Atlas of Transesophageal Echocardiography, 2nd Edition (2007)

Chapter 3. Aortic Valve, Aorta, and Aortic Branches

Transesophageal echocardiography (TEE) can substantially augment the transthoracic echocardiogram in the workup of the aortic valve and the aorta.

Aortic Valve

Views

The mid-esophageal short- and long-axis views are the most commonly used views. To obtain an optimal short-axis view, the TEE image is rotated from 0° to between 30° and 60°, with flexion of the probe as necessary. The optimal short-axis view is the one in which the valve appears most circular and the three thin leaflets are seen clearly, surrounded by the noncoronary cusp in the upper left and the left and right cusps as one looks clockwise from the noncoronary cusp. This view is particularly useful for determining the number of aortic valve leaflets and assessing their thickening and fusion, as well as for determining the area of the aortic valve and diagnosing and assessing the severity of aortic insufficiency. The approach to positioning for aortic valve planimetry to obtain valve area is discussed in the subsequent text.

The long-axis view of the aortic valve is generated by further rotation of the probe to an angle usually between 90° and 160°, again with flexion as necessary, to optimize the image. This view demonstrates the aortic outflow tract (AOT), aortic valve and sinuses of Valsalva, and the proximal aorta. The normal valve leaflets appear as thin, pliable, widely opening structures. It is important not to misdiagnose the normal mild thickenings at the coaptation point of the aortic valve leaflets (nodules of Arantius) as pathologic. This view is particularly useful for determining the level of aortic outflow obstruction: subvalvular, valvular, or supravalvular. Leaflet structure and separation are well seen in this view. The presence of valve redundancy can be assessed and can be generally distinguished from the presence of vegetation. Eversion of the leaflets (“rolling up” of the edges) is also well demonstrated.

A less commonly used view is the deep transgastric view, the central utility of which is to try to align the ultrasound beam with the aortic jet in order to determine the pressure gradient across the aortic valve. These views are obtained by advancing the scope into the transgastric position and then flexing it to obtain a view that places the aorta and aortic valve in line with the ultrasound beam. This facilitates the measurement of gradients but does not allow sufficient maneuver to ensure that the probe is aligned so as to provide the highest velocity aortic jet.

Aortic Outflow Obstruction

Using TEE, it is possible to diagnose aortic outflow obstruction, determine the level (subvalvular, valvular, or supravalvular), and quantify the severity. Aortic stenosis (AS) is the only valvular lesion commonly associated with sudden cardiac death. It becomes more common with advancing age, so a progressively aging population results in an increase in the prevalence of the lesion. Subvalvular and supravalvular outflow obstruction are less common.

When an adequate study is performed, transthoracic echocardiography (TTE) can be effective for the workup of AS. On TTE, the diagnosis of AS is made by demonstrating a thickened aortic valve and either a high (>approximately 50 mm Hg) transvalvular gradient or a diminished aortic valve area (AVA) (using the continuity equation). In order to estimate the gradient, the beam is aligned with the axis of the highest velocity aortic jet and the velocity recorded. This may require interrogating in multiple views, including the apical five-chamber, suprasternal notch, and right parasternal views. Using a simplified conservation of energy (Bernoulli) equation, the peak gradient is

Δ Pmax = 4 (Vmax - VOT)2

where Vmax is the peak aortic velocity and VOT is the outflow tract velocity. The mean aortic gradient can also be estimated using the time velocity integral.

An indirect calculation of the AVA can be obtained from the continuity equation, which is a statement of the conservation of mass. Assuming the AOT to be circular, its area (AOT) can be estimated from the measured diameter on the parasternal long-axis view and the outflow tract velocity (VOT), obtained from pulsed-Doppler examination in the parasternal five-chamber view. The peak velocity across the aortic valve is known, and with a variety of simplifying assumptions, the AVA is calculated as

AVA = VOTAOT/Vmax

This equation is valid even in the presence of aortic insufficiency.

