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CHAPTER
49
ECHOCARDIOGRAPHY
IN CARDIAC SURGERY
Samia Mora, Katherine C. Wu
PRINCIPLES OF ECHOCARDIOGRAPHY
DOPPLER ECHOCARDIOGRAPHY
Since 1976, echocardiography (echo) has been used to
evaluate cardiac structure and function. Echo uses sound
in the high-frequency range (2 to 10 MHz). Frequency
ranges between 2 and 5 MHz are typically used for imaging adults, while frequencies of 7.5 to 10 MHz are used for
children and specialized adult applications. The transducer
contains a piezoelectric crystal that converts electrical to
sound energy, producing sound waves that are transmitted
in the form of a beam. A complete transthoracic echocardiogram (TTE) consists of a group of interrelated applications including two-dimensional (2D) anatomic imaging,
M-mode, and three Doppler techniques: pulsed-wave
(PW), continuous-wave (CW), and color-flow (CF) imaging.1–7 In addition, the quantification of cardiac chamber
dimensions, areas, and volumes is an important aspect of a
complete examination. Using a combination of these ultrasound techniques, one can assess the anatomy and function
of the cardiac valves, myocardium, and pericardium.
The Doppler effect is the phenomenon whereby the frequency of sound waves increases or decreases as the sound
source moves toward or away from the observer. The
resultant Doppler frequency shift can be detected and
translated into blood-flow velocity. The velocity of blood
can then be used to calculate valvular gradients and
areas, intracardiac pressures, and volumetric flow.
Pulsed-wave doppler
Pulsed-wave (PW) Doppler is obtained when a pulse of
ultrasound is transmitted intermittently, allowing for
estimation of blood-flow velocity at a specific region of
interest. It is thus “site-specific.” Its disadvantage is aliasing (or wraparound) of the signal at velocities that are
one-half of the pulse repetition frequency (Nyquist limit).
This property limits the maximal velocity that can be
accurately measured with PW.
Continuous-wave doppler
TWO-DIMENSIONAL ECHOCARDIOGRAPHY
Continuous-wave (CW) Doppler records all the velocities along the path of the ultrasound beam. Using CW,
the magnitude of the blood-flow velocity and its direction can be accurately recorded. Its disadvantage is that it
does not allow localization of the specific site of the
velocity obtained along the beam path. CW is used to
measure high-velocity jets associated with valvular dysfunction or intracardiac pressure gradients. The simplified Bernoulli equation can then be used to convert
velocities into pressure gradients (P 4V2).
Standard views are obtained along three orthogonal planes
of the left ventricle (LV): long-axis, short-axis, and the 4chamber plane (Fig. 49-1A to C). The long axis is parallel to
the long axis of the LV. The short axis cuts the LV cross-sectionally, similar to slices of bread in a loaf, and is orthogonal
to the long axis. Four standard transducer locations are used
to obtain complete visualization of the entire heart: parasternal, apical, subcostal, and suprasternal.
M-MODE ECHOCARDIOGRAPHY
Color-flow doppler
M mode is a one-dimensional “ice pick” view of the heart
(Fig. 49-1D) and is often used for measuring LV systolic
and diastolic chamber dimensions and wall thickness.
Color-flow (CF) Doppler transforms Doppler velocity
information into a color-coded scheme. Red denotes
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A
B
C
D
Figure 49-1 Standard 2D TTE (A to C) and M-mode (panel D) views in a normal individual. A. Parasternal long-axis view of the right ventricle (RV), interventricular septum, left
ventricle (LV) cavity and posterior wall, and both mitral and aortic valves. Since the RV is
the most anterior structure, it will be located closest to the transducer beam and is seen at
the top of the image display, while the LV and LA (both posterior structures) are farther
away from the transducer and are seen at the bottom of the image. B. Parasternal shortaxis view of the ventricles at the papillary muscle midventricular level obtained by rotating
the transducer 90 degrees. C. Apical four-chamber view, important for evaluation of ventricular function, apical thrombus, mitral and tricuspid valve function. D. M-mode view
through the RV and mitral leaflets. This view is useful for detecting RV diastolic collapse in
tamponade.
flow toward the transducer, while blue represents flow
away from the transducer. The relative velocity of blood
flow is also depicted, with brighter shades of blue or red
representing higher velocities. Turbulent flow is seen as
multicolored jets (e.g., due to valvular disease or intracardiac shunts).
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
TEE was first introduced clinically in the United States
in the 1980s. By placing an echocardiographic probe in
the esophagus, which is in close proximity to cardiac
structures, TEE obtains significantly enhanced images
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Chapter 49 ● Echocardiography in Cardiac Surgery
with excellent resolution. The development of transducer
crystals that rotate from 0 to 180 degrees also allows for
examination of each cardiac structure from different
planes and angles. Acquisition of images is from two basic
locations: midesophageal (30 to 35 cm from the incisors)
and midgastric (40 to 45 cm from the incisors).
Indications
TEE is useful for the evaluation of patients with limiting
body habitus, such as obesity or emphysema, who are not
optimally imaged by the transthoracic approach. In addition, certain structures that are not well visualized by
transtracheal echo (TTE) [such as the left atrial (LA)
appendage, thoracic aorta, and prosthetic valves] can be
assessed by the transesophageal approach. A third common
indication is to guide intraoperative management during
cardiac surgery. Class I indications for perioperative TEE
(conditions for which there is evidence and/or general
agreement that TEE is useful and effective) are listed in
Table 49-1.8 There are other situations in which TEE may
also be useful but is not required (i.e., class II indications:
conditions in which there is a divergence of opinion about
the usefulness/efficacy of a procedure but in which the
weight of opinion is in favor of usefulness/efficacy). These
include ongoing surgical procedures in patients at increased
risk of myocardial ischemia or hemodynamic instability,
during minimally invasive surgery or the Cox-Maze procedure cardiac tumor resection or aneurysm repair, intracardiac thrombectomy or pulmonary embolectomy, for
detection of intracardiac air or aortic atheromatous disease,
and for selecting anastomotic sites during heart/lung
transplantation.8 Antibiotic prophylaxis for infective endocarditis is usually unnecessary but is optional in the high-risk
patient (e.g., complex congenital heart disease, prosthetic
valve, poor dentition, or prior history of endocarditis).9
Contraindications and complications
Relative contraindications for TEE include significant
esophageal pathology (e.g., strictures, varices), history
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of radiation therapy to the mediastinum, and recent
esophageal or gastric surgery. Serious complications of TEE
are uncommon ( 1 percent) but may include aspiration
and other problems related to oversedation, mucosal
trauma, laryngospasm, esophageal or pharyngeal laceration
or perforation, methemoglobinemia, and rarely death.
TEE probe passage is “blind” and is done without direct
visualization. The more severe complications of esophageal
or pharyngeal trauma are signaled by patient complaints of
severe pain and inability to swallow, which usually occur
after the procedure has ended and sedation has worn off.
Esophageal perforation during intraoperative TEE can go
undetected for a period of time because of the anesthetized
state of the patient and the lack of patient feedback regarding pain during probe passage.
ASSESSMENT OF VENTRICULAR FUNCTION
Routinely, a qualitative “eyeball” estimate of global LV
systolic function is obtained visually by examining LV wall
thickening and motion. In addition, quantitative measures
of LV systolic function can also be obtained. LV segmental wall function can be analyzed using a semiquantitative
grading scale (wall motion score).
LEFT VENTRICULAR EJECTION FRACTION
Ejection fraction (EF) is often reported qualitatively as
increased (hyperdynamic), normal, mildly, moderately, or
severely reduced.8 In addition, the reader often assigns an
estimated value to the qualitative assessment. Normal LV
EF is 61 10 percent.10
Visual estimation of EF by experienced readers is generally reliable but is limited by reader variability and
depends on optimal echocardiographic delineation of the
endocardium.
EF can also be quantified from the equation below
after determining end-diastolic volume (EDV) and endsystolic volume (ESV):
EF SV/EDV (EDV – ESV)/EDV
Table 49-1
Class I indications for perioperative
transesophageal echocardiography
Acute and life-threatening hemodynamic instability
Valve repair or complex valve replacements
Hypertrophic obstructive cardiomyopathy
Aortic dissection with possible aortic valve involvement
Endocarditis (perivalvular involvement)
Congenital heart surgery
Pericardial windows (posterior or loculated effusions)
Placement of intracardiac devices
Source: Data modified from Cheitlin MD, Armstrong WF, Aurigemma GP,
et al. ACC/AHA/ASE 2003 guideline update for the clinical application of
echocardiography: summary article: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines
(ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical
Application of Echocardiography). Circulation 2003;108:1146–1162.
Where SV stroke volume, EDV end-diastolic volume, and ESV end-systolic volume.
Volumes can be obtained by the modified Simpson’s
method, which divides the LV cavity into a series of
stacked cylinders of equal height that are summed to
estimate the entire ventricular volume at end-diastole
and end-systole. Further details of the technique can be
found in several of the references.1,2,11
LEFT VENTRICULAR FRACTIONAL
SHORTENING (PERCENT FRACTIONAL
SHORTENING)
Percent FS is another method for estimating LV systolic function and reflects a percent change in LV
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dimension with systolic contraction. It is calculated
from LV end-diastolic and end-systolic dimensions measured by M mode. For ventricles that are roughly symmetrical without regional wall motion abnormalities, EF
is approximately 2 (percent FS).
