ECHOCARDIOGRAPHY IN CARDIAC SURGERY - TSDA

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CHAPTER 

49 

ECHOCARDIOGRAPHY 

IN CARDIAC SURGERY 

Samia Mora, Katherine C. Wu 

PRINCIPLES OF 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. 

TWO-DIMENSIONAL ECHOCARDIOGRAPHY 

Standard views are obtained along three orthogonal planes 

of the left ventricle (LV): long-axis, short-axis, and the 4- 

chamber 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 

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. 

DOPPLER ECHOCARDIOGRAPHY 

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 

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 4V 2 ). 

Color-flow doppler 

Color-flow (CF) Doppler transforms Doppler velocity 

information into a color-coded scheme. Red denotes 

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944 PART II ● ADULT CARDIAC SURGERY 

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


Chapter 49 ● Echocardiography in Cardiac Surgery 945 

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 

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. 

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 

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



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 

anesthesiologists 12 [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 

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.) 

Mitral valve inflow 

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).



LA pressure seen after MV opening. The fourth velocity is 

the atrial flow reversal velocity (PV a 

) 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 PV S2 

is much less than PV D 

. When 

higher filling pressures are present, both the duration and 

peak velocity of PV a 

are increased. Another sign of elevated 

LA pressure is when the duration of PV a 

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 (PV S1 

) 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 (PV S2 

) 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 (PV D 

). 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 (PV S1 

, 

PV S2 

, PV D 

, PV a 

). Duration of peak reverse flow velocity during atrial contraction (PV a 

dur) 

is also measured. (From Oh et al. 11 With permission.)



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 cm 2 . 

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 

score 15 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 (cm 2 ) 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 4V 2 

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.) 

Where P MV pressure gradient (mmHg) and V 

velocity of blood flow across the MV (ms). 

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



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 of mitral stenosis 

Mitral valve area Mean gradient a 

Severity (cm 2 ) (mmHg) 

None 4–6 — 

Mild 1.6–2.0 5 

Moderate 1.1–1.5 5–10 

Severe 1 10 

a Assumes 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.



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). 

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 MR 4,16 include: 

● 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 cm 2 . 

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 

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 

Table 49-3 

Morphology 

Stenosis 

Regurgitation 

Echocardiographic assessment of the 

mitral valve 

Mitral annulus, leaflets, chordae, papillary 

muscles, LV size and function, 

LA size, pulmonary hypertension (RVSP) 

Often rheumatic 

Echo score: leaflet mobility, thickening, 

subvalvular thickening, calcifications, 

8 favors valvuloplasty 

Severe MS: area 1 cm 2 or mean gradient 

10 mmHg 

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.



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 MVP 20 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. 

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. 

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 

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



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 cm 2 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



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 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. 


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. 

Aortic valve area 

In aortic stenotic lesions, the AV area decreases by approximately 

0.1 cm 2 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: 

A 1 

V 1 

A 2 

V 2 

Where A area or r 2 ; V velocity; A 1 

V 1 

flow proximal 

to the valve (LVOT); A 2 

V 2 

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 (r 1 

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 4V 2 

Where P AV pressure gradient (mmHg) and V 

velocity of blood flow across the AV (ms).



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 

Velocity Area Mean gradient a 

Severity (ms) (cm 2 ) (mmHg) 

None 1 3–4 — 

Mild 2.5–2.9 1.5 25 

Moderate 3–4 1–1.5 25–50 

Severe 4 1 50 

a Assumes normal cardiac output. 

Source: ACC/AHA Guidelines for the Management of Patients with 

Valvular Heart Disease. 9 With permission.



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. 


This is helpful for evaluating LV size and function, AV 

structure and leaflet mobility, aortic root dilatation, aortic 

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.



Table 49-5 

Morphology 

Stenosis 

Regurgitation 

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. 

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 

Echocardiographic assessment of the 

aortic valve 

Three semilunar leaflets/cusps, LV size and 

function 

Often degenerative/calcific 

Severe AS: area 1 cm 2 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. 

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 abnormality 

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 include 16 : 

● A large regurgitant (color) jet ( 10 cm 2 ), 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 

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 4V 2 ) 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 P RV 

P RA 

). In 

the absence of elevated RA pressures, the right atrial 

pressure (P RA 

) is estimated at 10 mmHg. Therefore, 

RVSP P RA 

P 10 4V 2 

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.