In patients with a markedly reduced stroke volume, valve opening can be reduced. Therefore, the low stroke volume results in both a reduced pressure gradient and a smaller valve area. In patients with a low gradient due to low stroke volume, a dobutamine infusion can be used to clarify the picture. With inotropic stimulation, the computed valve area of a normal valve (or one that is not rigid or severely stenosed) will increase with a minimal rise in gradient. A more rigid, severely stenosed valve, on the other hand, will demonstrate an increase in the transvalvular gradient without an increase in the computed valve area.

These same calculations can be performed on the basis of data derived from the TEE transgastric views. However, in practice, this approach is rarely used. The appropriate deep transgastric view is hard to obtain and it is not possible to maneuver the view sufficiently to be certain that the maximum jet is found.

TEE has assumed a prominent role in the echocardiographic examination of the aortic valve because of the superior imaging detail that it provides compared to TTE. Because the multiplane probe permits great flexibility in the selection of the imaging plane, it is far more effective than single and biplane probes in providing a complete study of a variety of lesions. TEE should be considered a complement to, but not a replacement for, TTE.

A number of findings suggest or are consistent with AS. Thickening of the aortic valve is clearly seen on TEE; when limitation of motion is also present, this is consistent with AS. Color Doppler detection of a narrow (7 mm or less at its origin) systolic jet indicates severe stenosis.

Planimetry of the minimum orifice area in the short-axis view (usually best imaged at 30° to 60°) has been shown to correlate well with catheterization-derived AVA. The stenotic valve often has the geometry of a truncated cone. It is important that the topmost part of this cone be studied, because it is the flow-limiting orifice. To ensure that the minimum orifice is imaged, the probe is first moved up the esophagus in the short-axis view until the aortic valve disappears. The probe is then advanced until the full perimeter of the valve just comes into view, which should demonstrate the minimum cross-sectional area (flow-limiting orifice). Gain must be carefully adjusted to minimize the “blooming” effect of the extensive calcium that is usually present in adults, and the probe must be manipulated to avoid acoustic shadowing by the calcium. In the presence of severe calcification it may be difficult to identify the orifice. When this difficulty arises, color Doppler is often helpful because the first signals appear in the orifice at the beginning of systole.

An attempt can be made to position the TEE image so that a pressure gradient can be measured between the left ventricle and the aorta using the transgastric view. If a high gradient is obtained, AS can be diagnosed. However, it is difficult to be certain that the maximum gradient has been measured because TEE has limited capacity for looking for the maximum jet at multiple angles.

Left ventricular hypertrophy is well imaged by TEE and commonly accompanies AS. It is particularly important to exclude the presence of coexisting hypertrophic cardiomyopathy (HCM) because the hypertrophied muscle can be resected at the time of aortic valve replacement. A narrow left ventricular outflow tract (LVOT) (<20 mm) and hypertrophy that is out of proportion to what would be expected from the degree of AS present alert the echocardiographer to the possibility of coexisting HCM. Systolic anterior motion of the mitral valve may be absent in HCM patients with severe AS.

An interesting lesion that can be identified by TEE is the supravalvular AS. This lesion may be congenital, or it may be present in patients with atherosclerosis and very high cholesterol levels.

The morphologic data available from TEE allow detailed examination of the aortic valve. The multiplane probe is substantially more effective than are single or biplane probes. The mild thickening normally present at the points of leaflet coaptation (nodules of Arantius) also may be identified. TEE effectively defines the number of leaflets and the degree of commissural fusion present. The median raphe of a bicuspid valve can be clearly seen. The distinction between tricuspid and bicuspid aortic valve is important because of the difference in prognosis and the implications for valve repair versus valve replacement. The presence of valve redundancy, which may be confused with a vegetation on transthoracic echo, can be delineated. Eversion of the leaflets is also well demonstrated.

Aortic Regurgitation

The causes of aortic regurgitation (AR), including thickening, eversion of the leaflets, infection, dilatation of the proximal aorta with loss of leaflet coaptation, and redundancy, can be delineated. Intermittent AR, caused by varying coaptation points resulting from valve redundancy (especially in a bicuspid valve), can also be detected. Small fenestrations as well as large holes and their exact location and size can be imaged.