Percent FS (EDD – ESD) / EDD 100
Where EDD end-diastolic dimension and ESD endsystolic dimension.
LEFT VENTRICULAR REGIONAL
WALL MOTION
For the assessment of LV regional wall motion, the LV is
divided into 16 segments (Fig. 49-2), each of which is
given a score from 1 to 5 (1, normal or hyperkinetic; 2,
hypokinetic; 3, akinetic; 4, dyskinetic; 5, aneurysmal or
diastolically deformed). This grading system differs from
the 1-to-5 grading system of TEE often used by cardiac
anesthesiologists12 [1, normal ( 30 percent thickening);
2, mildly hypokinetic (10 to 30 percent thickening); 3,
severely hypokinetic ( 10 percent thickening); 4, akinetic (no thickening); 5, dyskinetic (paradoxical systolic
motion)]. The wall motion score index is calculated as
the sum of segmental wall motion scores divided by the
number of segments seen. A score of 1 is normal and
higher wall motion scores indicate more extensive ventricular dysfunction. However, this grading system is
more useful for research databases than for clinical use.
LEFT VENTRICULAR FILLING
LV preload is the LV volume at end-diastole. Normal LV
end-diastolic size is 3.5 to 5.7 cm in the parasternal longaxis view. The size of the ventricles and atria may be used
for the qualitative evaluation of filling pressures and
assessment of hyper- or hypovolemia, particularly intraoperatively with TEE.13 Small LA size and near cavity
obliteration of the LV can indicate hypovolemia.14
Conversely, ventricular and atrial enlargement may indicate hypervolemia. Doming of the interatrial septum
toward the right suggests elevated LA pressure and
increased LV preload (the septum bulges toward the side
with lower pressure). One limitation to using TEE for
indirect measurement of volume status is that the LV
may be foreshortened; it is therefore recommended that
the LV be imaged from several different planes to get a
more accurate estimate of LV volume.14
LEFT VENTRICULAR DIASTOLIC FUNCTION
Doppler echo is the most common diagnostic tool for
assessing diastolic function. Indices of transmitral and
pulmonary venous Doppler flows are commonly used to
identify patterns of diastolic dysfunction.11
Mitral valve inflow
Figure 49-2 Sixteen-segment model of the left ventricle.
According to guidelines of the American Society of
Echocardiography and the Society of Cardiac Anesthesia,
the left ventricle is divided into 16 segments (6 basal, 6 mid
ventricular, and four apical segments) for evaluation of wall
motion and calculation of the wall motion score. (From
Shanewise et al.12 With permission.)
When sinus rhythm is present, PW Doppler at the level of the
mitral valve (MV) leaflets records two velocities separated by
a period of diastasis (no flow), as shown in Fig. 49-3. After
the MV opens, early rapid (E wave) diastolic filling of the
LV occurs, followed by a period of diastasis, after which late
filling occurs due to atrial contraction (A wave). Normally,
in individuals less than 60 years old, the peak E:A wave
velocity ratio is greater than 1. When there is impaired
relaxation without elevated filling pressures, the peak E
decreases, hence the E:A ratio becomes less than 1. In contrast, a “restrictive” filling pattern is seen when both
impaired relaxation and elevated filling pressures are present, resulting in a smaller contribution of atrial contraction
and an increased E:A ratio ( 1.5 to 2).
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LA pressure seen after MV opening. The fourth velocity is
the atrial flow reversal velocity (PVa) that is related to LA
contraction. A pulmonary vein systolic velocity peak less
than the diastolic velocity peak is suggestive of elevated LA
pressures. Restrictive filling indicative of very high filling
pressures is seen when PVS2 is much less than PVD. When
higher filling pressures are present, both the duration and
peak velocity of PVa are increased. Another sign of elevated
LA pressure is when the duration of PVa is longer than the
duration of the mitral inflow A wave (by 0.03 s).
Figure 49-3 Pulsed-wave (PW) Doppler of the mitral valve
inflow. This figure shows a normal pattern of blood flow
through the mitral valve in diastole. The two peaks indicate
early (E wave) and late (A wave) diastolic filling separated
by a brief period of diastasis (no flow). In individuals less
than 65 years old, a normal E:A ratio is 2:1. Deceleration
time is the time interval from peak E velocity to baseline.
Pulmonary vein flow
Four velocities are seen in PW Doppler of the pulmonary
veins (Fig. 49-4). Occurring in early systole, the first systolic forward flow velocity (PVS1) is due to the relaxation
of the LA, which promotes pulmonary venous flow into
the LA. In mid- to late systole, a second systolic forward
flow (PVS2) occurs that is produced by the increase in
pulmonary venous pressure occurring after right ventricular (RV) systole. In diastole, a third pulmonary vein
velocity is seen (PVD). This is related to the decrease in
RIGHT VENTRICULAR FUNCTION
AND FILLING PRESSURES
Qualitative evaluation of RV wall thickening and motion is
done visually, as in the evaluation of LV function, although
it is more difficult to estimate RV function. Normal RV
size is less than two-thirds of LV size (see Fig. 49-1). Septal
wall flattening (resulting in a D-shaped LV in the shortaxis view) or septal deviation into the LV can be see in both
pressure- and volume-overload conditions of the RV.12
When tricuspid regurgitation is present, the RV systolic
pressure (RVSP) can be estimated (see also “Pulmonary
Hypertension,” below), although TTE is preferred to
TEE for measuring RVSP because of better alignment
of the transducer beam with the direction of the regurgitant jet.
Examination of the size and respiratory changes of the
venae cavae and hepatic veins can give helpful clues to
the patient’s volume status and is also used in the evaluation of pericardial disease. Although TTE is preferred for
examination of respirophasic collapse of the inferior vena
Figure 49-4 Pulsed-wave (PW) Doppler of the pulmonary vein. This figure shows a normal pattern of blood flow through the pulmonary veins with four velocities seen (PVS1,
PVS2, PVD, PVa). Duration of peak reverse flow velocity during atrial contraction (PVa dur)
is also measured. (From Oh et al.11 With permission.)
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cava, TEE provides better visualization of the superior
vena cava. Dilatation of the superior vena cava (greater
than one-half the aortic dimension in the short-axis
view) is suggestive of hypervolemia.14
VALVULAR DISEASE
MITRAL VALVE
Mitral valve morphology
Normal MV function depends on the normal function
of all its component parts, including the mitral leaflets,
annulus, chordae tendineae, papillary muscles, and LV.
The rectangular posterior leaflet is composed of three
scallops (P1, P2, P3), while the semicircular anterior
leaflet is divided into thirds for descriptive purposes
(Fig. 49-5). Normal MV area is 4 to 6 cm2.
Mitral stenosis
Rheumatic heart disease is the most common cause of
mitral stenotic lesions (Fig. 49-6), with leaflet thickening
and fusion of the commissures (characteristic fish-mouth
valve in the short-axis view and hockey-stick appearance
in the long-axis view).
Two-dimensional (2D) echo is the “gold standard” for
evaluating mitral stenosis (MS) and allows assessment of
the structure and function of the mitral annulus, leaflets,
chordae, papillary muscles, LV size and function, LA size,
and pulmonary hypertension (RVSP). The Wilkins echo
score15 for rheumatic MS is based on four variables (leaflet
mobility, leaflet thickening, subvalvular thickening, and
calcifications). Each variable receives a score of 1 to 4 and
the individual scores are summed up. A total score equal
to or greater than 8 is associated with better outcomes for
mitral balloon valvuloplasty. For valves with less favorable
scores ( 8), cardiac surgery with valve replacement may
be the preferred treatment modality.
Mitral valve area
Calculation of MV area is usually obtained using the
pressure half-time (PHT) method. PHT is the time (milliseconds) for the maximal pressure gradient to decrease
by half and is usually equal to the deceleration time multiplied by 0.29.
MV area (cm2) 220 / PHT (ms)
The PHT method has several important shortcomings.
It is affected by concomitant aortic regurgitation or
decreased LV compliance.4 The rapid increase in LV diastolic pressure associated with either of these conditions
may shorten the PHT and underestimate the extent of
stenosis. Other techniques to estimate valve area include
planimetry and the continuity equation.1,4 The latter
approach is also less reliable in the presence of significant
aortic and mitral regurgitation. Details of this approach
are outlined in the references 1 through 11.
Mitral valve pressure gradients
As the degree of obstruction to blood flow caused by a
stenotic valve increases, the velocity of the blood flow also
increases in order to maintain constant flow (conservation of mass or flow). Velocities can then be transformed
into pressures with the simplified Bernoulli equation:
ΔP 4V2
Where P MV pressure gradient (mmHg) and V velocity of blood flow across the MV (ms).
Figure 49-5 Mitral valve structure. The mitral valve consists of two leaflets, the anterior and posterior leaflets,
which are separated at the annulus by the posteromedial
and anterolateral commissures. The posterior leaflet is rectangular and composed of three scallops (P1, P2, P3). The
anterior leaflet is semicircular and is divided into three segments for descriptive purposes (A1, A2, A3). (From
Shanewise et al.12 With permission.)