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 18–25 

Mild 30–40 

Moderate 40–70 

Severe 

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 P 4V 2 

Valve area 

MV prostheses: area 220/PHT 

AV or MV prostheses: A 1 

V 1 

A 2 

V 2 

Regurgitation/leaks Size, symmetry, velocity, eccentricity 

Leaflet mobility/ Degree of leaflet excursion 

restriction 

LV size/function LV dimensions, EF 

Pulmonary RVSP 4V 2 10 

hypertension 

Compare with Change in gradients, area, leaks 

prior echo 

P pressure gradient; V velocity; MV mitral valve; PHT 

pressure half-time; AV aortic valve; A 1 

V 1 

flow (area 1 

velocity 

1 

) proximal to the valve prosthesis; A 2 

V 2 

flow (area 2 

velocity 

2 

) across the valve prosthesis; LV left ventricle; EF ejection 

fraction; RVSP right ventricular systolic pressure. 

Source: From Zabalgoitia. 28 With permission.



Table 49-8 

Paravalvular leak 

Pannus formation 

Structural 

deterioration 

Nonstructural 

dysfunction 

Thrombosis 

TEE Findings in prosthetic valve 

complications 

Source: From Zabalgoitia. 28 With permission. 

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 

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 findings 4 of normal prosthetic valve regurgitation 

include: 

1. AV: regurgitant area 1 cm 2 and length of jet 

1.5 cm 

2. MV: regurgitant area 2 cm 2 and length of jet 

2.5 cm 

3. Characteristic flow patterns (Medtronic-Hall, one 

central jet; Star-Edwards, two curved side jets; Bjork- 

Shiley, 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 

equation (P 4V 2 ). 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 (A 1 

V 1 

A 2 

V 2 

) 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 A 1 

. 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 

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



A 

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 Small, narrow Large, wide 

Symmetrical Yes No 

Velocity Low High 

Eccentric No 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



Table 49-10 Echocardiographic characteristics of vegetative and nonvegetative valvular masses 

Characteristic Vegetation Nonvegetation 

Echogenicity Similar to myocardium Similar to pericardium 

Low echogenicity/gray 

High echogenicity/white 

Location Upstream surface of valve near the Downstream surface of valve 

regurgitant jet 

Motion Mobile, prolapses Less mobile 

Shape Amorphous, lobulated Filamentous, strand-like narrow base of 

Wide base of attachment 

attachment 

Regurgitation Severe regurgitant jet Mild or no regurgitant jet 

Vegetation located near jet 

Other Paravalvular abscess/leak None 

Fistula 

Valve dehiscence 

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.



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 

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 

Postinfarct ventricular septal defect 

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 

B 

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.



Table 49-11 

Diagnostic tests for acute aortic dissection 

Sensitivity Specificity 

Test (%) (%) Pluses and minuses 

TEE 99–100 89 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 

CT 90 85 Pluses: Quick, noninvasive 

Minuses: Cannot assess branch vessels or IH, dye load/allergy 

MRI 98–100 100 Pluses: Noninvasive, assesses branch vessels, IH 

Minuses: Slow, may not be available, pacemakers/device, breath-hold 

necessary 

Angiography 88–91 95 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 TEE 32 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 

True lumen 

False lumen 

Systole Expansion Collapse 

Diastole Collapse Expansion 

SEC/thrombus Absent or minimal Present 

Blood flow Systolic forward flow Reversed or 

absent flow 

SEC spontaneous echo contrast. 

Source: Erbel et al. 32 With permission.



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.



Table 49-13 

RA collapse 

RV diastolic collapse 

LA, LV collapse 

Abnormal 

interventricular 

septal motion 

Respiratory variation 

in ventricular size 


in transvalvular 

inflow velocities 


in PV and HV 

velocities 

Dilated IVC and 

blunted respiratory 

changes 

Echocardiographic signs of cardiac 

tamponade 

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 

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. 

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 Oh 4 and Munt et al. 35 With permission. 

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 

Table 49-14 

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 

Echocardiographic signs of constriction 

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 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. 

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 

(Q p 

:Q s 

) 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).



A 

B 

C 

D 

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 features 37 (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



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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