TEE is of particular importance in the workup for endocarditis. TEE is far more sensitive for the assessment of vegetations than is TTE. For this reason, in the appropriate clinical setting, the absence of a vegetation on TTE should prompt the performance of TEE. Abscesses are also far more likely to be seen on TEE than TTE. Their anatomic location and extent are readily imaged, and their communication with other structures is diagnosed using color-flow Doppler.

Assessment of the severity of AR is based on semiquantitation using the fraction of the LVOT at the origin of the diastolic jet on the ventricular aspect of the aortic valve that is covered by the jet. The percent ratio of proximal jet width to LVOT diameter (taken at the same location) of <25% represents mild regurgitation, 25% to 65% represents moderate severity, and >65% is a demonstration of severe regurgitation. Two technical points are important. First, the assessment must be made at the origin of the jet (vena contracta level). Second, the Nyquist limit is important. If it is set higher than 40 to 50 cm/sec, changes in the color filter result in the loss of imaging of lower velocities and therefore changes the size of the proximal jet.

Aorta

Defining aortic anatomy is another important application of TEE. The location and extent of aortic aneurysms are more effectively visualized using TEE than TTE. The ability of TEE to image the entire aorta is an important advantage over TTE. Evidence of rupture can be sought and the extent of associated AR can be assessed using color-flow Doppler. In many centers, TEE is the modality of choice for diagnosing aortic dissection because of its ability to rapidly and accurately make the diagnosis. This is important because these patients may die suddenly if surgery is not performed immediately.

The diagnosis of dissection is based on the demonstration of a flap that separates the true lumen (TL) and the false lumen (FL). It is necessary to examine the aorta in multiple planes because the flap is not well seen in all views. The flap is usually, but not always, mobile, which aids in making the diagnosis. Flow in opposite directions on the different sides of the flap, if present, helps to confirm the diagnosis. A number of features aid in differentiating the TL from the FL and may help confirm the diagnosis of aortic dissection. Flow in the TL usually has higher velocity than flow in the FL; as a result, the signals are generally brighter. In addition, the TL expands in systole and the FL expands in diastole. When a clot is present it is usually in the FL. Communications between the TL and FL seen on color Doppler are helpful in confirming the diagnosis. Because the entire thoracic and proximal abdominal aorta can be imaged using the multiplane probe, the exact location and full extent of dissection can be delineated.

Dissections that involve the ascending aorta, arch, or both, and the descending aorta are DeBakey type I. Dissections that involve the ascending aorta, arch, or both (but not the descending aorta) are DeBakey type II, and those that involve only the descending aorta are Type III. In the Stanford classification, any dissection involving the ascending aorta, the arch, or both is type A, whereas dissection involving only the descending aorta is type B.

TEE is useful in assessing prognosis and making management decisions. A clotted FL has a better prognosis than a flow-filled FL because it acts as a buttress for the TL, thereby diminishing the chance of rupture. Assessment of the cause and severity of AR in patients who had dissection helps in making a decision regarding the necessity of resuspension or replacement of the aortic valve. Involvement of the coronary arteries in the dissection can also be diagnosed. Dissections that involve only the descending aorta do not require surgery unless there is evidence of impending rupture or compromise of organ flow, which occurs rarely.

Atherosclerotic plaques in the aorta are readily identified by TEE. The presentation varies from uniform intimal thickening to large mobile plaques protruding into the lumen. Atherosclerosis in the aorta is a risk factor for stroke and emboli to other parts of the body. The greater the mobility, the higher the risk of embolization. Fixed plaques protruding >5 mm into the lumen are also at high risk for embolization.

FIGURE 3.1. Aortic stenosis. A,B. The valve is mildly thickened and doming but opens well, consistent with mild aortic stenosis (AS). AO, aorta; LA, left atrium, LV, left ventricle; MV, mitral valve; PA, pulmonary artery; RA, right atrium; RV, right ventricle. C–E. Patient with severe calcific AS. The valve is markedly thickened and calcified (arrows), and the opening of the valve is severely restricted. Flow acceleration (arrowheads) and turbulence in the aortic root (E) are indicative of significant AS. This patient underwent aortic valve (AV) replacement. F. The wide aortic jet (arrowheads) in another patient suggests an absence of significant AS. G. The jet (arrowhead) shown in this illustration, on the other hand, is narrow (<7 mm) at its origin, indicative of severe AS. Marked poststenotic dilatation of the aorta is present. It is important to assess the jet width at its exit point from the aortic valve. At surgery, this patient was found to have a heavily calcified, severely stenotic aortic valve. He underwent CarboMedics aortic valve replacement.