Severity of mitral stenosis
The mean MV pressure gradient and MV area are used
to estimate the severity of mitral stenosis and the need
for intervention (Table 49-2).
Mitral regurgitation
There are three basic mechanisms of mitral regurgitation
(MR): primary abnormalities of the mitral leaflets, commissures, or annulus; malfunctioning of the subvalvular
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A
B
Figure 49-6 Rheumatic mitral stenosis. A. Transesophageal transgastric
long-axis view of the left ventricle, the anterolateral papillary muscle
(ALPM), the posteromedial papillary muscle (PMPM), mitral valve (MV)
leaflets, and left atrium (LA). Note the thickened and partially calcified
subvalvular and valvular structures (short arrow). The patient had severe
three-vessel coronary artery disease in addition to rheumatic aortic stenosis and atrial fibrillation and underwent successful mitral and aortic valve
replacements and coronary artery bypass grafting. B. Continuous-wave
(CW) Doppler of the mitral valve intraoperatively. MR mitral regurgitation; MS mitral stenosis.
structures (chordae tendineae and papillary muscles); and
alterations in LV and LA dimensions and function.
The most common cause of isolated severe MR is
myxomatous degeneration (Fig. 49-7). The valve itself
can also be deformed from rheumatic fever, mitral annular calcification, infective endocarditis, and congenital
lesions (cleft MV). Other less common causes of leaflet
abnormalities include endomyocardial fibrosis, carcinoid
Table 49-2
Severity
None
Mild
Moderate
Severe
aAssumes
Severity of mitral stenosis
Mitral valve area
(cm2)
Mean gradienta
(mmHg)
4–6
1.6–2.0
1.1–1.5
1
—
5
5–10
10
normal cardiac output.
Source: ACC/AHA Guidelines for the Management of Patients with
Valvular Heart Disease.9 With permission.
disease, drugs (e.g., fenfluramine hydrochloride and
phentermine, or Fen-Phen), radiation therapy, trauma,
and collagen vascular disease.
Abnormalities in the subvalvular structures include
dysfunctional and/or ruptured chordae tendineae and
papillary muscles. Ruptured chordae tendineae account
for a large proportion of MR lesions. Etiologies include
idiopathic causes, MV prolapse, infective endocarditis,
and thoracic trauma. Papillary muscle dysfunction (with
or without frank rupture) is most often seen in the setting of myocardial ischemia or infarction. The posteromedial head of the papillary muscle is most vulnerable to
ischemia because of its end-artery vascular supply. Other
causes of dysfunction include dilated cardiomyopathy,
myocarditis, hypertension, and chest trauma.
Global or regional LV enlargement may dilate the
mitral annulus and change the position and axis of contraction of the papillary muscles, leading to dysfunction.
Progressive LA and LV enlargement associated with
chronic MR further exacerbate the extent of MR because
of continued changes in chamber geometry.
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degree preoperatively, particularly for ischemic MR,
because of different hemodynamic and ischemic conditions (e.g., lower blood pressure or relief of ischemia will
reduce the amount of regurgitation).17
Severity of mitral regurgitation
Echo findings in severe MR4,16 include:
A
●
●
●
●
●
●
●
●
●
B
Figure 49-7 Myxomatous mitral valve prolapse and mitral
regurgitation. A. Transthoracic parasternal long-axis view
of the mitral valve with a greater than 2-mm prolapse of the
posterior leaflet (MVP) beyond the plane of the annulus.
B. Apical four-chamber view shows biatrial enlargement.
C. Color-flow Doppler shows severe mitral regurgitation
(MR) with an eccentric jet that is “wall hugging” and anteriorly directed (opposite the side of leaflet prolapse).
Two-dimensional echocardiography
Unlike the case in MS, where echo is the accepted gold
standard for diagnosis, there is no gold standard for the
assessment of MR; therefore multiple parameters are
used in estimating the severity of MR.16 The purpose of
echo in MR is to determine the etiology, mechanism,
and severity of regurgitation; determine the need for
surgery and the type of surgery that is necessary; and
evaluate other valves, RV and LV function, and the presence of pulmonary hypertension. The most important
aspect is to determine the hemodynamic significance of
the regurgitation based on LV size (particularly end-systolic dimension), LV systolic function (EF), and the
presence and degree of LA enlargement and pulmonary
hypertension (RVSP). Regurgitant jet size and area may
contribute to the assessment of MR but often correlate
poorly with MR severity.16 The degree of MR intraoperatively may appear less or more severe compared to the
●
Large regurgitant jet: 40 percent of LA area.
Wide vena contracta (the narrowest part of the regurgitant color jet at its origin): 7 mm.
Eccentric wall-impinging regurgitant jet (Fig. 49-7B).
Dilated LV: end-systolic dimension 45 mm or enddiastolic dimension 70 mm.
LV EF 55 to 60 percent.
Dilated LA ( 5.5 cm), although the LA may not be
dilated in acute MR.
Pulmonary hypertension: resting RVSP 50 mmHg.
Restrictive mitral filling pattern: high peak early transmitral velocity (E wave) 1.5 ms.
Pulmonary vein systolic flow reversal: A normal pulmonary vein Doppler pattern has a systolic (S) wave
larger than the diastolic (D) wave. As the MR progresses, the S wave decreases until it may become
reversed. While a reduced S wave is a nonspecific finding,18 the presence of a reversed S wave has high specificity for significant MR. The absence of a reversed S
wave does not exclude significant MR.
Effective orifice area (ERO) 0.4 cm2.
Table 49-3 summarizes the important echo features of
MV stenosis and regurgitation.
Mitral valve prolapse
Mitral valve prolapse (MVP) is the most common cause
of MR in patients undergoing cardiac surgery in the
United States.19 MVP is the systolic billowing or displacement of at least 2 mm of either mitral leaflet into
Table 49-3
Echocardiographic assessment of the
mitral valve
Morphology
Mitral annulus, leaflets, chordae, papillary
muscles, LV size and function,
LA size, pulmonary hypertension (RVSP)
Stenosis
Often rheumatic
Echo score: leaflet mobility, thickening,
subvalvular thickening, calcifications,
8 favors valvuloplasty
Severe MS: area 1 cm2 or mean gradient
10 mmHg
Regurgitation Regurgitant jet size does not correlate well
with severity
Severe MR: dilated LV (ESD 45 mm), ↓ LV
systolic function (EF 55–60%), dilated LA,
pulmonary hypertension (RVSP 50)
LV left ventricle; RVSP right ventricular systolic pressure;
MS mitral stenosis; MR mitral regurgitation; ESD endsystolic dimension; LA left atrium; EF ejection fraction.
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Chapter 49 ● Echocardiography in Cardiac Surgery
the LA beyond the plane of the mitral annulus in the
parasternal or apical long-axis views (see Fig. 49-7).
Recent criteria for echo diagnosis of MVP20 have
become more stringent, leading to increased specificity
of the criteria for MVP while at the same time preserving
sensitivity for the detection of MVP complications.
Classic MVP is defined as equal to or greater than 5 mm
of leaflet thickening (myxomatous changes) of the prolapsing leaflet, while nonclassic prolapse is leaflet thickening less than 5 mm. Compared to nonclassic MVP,
classic MVP has a worse prognosis, with most complications of MVP (significant MR and congestive heart failure, MV surgery, infectious endocarditis) arising in
patients with classic MVP.19 Asymmetrical prolapse of
the leaflets is associated with progression to more significant disease (flail leaflet and severe MR).
Determining which segment of the mitral leaflet tissue
is prolapsing is essential for proper MV repair. MR associated with MVP often has an eccentric jet directed
opposite to the prolapsing leaflet (e.g., anteriorly
directed jet if posterior leaflet prolapse is present). In
contrast, in MR associated with rheumatic mitral stenosis, the regurgitant jet is directed toward the affected
leaflet due to restricted leaflet motion (e.g., anteriorly
directed jet if the anterior leaflet is calcified). MR associated with MVP may be due to flail leaflet or chordal rupture resulting from myxomatous involvement of the
chordae or leaflet. Chordal rupture is diagnosed when
the chords are seen as mobile echodensities attached to a
flail or partially flail leaflet (Fig. 49-8).21 These may be
confused with or may be difficult to distinguish from
vegetations of infective endocarditis. Mitral annulus calcification (MAC) may also be seen in patients who have
MVP.
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Figure 49-9 Flail mitral leaflet with severe mitral regurgitation. Intraoperative transesophageal echocardiogram with
color-flow Doppler consistent with severe mitral regurgitation. This patient underwent successful mitral valve repair
with posterior leaflet quadrangular resection and an annuloplasty band.
Flail leaflet
Flail leaflet encompasses a spectrum of disease severity
from partially to completely flail leaflets, resulting in
excessive motion of the mitral leaflets and various degrees
of MR (Fig. 49-9). Flail mitral leaflet is diagnosed when
the leaflet tip is “upturned” toward the LA during MV
closure (due to loss of coaptation). Most commonly, it is
caused by MVP or endocarditis resulting in chordal rupture, but it may also be caused by ischemia or infarction
of the papillary muscle (usually affecting the posteromedial
papillary muscle). A partially flail leaflet (due to chordal
rupture) is usually associated with moderate to severe MR,
while a completely flail mitral leaflet is almost always associated with severe MR necessitating surgery.21
Ruptured papillary muscle
Dysfunction of the papillary muscle results in severe MR
and is most often due to acute myocardial infarction.
