mobile
nature of these thrombi in the real-time image.
FIGURE 15.66A. Apical four-chamber view recorded without (A) and with (B)
intravenous contrast for left ventricular opacification. A: Note the vague suggestion of a
filling defect in the apex of the left ventricle (LV) (arrows). B: After injection of
intravenous contrast, the entire left ventricular cavity is opacified and the thrombus
appears as a slightly mobile spherical filling defect in the left ventricular apex (arrows).
RV, right ventricle.
FIGURE 15.66A. Apical four-chamber view recorded without (A) and with (B)
intravenous contrast for left ventricular opacification. A: Note the vague suggestion of a
filling defect in the apex of the left ventricle (LV) (arrows). B: After injection of
intravenous contrast, the entire left ventricular cavity is opacified and the thrombus
appears as a slightly mobile spherical filling defect in the left ventricular apex (arrows).
RV, right ventricle.
FIGURE 15.68. Apical four-chamber view recorded in a
patient with an ischemic cardiomyopathy and restricted
posterior leaflet motion. A: Recorded in diastole. Note the
position of the posterior leaflet (arrow). In systole (B),
there is normal motion of the anterior leaflet toward the
tip of the posterior leaflet, which has remained tethered in
position (arrow) due to the underlying wall motion
abnormality. This abnormal coaptation results in
functional mitral regurgitation. LA, left atrium; LV, left
ventricle.
FIGURE 15.76. Apical view recorded in a patient status post-cardiac transplantation
who has undergone multiple right ventricular endocardial biopsies. A: Note the
continuous turbulent flow in the right ventricular apex, which is the result of an
iatrogenic coronary artery fistula into the cavity of the right ventricle (RV). B: A color
Doppler M-mode recording through that area demonstrates the continuous flow. LV,
left ventricle; RA, right atrium.
FIGURE 15.77. Parasternal short-axis view recorded at the base of the heart in a child
with Kawasaki disease and aneurysmal dilation of the right coronary artery (RCA). Note
size and location of the aorta (Ao) and pulmonary artery and a markedly dilated right
coronary artery that measures approximately 8 mm in diameter. LMCA, left main
coronary artery; RA, right atrium; RVOT, right ventricular outflow tract.