FIGURE 3.2. Aortic stenosis. A,B. A thickened aortic valve with markedly restricted opening (arrow). The inset in B shows the valve orifice imaged in short axis. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RV, right ventricle; RVO, right ventricular outflow tract. C. Planimetry of the orifice of a thickened valve in the short-axis view is shown in another patient. An area of 0.74 cm2 is found in this patient. The bottom inset in C demonstrates that color Doppler can help to identify the orifice; the top inset shows a narrow jet (arrowheads) consistent with severe stenosis. The probe must be moved carefully up and down the esophagus until the minimum cross-sectional area is found. This yields the flow-limiting orifice area. This point is emphasized in D, which shows that planimetry of the minimum area yields a valve area of 0.68 cm2, whereas planimetry more proximally gives an area of 1.43 cm2PA, pulmonary artery. E–G. Gross specimens of thickened tri-leaflet aortic valves show calcium in the cusps that restricts opening. (C reproduced with permission from 

Kim KS, Maxted W, Nanda NC, et al. Comparison of multiplane and biplane transesophageal echocardiography in the assessment of AS. Am J Cardiol 1997;79:436–441.

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FIGURE 3.3. Aortic stenosis. A. Planimetry reveals severe bicuspid aortic stenosis (AS) with a valve area of 0.52 cm2Upper inset panel: A very narrow jet consistent with severe AS. Lower inset panel: Acoustic shadowing that results in the dropout of part of the image so that color does not fill the entire orifice. Careful positioning of the probe is necessary if the valve is to be accurately planimetered. B. Severe bicuspid aortic valve stenosis is seen in another patient. C. Gross specimen shows a thickened and calcified bicuspid aortic valve. AV, aortic valve; LA, left atrium; RVO, right ventricular outflow tract; SVC, superior vena cava. (A reproduced with permission from 

Kim KS, Maxted W, Nanda NC, et al. Comparison of multiplane and biplane transesophageal echocardiography in the assessment of AS. Am J Cardiol 1997;79:436–441.

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FIGURE 3.4. Aortic stenosis. A,B. A bicuspid valve mimicking a tricuspid aortic valve. Although the valve appears to have three leaflets, it was found to be tricuspid at surgery.AO, aorta; AV, atrial valve; LA, left atrium; LAA, left atrial appendage; PA, pulmonary artery; RA, right atrium; RV, right ventricle; RVOT, right ventricular outflow tract; TV, tricuspid valve. C,D. This valve (arrowheads) appeared to be bicuspid but was surgically shown to be tricuspid. E. The narrow jet (arrow) confirms the presence of severe stenosis in this patient. F. In another patient, color Doppler examination was helpful in identifying the eccentric severely stenotic orifice. This patient underwent aortic valve replacement. G. The surgically resected specimen from the patient in F shows a heavily calcified, severely stenotic bicuspid valve.

FIGURE 3.5. Aortic stenosis. Two patients with fixed stenotic orifices are shown. A. Size of the orifice (arrow), which measures 0.36 cm2, does not change from diastole to systole. Color Doppler examination (inset) was helpful in delineating the orifice. AV, atrial valve; LA, left atrium; PA, pulmonary artery; RA, right atrium. B–D. Another patient with a fixed stenotic orifice (arrowheads), which does not change in size from diastole (B) to systole (C). In such cases, color Doppler examination is useful in identifying the orifice (D). (A reproduced with permission from 

Kim KS, Maxted W, Nanda NC, et al. Comparison of multiplane and biplane transesophageal echocardiography in the assessment of AS. Am J Cardiol 1997;79:436–441.