Papillary muscle dysfunction should be differentiated
from acute chordal rupture. Papillary muscle rupture is
diagnosed in the appropriate clinical context when a triangular mass (the head of the papillary muscle), seen
attached to the flail leaflet, prolapses into the LA during
systole, accompanied by severe MR.17
Figure 49-8 Ruptured chord attached to a flail segment of
the posterior mitral leaflet due to myxomatous disease.
Intraoperative transesophageal echocardiogram showing
the ruptured chord as an echodense linear filament
attached to the flail leaflet, prolapsing into the left atrium
during systole.
Leaflet perforation
This is most commonly caused by valvular endocarditis,
while less common etiologies include congenital (cleft
MV) or iatrogenic causes. With leaflet perforation, the
regurgitant jet is often eccentric and originates at the site
of perforation.
Mitral valve repair
TEE is essential in determining the suitability of a valve
for repair. It can assess the mechanism and severity of
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Figure 49-10 Posterior leaflet prolapse and dilated mitral annulus. Note the
anteriorly directed eccentric jet of mitral regurgitation seen on transesophageal
echocardiography. Following the repair (posterior leaflet quadrangular resection
and annuloplasty ring), the patient had good ventricular function and no residual
mitral regurgitation.
MR, identify the affected leaflets, determine the presence
of coexisting valvular lesions, and estimate RV and LV
function. The prognosis of MV repair differs based on
the mechanism of MR (organic/primary vs. functional/secondary) and is strongly influenced by the preoperative EF. The most common indication for MV
repair is myxomatous disease. Determining which leaflet
or segment is involved is important in deciding on the
suitability of the repair, the likelihood of successful repair
(better with posterior leaflet prolapse), and the method
of repair. This is done by analyzing the motion of the
leaflets and the direction of the regurgitant jet.
TEE is also helpful intraoperatively to assess the success of the repair. Immediately postrepair (Fig. 49-10),
the competency of the valve can be assessed for residual
MR (1
, mild; 2
, moderate; 3
, moderate to severe;
4
, severe). Phenylephrine and volume may be administered in order to assess the effect of increased afterload
and preload on the degree of residual MR. If there is MR
postrepair equal to or greater than 2
, further surgery is
indicated. Repeat imaging is also done after the patient is
off cardiopulmonary bypass. Other findings that may be
detected on TEE include residual mitral stenosis, global
or regional LV systolic dysfunction, suture dehiscence or
leaflet perforation, and MV systolic anterior motion
(SAM) with outflow obstruction. Limitations to intraoperative TEE include the effect of changing hemodynamics, which may significantly affect the appearance and
severity of valvular lesions, since the evaluation depends
on preload and afterload conditions as well as ventricular
function. Hence, it is important that loading conditions
be similar in comparing the severity of MR.
AORTIC VALVE
Aortic valve morphology
Normally, the aortic valve (AV) is composed of three semilunar leaflets (cusps) that open and close passively due to
pressure differences between the LV and the aorta. Small
strands may be seen on the cusps (Lambl’s excrescences),
particularly on TEE, and represent a normal variant.
Bicuspid and rarely unicuspid or quadricuspid valves may
be seen on echo (Fig. 49-11). The normal valve area is
3 to 4 cm2 with a 2-cm leaflet separation during systole.
A bicuspid AV is the most common congenital heart
defect and occurs in about 1 to 2 percent of the U.S. population. The morphologic features of a bicuspid AV are
somewhat variable. In some patients, there are two equalsized cusps with a single central commissure. In many others, the cusps may be unequal in size with an eccentric
commissure, with the larger of the two cusps containing
a raphe.1,22 In the parasternal long-axis views, bicuspid
valves are characterized by systolic doming. In the shortaxis views, the hallmark is an elliptical “football”-shaped
systolic orifice. The valve leaflets themselves may be thickened and fibrotic, particularly with increasing patient age.
A bicuspid valve may be functionally normal with no significant stenosis or regurgitation, particularly in adolescents
and young adults, among whom up to one-third have no
significant valvular dysfunction.23 However, over time,
progressive “wear and tear” with resulting fibrosis and
valve calcification leads to functional abnormalities. By the
age of 60 years, over 50 percent of bicuspid valves are significantly stenotic. Valve regurgitation is frequently present
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Figure 49-11 Bicuspid, tricuspid, and quadricuspid aortic valves. The normal
aortic valve is trileaflet (central panel). Bicuspid valve is the most common congenital anomaly of the aortic valve (left panel), with quadricuspid (right panel)
aortic valves being much less common.
as well and may be the predominant functional abnormality in younger patients. Etiology of the regurgitation may
be retraction and fibrosis of the commissures or leaflets,
cusp prolapse, dilatation of the aortic root or valve annulus, or damage from infective endocarditis.
It is important to recognize that bicuspid AVs are
often associated with abnormalities of the aorta.
Concomitant aortic coarctation occurs in a minority.
Aortic dissection is another known association, with 5 to
9 percent of patients with dissecting aortic aneurysms
having bicuspid valves. Aortic root dilatation may be due
to a common developmental defect that affects both the
aorta and the valve.24 Poststenotic dilatation of the
ascending aorta can also occur.
Aortic valve area
In aortic stenotic lesions, the AV area decreases by approximately 0.1 cm2 per year, although large variations from
patient to patient exist.25 The AV area is usually determined
using the continuity equation. Direct planimetry (visualization of the orifice area) is less reliable for patients with heavily calcified valves (due to shadowing of the valve) and for
critical (“pinhole”) stenoses.22 The continuity equation is
based on the principle of conservation of flow (or mass),
whereby flow before the valve must equal flow across the
valve. Since the area of the LV outflow tract (LVOT) can be
directly measured, as can velocities in the LVOT and across
the valve, the AV area can then be calculated:
A1V1 A2V2
Aortic stenosis
Rheumatic aortic stenosis (AS) (Fig. 49-12A) is usually
associated with MV disease. Calcium deposits are present
on both sides of the aortic cusps, resulting in commissural
fusion and aortic regurgitation. Degenerative calcific disease is the most common cause of AS in the United States.
It is often associated with MAC and coronary artery disease. Nodular calcification is often present on the aortic
aspect of the valve along the bases of the cusps and may
protrude into the sinuses of Valsalva (Fig. 49-12B and C).
In contrast to rheumatic AS, there is no commissural fusion
in degenerative AS, hence aortic regurgitation is rare.
Two-dimensional echocardiography
A thorough echo evaluation includes assessing the thickness and calcification of the leaflets, their mobility, looking for the etiology of stenosis (e.g., bicuspid, rheumatic,
degenerative calcific) and its extent, the presence of
other valvular lesions, and assessing LV size and function. TTE is often superior to TEE in assessing the severity of AS because obtaining maximal velocity jets (i.e.,
absolutely parallel to flow) is often difficult with TEE.
Where A area or r2; V velocity; A1V1 flow proximal to the valve (LVOT); A2V2 flow across the valve.
The major limitation to the continuity equation is
that small errors in the LVOT diameter become magnified in estimating the AV area (since the radius is squared
in the equation). As a general rule, one may assume that
the LVOT diameter is 2 cm (r1 1 cm) with generally
good estimates of the AV area. Another limitation is in
obtaining the maximal aortic jet velocity, which requires
that the echocardiographic Doppler beam be exactly parallel to the direction of blood flow.
Aortic valve pressure gradients
Like pressure gradients obtained for mitral stenosis, the
simplified Bernoulli equation is used for estimating AV
pressure gradients:
P 4V2
Where P AV pressure gradient (mmHg) and V velocity of blood flow across the AV (ms).
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A
B
C
D
Figure 49-12 Rheumatic and calcific aortic stenosis. A. Rheumatic aortic stenosis with
calcium deposits in the commissures resulting in commissural fusion. B and D. Short and
long-axis views: Calcific aortic stenosis, with calcium deposits on the aortic aspect of the
valve on the bases of the cusps and no commissural fusion. C. Continuous-wave (CW)
Doppler of the aortic valve (shown in B and C) is consistent with severe aortic stenosis
(aortic velocity 4 ms, mean gradient 50 mmHg). RA right atrium; LA left atrium;
AV aortic valve; LAA left atrial appendage; IAS interatrial septum; Ao aorta;
PG peak gradient; MG mean gradient.
AV pressure gradients may be significantly underestimated because of inadequate envelopes (because the
Doppler beam is not parallel to the blood flow) or an
inadequate number of measurements from different
locations. Maximal velocities may be present or obtainable from only certain locations in an individual patient.
Hence complete assessment from all locations is needed.
In addition, the velocity of flow is highly dependent on
overall LV function. Pressure gradients may significantly
underestimate the severity of AS in the presence of severe
LV dysfunction (“low-gradient AS”). The opposite is
also true, whereby increased flow velocity across the
valve is seen in situations of increased cardiac output
(i.e., anemia, aortic regurgitation, hyperthyroidism) and
may not reflect true aortic stenosis. In such situations,
valve area calculations may be more accurate, and correlation with valve morphology and visual assessment of
leaflet mobility is important.
Severity of aortic stenosis
The mean AV pressure gradient and the AV area are used
to estimate severity of AS and the need for surgical intervention (Table 49-4). If there is a significant discrepancy
between the pre- and intraoperative grading of the severity of AS, the following should be considered:
1. Change in hemodynamic conditions: changes in
heart rate or rhythm, contractility, and hemodynamics influence the gradients across the AV. The AV area
is usually less affected by loading conditions.
2. Measurement variability in data recording: measurement errors in the LVOT diameter greatly influence
the AV area, since the LVOT radius is squared in the
continuity equation.
Table 49-4
Severity of aortic stenosis
Severity
Velocity
(ms)
Area
(cm2)
Mean gradienta
(mmHg)
None
Mild
Moderate
Severe
1
2.5–2.9
3–4
4
3–4
1.5
1–1.5
1
—
25
25–50
50
aAssumes
normal cardiac output.
Source: ACC/AHA Guidelines for the Management of Patients with
Valvular Heart Disease.9 With permission.
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Chapter 49 ● Echocardiography in Cardiac Surgery
Aortic regurgitation
Echo assessment of aortic regurgitation (AR) includes a
comprehensive examination of AV morphology, aortic
root dilatation, and LV size and function.16 TTE is generally the initial diagnostic test used for evaluating the
severity of AR. However, TEE is also helpful particularly
for patients with poor transthoracic windows, if prosthetic valves are present, and intraoperatively to guide
surgical repair. TEE is particularly useful for determining
the mechanism of regurgitation by distinguishing
valvular from nonvalvular causes of AR. Common etiologies for AR include congenital malformations (bicuspid valves); degenerative calcific, rheumatic, and infective
endocarditis; aortic aneurysm (Fig. 49-13) or dissection,
Marfan’s syndrome, drug-induced (e.g., Fen-Phen) AR,
and prosthetic valve dysfunction.9 Acute and chronic AR
differ in both pathophysiology and echo findings. Many
of the echo findings in chronic AR (e.g., LV dilatation
and systolic dysfunction) may not be present in acute
AR. Chronic AR is a state of both pressure and volume
overload of the LV, resulting in LV hypertrophy and
dilatation.
Two-dimensional echocardiography
This is helpful for evaluating LV size and function, AV
structure and leaflet mobility, aortic root dilatation, aortic
955
dissection, associated vegetations, diastolic fluttering
motion of MV leaflets, and premature MV closure (indicative of significant AR).
Severity of aortic regurgitation
In assessing the severity of chronic AR, it is essential to
combine data on LV size and function with Doppler data
and not to rely solely on color Doppler, since it is often
misleading. No study has yet demonstrated that quantification of the severity of AR by Doppler criteria alone is
predictive of outcome. Instead, LV size and function are
used for risk stratification of asymptomatic patients with
chronic AR. Echo findings in severe AR include:
●
●
●
●
●
●
●
Dilated LV: minor-axis dimension 50 to 55 mm in
systole or 70 to 75 mm in diastole
LV ejection fraction 55 percent
Pressure half-time 200 ms
Proximal regurgitant color jet width/LVOT diameter
65 percent
Vena contracta 6 mm
Holodiastolic flow reversal in the descending thoracic
aorta
Restrictive filling pattern to the MV inflow
In comparison to men, women with AR should be considered for surgery before severe symptoms have developed
Figure 49-13 Aortic aneurysm of the sinuses of Valsalva and secondary aortic regurgitation. The aortic wall is thin at the sinuses of Valsalva and aneurysmal dilatation results in
aortic regurgitation. Note the wide base of the regurgitant jet (vena contracta) consistent
with severe aortic regurgitation (arrow). SoV sinuses of Valsalva; LV left ventricle;
Ao aorta; LA left atrium; AR aortic regurgitation.
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Table 49-5
Morphology
Stenosis
Regurgitation
Echocardiographic assessment of the
aortic valve
Three semilunar leaflets/cusps, LV size and
function
Often degenerative/calcific
Severe AS: area 1 cm2 or mean gradient
50 mmHg
Regurgitant jet size does not correlate well
with severity
Severe AR: dilated LV (ESD 50–55 mm),
LVH, ↓ LV systolic function (EF 55%)
Acute AR: LV dilatation/systolic dysfunction
may be absent
LV left ventricle; AS aortic stenosis; AR aortic regurgitation;
ESD end-systolic dimension; LVH left ventricular hypertrophy;
EF ejection fraction.
and for smaller LV dimensions. In a recent study, intraoperative mortality was similar for men and women, but
10-year survival was significantly worse for women than
for men (39 vs. 72 percent, respectively).26
In acute AR, many of the features of chronic volume
overload will not be present. The severity will be need to
be assessed by evaluation of color-flow Doppler jet
width, presence of significant pulmonary hypertension,
and evidence by Doppler of rapid equilibration of aortic
and LV diastolic pressure (short diastolic half-time
200 ms, short mitral deceleration time 150 ms, or
premature closure of the MV). Echo assessment of the
AV is summarized in Table 49-5.
mality of the TV. Mild TR is a normal finding in 70 percent of individuals.16 Pathologic TR is often secondary
to RV dysfunction, RV dilatation, or significant systolic
pulmonary hypertension (systolic pulmonary artery pressures 55 mmHg). Primary causes of TR are less common (Ebstein’s anomaly, endocarditis, trauma, anorectic
drugs, carcinoid, myxomatous or rheumatic valvular disease, radiation). Patients with severe TR of any cause
have poor long-term outcomes because of RV dysfunction and/or systemic venous congestion. TV reconstruction, annuloplasty, or valve replacement is indicated in
some cases of severe TR.
TEE is useful intraoperatively to assess the need for
TV surgery when TR is secondary to annular dilatation
and/or elevated pulmonary artery pressures, particularly during MV surgery. After correction of MV disease, TV surgery may be required if persistent severe
TR or annular dilatation ( 30 mm) is still present
(Fig. 49-14).27
Severity of tricuspid regurgitation
Echo findings in severe TR include16:
●
●
●
●
●
●
A large regurgitant (color) jet ( 10 cm2), vena contracta 7 mm, or eccentric jet
Annular dilatation ( 30 mm), leaflet coaptation,
anatomic clues (e.g., vegetations, myxomatous disease)
Dilated right atrial (RA)
Dilated RV and paradoxical interventricular septal wall
motion
Pulmonary hypertension
Dilated venae cavae and hepatic veins with minimal
respiratory flow variation and systolic flow reversal
TRICUSPID VALVE
Tricuspid valve morphology
Normal function of the TV depends on the normal function of its components: annulus, leaflets, chordae, papillary muscles, right atrium, and ventricle.
Tricuspid stenosis
The most common cause of tricuspid stenosis (TS) is
rheumatic, which results in both stenosis and regurgitation of the TV and is often associated with concomitant
mitral or AV disease. Echo assessment of TS is similar to
that of MS. The mean gradient across the TV is normally
2 mmHg. Tricuspid stenosis is considered severe when
the mean gradient is 7 mmHg and the pressure halftime (PHT) is 190 ms.
Tricuspid regurgitation
As in the case of the AV and MV, TTE or TEE evaluation
of tricuspid regurgitation (TR) focuses on the identification of the etiology or mechanism of TR as well as its
hemodynamic severity. TR is the most common abnor-
Pulmonary hypertension
In the absence of pulmonary stenosis, pulmonary artery
systolic pressure is equal to RV systolic pressure (RVSP).
RVSP is estimated using the simplified Bernoulli equation (P 4V2) from the peak TR velocity (V). P is
then the pressure gradient across the TV, or the pressure
difference between the RA and RV (P PRV PRA). In
the absence of elevated RA pressures, the right atrial
pressure (PRA) is estimated at 10 mmHg. Therefore,
RVSP PRA P 10 4V2
Where RVSP RV systolic pressure and V peak TR
velocity (ms).
Severity of pulmonary hypertension
Normal pulmonary artery systolic values are 18 to 25
mmHg with a mean of 12 to 16 mmHg.2 Pulmonary
hypertension is defined as systolic pulmonary artery pressure greater than 30 mmHg or mean pulmonary artery
pressure less than 20 mmHg at rest.2 Commonly used
values using RVSP to estimate the severity of pulmonary
hypertension are shown in Table 49-6.
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Figure 49-14 Tricuspid valve annuloplasty. This patient had infective endocarditis resulting in flail posterior mitral valve leaflet and tricuspid regurgitation. He underwent mitral
valve repair and tricuspid valve annuloplasty. Note the dilated atria and tricuspid annulus
preprocedure and the pacer spikes on the rhythm strip postprocedure. RA right atrium;
TR tricuspid regurgitation; RV right ventricle.
PROSTHETIC VALVES
Any evaluation of prosthetic valve function should
include an assessment of transvalvular pressure gradients and valve area, similar to the evaluation of native
valve function. TTE is helpful in the initial assessment of
prosthetic valve dysfunction. However, its sensitivity is
impaired by difficulty in visualizing structures around
and behind the prosthesis, particularly for mechanical
valves. Prosthetic material attenuates the ultrasound
beam and causes multiple reverberations, hampering
interpretation. TEE is often required for the complete
evaluation of prosthetic valve structure and function.