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FIGURE 3.6. Aortic stenosis. Associated LV hypertrophy is shown in the transgastric view. A. The wall thickness measures >20 mm. B,C. Fibroelastosis developing in another patient with aortic stenosis (AS). Note the thickened, hyper-refractile endocardium (arrowheads)

FIGURE 3.7. Aortic stenosis. A. Aortic stenosis (AS) coexisting with hypertrophic cardiomyopathy. A markedly thickened ventricular septum, narrow left ventricular outflow tract, systolic anterior motion (SAM) of the mitral valve, and aortic valve with restricted opening are seen. B,C. Another patient with SAM of the anterior mitral leaflet, hypertrophied ventricular septum, and a thickened aortic valve with marked restriction of the opening. This patient underwent aortic valve replacement for severe stenosis and left ventricular septal myomectomy. LV, left ventricle; RV, right ventricle.

FIGURE 3.8. Aortic valve thickening. A,B. Localized thickenings (arrowheads) called nodules of Arantius are often seen in healthy patients on the aortic valve at the points of leaflet coaptation. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; SAM, systolic anterior motion; VS, ventricular septum.C,D. Another patient with prominent localized thickening (arrow) of the right coronary cusp causing aortic regurgitation (arrow in D). E. Calcification results in mild narrowing of the aorta at the level of the sinotubular junction (arrows). Severe acquired supravalvular aortic stenosis can occur in patients with familial, homozygous hypercholesterolemia. F. Fibrotic thickening (arrowheads) is shown at the base of the aortic leaflets.

FIGURE 3.9. Aortic regurgitation. A,B. Mild aortic regurgitation (arrows). Note the narrow jet width at its origin. AO, aorta; LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle. C. The aortic regurgitation (AR) jet is seen between the left and right aortic cusps. LAA, left atrial appendage; RVOT, right ventricular outflow tract. D. A color M-mode shows a narrow, eccentric, pandiastolic AR jet. E,F. Somewhat wider jets, suggesting more severe AR than in the earlier panels, are seen. G. The width of the jet at its origin occupies approximately 60% of the left ventricular outflow tract (LVOT), indicating moderately severe (3/4) AR. H–J. The proximal regurgitant jet occupies the entire LVOT, indicative of severe AR (4/4). MR, mitral regurgitation. K,L. The effect of changing the Nyquist limit on the width of the regurgitant jet. At the lower Nyquist limit of 37 cm/sec (L) the jet width/LVOT width ratio is 81%, indicating severe aortic insufficiency, which was confirmed at cardiac catheterization. When the Nyquist limit is increased to 55 cm/sec (K), the ratio of jet width to LVOT width is reduced to 53%, consistent with moderately severe regurgitation. This illustrates that the Nyquist limit should be kept in the range of 35 to 45 cm/sec for accurate assessment of AR severity. The primary reason for the alteration in jet width with a change in the Nyquist limit is the associated change in the color filter.

FIGURE 3.10. Redundant aortic valve. A,B. Redundant (arrowhead) right coronary cusp is shown with and without color Doppler. The other cusps do not appear to be redundant. LA, left atrium; RA, right atrium; RVOT, right ventricular outflow tract. C,D. In another patient, the linear echo prolapsing into the left ventricular outflow tract (LVOT)(arrowhead) represents cusp redundancy. AO, aorta; LV, left ventricle; RV, right ventricle. E. An M-mode study shows systolic fluttering of the aortic valve (AV), which is a normal finding and is not necessarily related to the redundancy.

FIGURE 3.11. Redundant aortic valve. A. Redundant aortic valve (AV) (arrow) prolapsing into the left ventricular outflow tract. AO, aorta; LA, left atrium; RA, right atrium;LV, left ventricle; PA, pulmonary artery; RV, right ventricle. B,C. Eccentric jets of aortic regurgitation (AR) (arrows). In both patients the AR jet is directed posteriorly and abuts the mitral valve.