Cinefluoroscopy may also be a relatively quick and useful method for determining leaflet mobility in mechanical
valves and is indicated when mechanical valve thrombosis
is suspected. When valve dysfunction is suspected, 2D
echo with Doppler and color flow in addition to TEE
may be necessary for a comprehensive evaluation of
Table 49-6
Severity of pulmonary hypertension
RVSP (mmHg)
Normal
Mild
Moderate
Severe
18–25
30–40
40–70
70
RVSP right ventricular systolic pressure.
valve function. Such an evaluation of valve function is
summarized in Table 49-7.28 TEE findings in common
complications of prosthetic valves are shown in Table
49-8.28
Prosthetic valve pressure gradients
Like native valve gradients, prosthetic valve pressure
gradients can be obtained using the simplified Bernoulli
Table 49-7
Evaluation of prosthetic valves
Pressure gradients
Valve area
Regurgitation/leaks
Leaflet mobility/
restriction
LV size/function
Pulmonary
hypertension
Compare with
prior echo
P 4V2
MV prostheses: area 220/PHT
AV or MV prostheses: A1V1 A2V2
Size, symmetry, velocity, eccentricity
Degree of leaflet excursion
LV dimensions, EF
RVSP 4V2 10
Change in gradients, area, leaks
P pressure gradient; V velocity; MV mitral valve; PHT pressure half-time; AV aortic valve; A1V1 flow (area1 velocity1) proximal to the valve prosthesis; A2V2 flow (area2 velocity2) across the valve prosthesis; LV left ventricle; EF ejection
fraction; RVSP right ventricular systolic pressure.
Source: From Zabalgoitia.28 With permission.
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Table 49-8
TEE Findings in prosthetic valve
complications
Paravalvular leak
Pannus formation
Structural
deterioration
Large, wide, eccentric jet with
high-velocity turbulent flow
Dehiscence, regurgitation, stenosis
Calcific degeneration (bioprostheses)
Often due to inappropriate sizing,
stenosis, or regurgitation
Decreased range of motion or
maximum excursion
Stenosis ( regurgitation)
Distinguish from fibrin strands, which
are small filaments on the atrial
aspect of mitral or ventricular
aspect of aortic valves
Stenosis
Irregular echogenic mobile mass
or masses on valve
Regurgitation ( stenosis)
Leaflet destruction (bioprostheses)
Perivalvular abscess (valve rocking,
periaortic root thickening,
echolucency)
Perivalvular dehiscence, fistular tract
Nonstructural
dysfunction
Thrombosis
Source: From Zabalgoitia.28 With permission.
equation (P 4V2). Compared to normal native
valves, homografts and the newer nonstented bioprostheses have similar velocities and pressure gradients,
while mechanical valves have higher flow velocities.
Prosthetic valves except ball-cage valves normally have
pressure gradients since they are by design obstructive,
with gradients increasing as valve size decreases. High
gradients are often seen with 19-mm AV prostheses.
High gradients in prosthetic valves may be seen for
other reasons as well, such as high cardiac output, valve
obstruction, or significant valvular regurgitation (due to
increased flow).
Prosthetic valve area
As in the case of native valves, prosthetic valve area can
be calculated using the continuity equation or pressure
half-time method. For AV prostheses, the continuity
equation (A1V1 A2V2) is usually used. The LV outflow
tract (LVOT) diameter or outer diameter of the sewing
ring (not its internal diameter) should be measured for
accurate estimation of A1. For MV prostheses, use of the
continuity equation is preferred, since the pressure halftime equation may overestimate the true prosthetic MV
area. The continuity equation should not be used if
there is significant aortic regurgitation or MR. The same
equations may be used for the calculation of prosthetic
TV areas.
Paravalvular leaks
Normal amounts of regurgitation are expected with
prosthetic valves owing to the built-in transvalvular
regurgitation (“closing volume”). The amount of
regurgitation increases with valve size, the size of the
gap between the occluder and the rim, and lower heart
rates. Echo findings4 of normal prosthetic valve regurgitation include:
1. AV: regurgitant area 1 cm2 and length of jet
1.5 cm
2. MV: regurgitant area 2 cm2 and length of jet
2.5 cm
3. Characteristic flow patterns (Medtronic-Hall, one
central jet; Star-Edwards, two curved side jets; BjorkShiley, two unequal side jets; St. Jude Medical, two
side jets and one central jet)
Larger leaks in other locations (Fig. 49-15) are abnormal
and may be associated with significant hemodynamic
compromise, hemolysis, or valve dehiscence.28 TEE is
often required to fully assess prosthetic valve regurgitation
because of the limited sensitivity of TTE. Echo characteristics that differentiate physiologic from nonphysiologic
regurgitation are summarized in Table 49-9.28
INFECTIVE ENDOCARDITIS
TEE is the procedure of choice for the detection of
vegetations in infective endocarditis, with better sensitivity (50 percent for TTE vs. 90 percent for TEE) and
specificity (95 percent for TTE vs. 95 percent for
TEE) for native valve endocarditis compared to
TTE.29,30 Characteristics of valvular vegetations are
listed in Table 49-10.29 However, early in the course of
infective endocarditis, vegetations may not have these
typical characteristics and TEE should be repeated if
the clinical suspicion is high. Compared with native
valve endocarditis, it is more difficult to identify vegetations on prosthetic valves because of artifact from the
prosthetic materials. Often both TTE and TEE are
useful to detect vegetations, although TTE has lower
sensitivity compared with TEE for prosthetic valve
endocarditis.8 TEE is particularly sensitive for identifying ring abscesses. Complications of infective endocarditis (Fig. 49-16) include:
1. Paravalvular abscesses
2. Valve destruction or perforation, leaflet rupture, or
dehiscence of prosthetic valves
3. Fistulas
4. Pseudoaneurysms
5. Emboli
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A
959
B
Figure 49-15 Paravalvular and valvular leaks. A. Bileaflet mechanical mitral prosthesis
with severe paravalvular regurgitation secondary to endocarditis and partial valve dehiscence, requiring valve replacement. B. Aortic bioprosthesis with severe aortic regurgitation
due to calcific degeneration and a torn leaflet. LA left atrium; LV left ventricle; MR mitral regurgitation; Ao aorta.
EVALUATION OF SPECIFIC DISORDERS
CORONARY ARTERY DISEASE
Myocardial ischemia/infarction
The echo manifestation of myocardial ischemia is a
decrease in contractility or systolic wall thickening of the
ischemic territory that is manifest within seconds of the
onset of ischemia, prior to evidence of electrocardiographic ischemia.4 Abnormal wall thickening is a better
indicator of ischemia than wall motion, since infarcted
myocardium may be passively pulled or tethered by adjacent normal myocardium, resulting in apparent wall
motion without active contraction. Ancillary signs of
ischemia include an increase in end-systolic LV volume
and a decrease in global contractility or EF.4 Hypokinesis
is decreased contractility (30 percent wall thickening);
akinesis is the absence of contractility (10 percent wall
Table 49-9
Physiologic and nonphysiologic valvular
regurgitation
Regurgitant Jet
Physiologic
Nonphysiologic
Size
Symmetrical
Velocity
Eccentric
Small, narrow
Yes
Low
No
Large, wide
No
High
Yes
Source: Modified from Zabalgoitia.28 With permission.
thickening); and dyskinesis is outward motion during
systole. Echo is accurate at localizing the site of coronary
obstruction (Fig. 49-17). However, it usually overestimates infarct size due to myocardial stunning, which has
resulted in a lack of correlation between wall motion
abnormalities detected on echo in the setting of an acute
myocardial infarction and infarct extent.31
Ischemic, infarcted, stunned, or
hibernating myocardium?
Myocardial segments may be dysfunctional secondary
to ischemia, infarction/scar, or stunned or hibernating
myocardium. Stunned myocardium is postischemic ventricular dysfunction that occurs when reperfusion of the
occluded artery has been achieved but the wall motion
and thickening of the corresponding myocardial segment
remain abnormal—a condition that may last for days to
weeks. Hibernating myocardium results from chronic
ischemic dysfunction when the myocardial tissue is chronically hypoperfused owing to inadequate blood flow,
resulting in abnormal wall motion and thickening, but it
usually recovers after successful revascularization. Resting
echo may help differentiate viable (stunned or hibernating) myocardium from nonviable (infarcted or scarred)
myocardium based on wall thickness. Thicker myocardium
is more likely to be viable, while thinned and fibrotic
myocardium most likely represents scar.4 The specificity of
these criteria is quite low, however. Viability assessment
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Table 49-10 Echocardiographic characteristics of vegetative and nonvegetative valvular masses
Characteristic
Vegetation
Nonvegetation
Echogenicity
Similar to myocardium
Low echogenicity/gray
Upstream surface of valve near the
regurgitant jet
Mobile, prolapses
Amorphous, lobulated
Wide base of attachment
Severe regurgitant jet
Vegetation located near jet
Paravalvular abscess/leak
Fistula
Valve dehiscence
Similar to pericardium
High echogenicity/white
Downstream surface of valve
Location
Motion
Shape
Regurgitation
Other
Less mobile
Filamentous, strand-like narrow base of
attachment
Mild or no regurgitant jet
None
Source: Modified from Schiller.29 With permission.
can be significantly improved with dobutamine or stress
echocardiography.8 A biphasic response on dobutamine
echo is the most sensitive parameter for viable myocardium
and is associated with improved survival after revascularization. This is evidenced by an improvement in wall
motion and thickening or recruitment at low-dose dobutamine (10 to 20 g/kg/min) followed by worsening
of wall motion and thickening at higher doses (30 to
40 g/kg/min) when the ischemic threshold is reached.
Left ventricular aneurysm and mural thrombus
A true ventricular aneurysm consists of a thin wall ( 7
mm) that is echogenic (and sometimes calcified) and has
A
B
C
D
Figure 49-16 Complications of infective endocarditis. A. Large vegetation on bioprosthetic tricuspid valve seen on transesophageal echocardiogram. B. Sinus of Valsalva
aneurysm and aortic–right ventricular fistula. C. Bicuspid aortic valve with bacterial endocarditis complicated by large aortic root (annular) abscess (note the thickened perivalvular
tissue) and complete heart block requiring emergent surgery. D. Large aortic valve vegetation prolapsing into the left ventricular outflow tract during systole. LA left atrium; TV tricuspid valve; RV right ventricle; SoV sinus of Valsalva; Ao aorta; AV aortic
valve; LV left ventricle.
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myocardial infarcts. Spontaneous echo contrast (SEC) or
mural thrombus may be present within an LV aneurysm
and is associated with an increased risk of embolic events.
The appearance of an acute mural thrombus (same
echogenicity as myocardium) generally differs from that
of a chronic thrombus, which tends to be layered with
areas of calcification.31 Compared to TTE, TEE may be
limited in detecting apical thrombi because of the often
suboptimal visualization of the true LV apex with TEE.
Pseudoaneurysms can also be complications of acute
myocardial infarction and are characterized by the lack of a
true myocardial wall. They result from contained free wall
myocardial rupture in which a portion of the pericardial
space limits frank rupture. Pseudoaneurysms can generally
be differentiated from true aneurysms by the presence of a
narrow neck (less than half of the maximum diameter)
compared to the wider base of a true aneurysm.31
Postinfarct ventricular septal defect
Figure 49-17 Common myocardial perfusion patterns by
each of the three major coronary arteries. LAD left anterior descending; Cx left circumflex; RCA right coronary artery. (From Shanewise et al.12 With permission.)
outward motion in both systole and diastole.31 Most
aneurysms occur apically, with inferobasal aneurysms
being the second most common. Aneurysms are complications of adverse remodeling following transmural
Life-threatening mechanical complications after acute
myocardial infarction include free wall rupture, papillary
muscle dysfunction/rupture, and ventricular septal defect
(VSD) (Fig. 49-18). TTE is usually sufficient for the
diagnosis of mechanical complications, although TEE
may be used as an adjunct. Postinfarct VSD is uncommon
(less than 1 percent of total infarcts), although it is associated with the worst outcome of mechanical complications
in patients with cardiogenic shock. Unlike postinfarct
papillary muscle rupture, VSD occurs with approximately
equal frequency after anterior and inferior infarcts. The posteroapical septum is the most common site of postinfarct
A
Figure 49-18 Postinfarct ventricular septal defect (VSD). This patient had suffered an
acute anterior myocardial infarction that was treated with thrombolytics but subsequently
developed a high septal VSD. A. Intraoperative transesophageal echocardiogram with
color-flow Doppler diagnostic of VSD with high-velocity turbulent flow across the septum.
B. Surgical repair with a pericardial patch and coronary artery bypass grafting to the ostial
left anterior descending artery was successful. Color-flow Doppler shows no flow across
the septum. LV left ventricle; RV right ventricle.
B
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PART II ● ADULT CARDIAC SURGERY
Table 49-11 Diagnostic tests for acute aortic dissection
Test
Sensitivity
(%)
Specificity
(%)
TEE
99–100
89
CT
90
85
MRI
98–100
100
Angiography
88–91
95
Pluses and minuses
Pluses: Quick, semi-invasive, assesses AR, coronaries, pericardial effusion,
may assess IH
Minuses: Limited assessment of IH, “blind spot” of distal ascending aorta
and anterior aortic arch, reverberation artifact
Pluses: Quick, noninvasive
Minuses: Cannot assess branch vessels or IH, dye load/allergy
Pluses: Noninvasive, assesses branch vessels, IH
Minuses: Slow, may not be available, pacemakers/device, breath-hold
necessary
Pluses: Assesses coronaries, AR, branch vessels
Minuses: Slow, invasive, dye load, may miss dissection if lumen is
completely thrombosed, does not detect IH
IH intramural hematoma; AR aortic regurgitation.
Sources: From Erbel et al.,32 Sabatine,33 and Nienaber et al.34 With permission.
VSD. Echo is the gold standard for diagnosing ventricular
septal rupture complicating myocardial infarction. TTE
using color-flow Doppler has a sensitivity of 85 to 95 percent, while TEE has a sensitivity and specificity of 100 percent.31 Echo characteristics of postinfarct VSD, in addition
to the septal defect, include the presence of a small pericardial effusion with possible intrapericardial thrombus
(echogenic mobile mass in the pericardial space) and echo
evidence of tamponade.31
THORACIC AORTIC ANEURYSM
AND DISSECTION
TTE may diagnose aortic dissection by detecting an intimal flap in the aorta (specificity 95 percent), but it has
low sensitivity (80 percent) for ascending aortic dissection and even lower sensitivity for distal thoracic aortic
dissection (70 percent).32 TEE is one of three imaging
modalities used for the diagnosis of acute aortic dissection—TEE, computed tomography (CT), and magnetic
resonance imaging (MRI)33,34—and for the diagnosis of
perioperative aortic dissections (Table 49-11). The
choice of imaging modality depends primarily on the
availability of the imaging procedure and patient characteristics (e.g., hemodynamic instability, presence of a
pacemaker, or contrast allergy), since the overall diagnostic accuracy for TEE, CT, and MRI is comparable.32
TEE is the imaging procedure of choice for patients who
are hemodynamically unstable. Compared to CT or
MRI, one limitation of TEE is that it cannot image the
aortic segment located between the distal ascending
aorta and the proximal arch, which may decrease its sensitivity for detection of aortic dissection, hematoma, or
atheroma in this region.
The main criterion for TEE diagnosis of suspected
acute aortic dissection is the presence of two lumina
(false and true) separated by an intimal flap (Table 49-12
and Fig. 49-19). Other findings for diagnosing aortic
dissection by TEE32 include:
1. Tear or disruption of the flap continuity or jets seen
with color Doppler across the flap
2. Complete obstruction of the false lumen; presence of
thrombus
3. Central displacement of intimal calcification or separation of intimal layers from thrombus
4. Periaortic hematoma (echo-free spaces around the
aorta)
5. Intramural hematoma (crescent-shaped echodensity
with vacuolization within it on the aortic short-axis
view)
6. Pericardial or pleural effusion
7. AR
It is important to define the anatomic site and extension
of the dissection, the degree of AR, involvement of the
coronary arteries, LV dysfunction, and the presence of
pericardial effusion or tamponade.
Intraoperatively, TEE is used during reconstructive
surgery for hemodynamic status, entry/exit sites, evaluation of decompression of the false lumen, and assessment
of concomitant valve surgery.13 Postoperatively, TEE is
used for the detection of residual regurgitation and LV
dysfunction. TEE is also indicated for defining the
anatomic site and size of aortic aneurysms.
Table 49-12 True versus false lumen in aortic dissection
Systole
Diastole
SEC/thrombus
Blood flow
True lumen
False lumen
Expansion
Collapse
Absent or minimal
Systolic forward flow
Collapse
Expansion
Present
Reversed or
absent flow
SEC spontaneous echo contrast.
Source: Erbel et al.32 With permission.
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A
B
C
Figure 49-19 Dissection of the descending thoracic aorta. Transesophageal echocardiogram showing a large aortic dissection with the diagnostic flap separating the true (TL) and
false lumen (FL). A. Short-axis view. B. Long-axis view. C. Long-axis with color-flow
Doppler shows flow in both the true and false lumens.
PERICARDIAL DISEASE
Pericardial effusion and tamponade
Echo is the diagnostic test of choice for detection of
pericardial effusion (PE) and assessing its hemodynamic significance. TEE is usually superior to TTE for
evaluating pericardial thickness and adjacent structures,
although CT and/or MRI are preferred for evaluating
the pericardium. Normally, the pericardial space contains
10 to 50 mL of fluid and the pericardium measures 1 to
3 mm in thickness. An increase in the volume of the pericardial fluid results in elevated pericardial pressures, leading to reduced RV filling, followed by reduced LV filling
(Fig. 49-20). PE usually appears as an echo-free space
surrounding the myocardium, although as protein or
cellular debris increases in the fluid, it becomes increasingly echogenic.35 PE is differentiated from pleural effusion by the anterior location of PE relative to the
proximal descending thoracic aorta, while pleural effusion is located posteriorly to the aorta. Epicardial fat
may be confused with PE, since it is also echolucent,
although epicardial fat is usually more echogenic than
pericardial fluid and is usually located anteriorly.35 TEE is
useful in the postoperative patient with tamponade and a
small loculated PE that may be difficult to visualize on
TTE. Loculated PE in postoperative cardiac surgery
patients may cause tamponade in the absence of typical
Figure 49-20 Large pericardial effusion and cardiac tamponade. Transthoracic echocardiogram of the apical fourchamber view reveals an atrial myxoma attached to the
interatrial septal with a large echolucent circumferential
pericardial effusion (PE) and evidence of elevated intrapericardial pressure. Classic features of tamponade are shown
with right ventricular (RV) diastolic collapse and abnormal
interventricular septal motion (shifted toward the left during
inspiration). RA right atrium; LA left atrium; LV left
ventricle.
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Table 49-13
Echocardiographic signs of cardiac
tamponade
RA collapse
RV diastolic collapse
LA, LV collapse
Abnormal
interventricular
septal motion
Respiratory variation
in ventricular size
Respiratory variation
in transvalvular
inflow velocities
Respiratory variation
in PV and HV
velocities
Dilated IVC and
blunted respiratory
changes
Sensitive but not specific.
Ranges from inward dip to complete
collapse of RV free wall in diastole;
specific sign but may be absent if
elevated RV pressures or adhesions
tether RV.
May be the only sign of tamponade
in postoperative cardiac surgery
patients.
Inspiration: septum shifts to the left.
Inspiration: LV becomes smaller,
RV larger.
Inspiration: mitral inflow E velocity
decreases, tricuspid inflow velocity
increases.
Inspiration: PV velocities decrease
and HV velocities increase.
Table 49-14 Echocardiographic signs of constriction
Pericardial thickening
and calcification
Dilated RA, LA, IVC
Diastolic flattening of
the LV posterior wall
Abnormal interventricular
septal motion
Premature pulmonary
valve opening
Respiratory variation in
ventricular size
Respiratory variation in
transvalvular and
venous (pulmonary/
hepatic) flow velocities
TEE better than TTE, but additional
imaging with CT or MRI may
be necessary
Nonspecific findings
Secondary to reduced filling in
mid- to late diastole, sensitive
but not specific
Inspiration: septum shifts to
the left
RV diastolic pressure PA
diastolic pressure in middiastole
Inspiration: LV becomes smaller,
RV larger
As in tamponade, respiratory
variation may be more
prominent in constriction
RA right atrium; LA left atrium; IVC inferior vena cava;
LV left ventricle; RV right ventricle; PA pulmonary artery.
Sources: From Oh,4 Munt et al.,35 and Hoit.36 With permission.
Not very specific.
RA right atrium; RV right ventricle; LA left atrium; LV left
ventricle; PV pulmonary vein; HV hepatic vein; IVC inferior vena cava.
Sources: From Oh4 and Munt et al.35 With permission.
echo signs (Table 49-13). In these patients, any evidence
of LA or LV collapse or other localized chamber compression may be indicative of hemodynamically significant elevated intrapericardial pressures.
Constrictive pericardial disease
In constrictive pericardial disease, the pericardium is thickened (3 mm) and often calcified, which reduces ventricular filling in diastole and causes diastolic heart failure.
However, the absence of pericardial calcification does not
rule out the diagnosis of constriction. Although echo
signs of constriction (Table 49-14) are not very sensitive
or specific, a completely normal echo study usually rules
out constriction.36 Other imaging modalities, such as CT
or MRI, may be necessary to further evaluate the pericardium and distinguish constriction from restriction.
CARDIAC SOURCES OF EMBOLI
One of the most common indications for TEE is for the
evaluation for cardiac sources of emboli, since TTE does
not visualize well the potential sources of emboli (LA
appendage thrombus, aortic atheroma, patent foramen
ovale or atrial septal defect, LV thrombus, valvular
lesions, intracardiac tumors). Small thrombi in the LA or
LA appendage can be detected using TEE. In addition,
factors that may contribute to or accompany atrial
thrombi are often seen in the absence of an obvious
thrombus: LA or LA appendage enlargement, SEC consistent with blood stasis, and decreased LA appendage
contraction with low PW Doppler velocities ( 20
mm/s). Aortic atheromas are evaluated for mobile components, plaque rupture, and ulceration and are graded
as mild ( 1 mm), moderate (1 to 3.9 mm), and severe
( 4 mm).
ATRIAL SEPTAL DEFECTS
TEE is superior to TTE for visualizing atrial septal
defects (ASDs). The anatomic defect is visualized using
two-dimensional echo and confirmed with Doppler and
contrast (bubble study) using maneuvers that increase
RA pressure, such as Valsalva or cough. The hemodynamic significance of the shunt is assessed using Doppler
by quantifying the shunt size and determining the presence of pulmonary hypertension. Shunt quantification is
obtained as the ratio of pulmonary to systemic flow
(Qp:Qs) using Doppler cardiac outputs across the pulmonary valve and AV.4 All four pulmonary veins should
be visualized and the presence of associated anomalies
excluded. TEE plays an important role in determining
the suitability of ASDs for device closure versus cardiac
surgery based on the size of the ASD and the rim of tissue surrounding it as well as the degree of septal tissue
redundancy.23 TEE has become essential for guiding
placement of catheter-deployed closure devices and in
assessing residual shunts (Fig. 49-21).
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B
C
D
965
Figure 49-21 Secundum atrial septal defect (ASD) and clamshell closure. A. Secundum
ASD seen as a defect in the mid-interatrial septum along with a dilated right atrium (RA)
on transesophageal echocardiography. The size of the rim of tissue between the ASD and
the aortic valve is critical in determining likelihood of success with device closure. C.
Color-flow Doppler of the ASD shows a high-turbulence jet consistent with shunt (arrow).
B. The clamshell has been deployed across the ASD. D. Postprocedure color-flow
Doppler with small residual shunt that usually resolves spontaneously after a period of
several weeks to months. AV aortic valve.
CARDIAC TUMORS
TEE, because of its high sensitivity, is the imaging modality
of choice and is superior to TTE, CT, MRI, and angiography for detecting cardiac tumors.1,4 Although MRI may
not detect small cardiac tumors, it is usually performed
after TEE for further differentiation of thrombus (presence
of methemoglobin or hemosiderin) from neoplasm,
since it is superior to TEE for tissue characterization.
MRI examinations are multiplanar and typically include
fast T1- and T2-weighted techniques with administration
of gadolinium (a paramagnetic contrast agent) and a technique for imaging moving structures with single-slice
breath-hold, such as fast gradient-echo sequences (e.g.,
FLASH). Primary tumors are more likely to affect the
myocardium, while secondary tumors usually involve the
pericardium with secondary intramyocardial infiltation.37
Atrial myxomas are the most common (up to 25 percent)
primary cardiac tumors. Atrial myxomas as seen on TEE or
TTE show several typical features37 (Fig. 49-22A):
●
●
Ninety percent originate in the interatrial septum, near
the fossa ovalis.
A spherical mass with a speckled appearance is often
seen in RA myxomas, while a villous amorphous mass
may be seen in LA myxomas.
●
●
●
Ninety percent attach to the wall of the atrium via a
stalk, which may allow prolapse through the MV.
Intramural hemorrhage (cysts) and necrosis result in a
heterogeneous appearance of echodensity; calcifications are uncommon but may be seen.
They may be highly mobile and a cardiac source of
embolus.
Metastatic tumors to the heart most commonly arise
from the breast or lung but may include leiomyosarcoma
(Fig. 49-22B). Metastatic tumors usually affect the pericardium and result in pericardial effusion. In addition,
some tumors metastasize through the inferior vena cava
(renal cell, hepatoma), affecting the right heart more than
the left; TEE allows for visualization of the route of extension.37 Tumors involving the cardiac valves are rare (often
fibroelastomas) and may affect valve competence and
global LV function. MRI and ultrafast CT may be a useful
adjunct in delineating tumors of the cardiac valves.38
LEFT VENTRICULAR OUTFLOW
TRACT OBSTRUCTION
TEE is used intraoperatively for septal myectomy for treatment of obstruction of the LV outflow tract (LVOT) due
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PART II ● ADULT CARDIAC SURGERY
A
B
Figure 49-22 Cardiac tumors. A. Large atrial myxoma attached to the interatrial septum,
seen as a spherical mass with a speckled appearance. B. Metastatic leiomyosarcoma of
genitourinary tract origin with myocardial invasion of the left ventricular (LV) apex.
to hypertrophic cardiomyopathy. Systolic anterior motion
(SAM) of the MV may cause LVOT obstruction; TEE is
used to define the structures involved in the SAM (e.g.,
chordae, anterior leaflet). As in aortic stenosis, LVOT gradients may differ intraoperatively versus preoperatively
owing to different hemodynamics. Color-flow Doppler
typically demonstrates turbulent blood flow (mosaic pattern) at the site of LVOT obstruction. An eccentric jet of
MR may also be seen if there is abnormal coaptation of
the mitral leaflets (usually a posteriorly directed jet owing
to abnormal coaptation of the anterior mitral leaflet).
TEE is also helpful during resection of lesions causing
subaortic stenosis. It can determine the location and
severity of obstruction. It is also useful for evaluating the
success of the surgery in relieving the obstruction and in
detecting MR that may result from the surgery.22
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