FIGURE 3.12. Redundant aortic valve. The arrows show various components of a redundant, noninfected bicuspid aortic valve prolapsing into the left ventricular outflow tract(A–D) with a posteriorly directed regurgitant jet AO, aorta; LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RVOT, right ventricular outflow tract. (E,F).The flow acceleration (FA) is large, indicating significant regurgitation although the proximal jet width appears narrow. This is related to the eccentric geometry of the jet and to the high Nyquist limit of 49 cm/sec. G. The systolic frame in the same patient clearly shows a bicuspid aortic valve with a raphe (lower arrow). H. The diastolic frame mimics a tricuspid aortic valve, emphasizing the importance of examining the valve throughout the cardiac cycle. This patient underwent aortic valve annuloplasty.

FIGURE 3.13. Redundant aortic valve. A–C. The diastolic frames show central noncoaptation (NC) of the aortic valve (AV) leaflets that results in aortic regurgitation (arrow inC). LA, left atrium; PA, pulmonary artery; RA, right atrium; RVO, right ventricular outflow tract. D. Cusp separation in diastole is also well seen in the M-mode study.

FIGURE 3.14. Redundant aortic valve with hole in right coronary cusp. A,B. A hole (arrows) in the right coronary cusp of the aortic valve, which prolapses into the left ventricular outflow tract. AO, aorta; LA, left atrium; LV, left ventricle; RVOT, right ventricular outflow tract. C. An area of noncoaptation (arrow) between the left coronary cusps (LCC) and noncoronary cusps (NCC). D. Severe aortic regurgitation with a large flow acceleration (arrow). MV, mitral valve.

FIGURE 3.15. Flail aortic valve. A–C. A flail right coronary cusp (arrows) prolapsing into the left ventricular outflow tract (LVOT) in diastole, resulting in prominent diastolic noncoaptation seen in the long-axis views. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RV, right ventricle. D. High-frequency diastolic fluttering (arrow) indicative of a flail aortic valve (AV). There was no evidence of infection. E. Severe eccentric aortic regurgitation (AR) with a large flow acceleration. F,G. Systolic turbulence in LVOT was also seen in this patient and was due to associated hypertrophic cardiomyopathy (IHSS). At surgery, the right coronary leaflet was found torn from its attachment at the commissure between the right and left sinuses. A portion of the autologous pericardium was used to reconstruct the right coronary cusp, and the annulus size was reduced from 24 mm to 18 mm in diameter by performing a triple annuloplasty. MR, mitral regurgitation.

FIGURE 3.16. Eversion of the aortic valve. The distal portion of the left coronary cusp in this patient shows eversion causing noncoaptation with the right coronary cusp, which is only minimally everted. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RV, right ventricle.

FIGURE 3.17. Flail aortic valve in systemic lupus erythematosus. A. Prominent prolapse of the right coronary cusp (arrow) into the left ventricular outflow tract during diastole and noncoaptation of the valve leaflets. B. The long-axis view of the aortic valve demonstrates an eccentric jet of severe aortic regurgitation (AR) directed toward the mitral valve. Note the prominent flow acceleration (FA), which also suggests severe regurgitation. C. Excised aortic valve. There is destruction of the right coronary cusp near the commissure (bottom left). No vegetations are seen. D. Gross specimen from another patient shows lupus valvulitis of both mitral and aortic valves. AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (AC reproduced with permission from 

Mehta R, Agrawal G, Nanda NC, et al. Flail aortic valve in systemic lupus erythematosus. Echocardiography 1996;13:431–434.

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FIGURE 3.18. Aortic valve vegetation. A–C. A large vegetation (arrow) moving into the left ventricular outflow tract in diastole and back into the aortic root in systole. AO, aorta; LA, left atrium; LV, left ventricle; MV, mitral valve; RPA, right pulmonary artery; RV, right ventricle.

FIGURE 3.19. Aortic valve vegetation. A–C. A large vegetation (V) is shown prolapsing into the outflow tract with severe aortic regurgitation (AR). D. Pulsed-Doppler of the distal ascending aorta demonstrates prominent pandiastolic backflow resulting from significant AR. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; MV, mitral valve; RV, right ventricle.

FIGURE 3.20. Aortic valve vegetation. A. A large vegetation (V) involving the aortic valve leaflets. AV, aortic valve; LA, left atrium; PA, pulmonary artery; TV, tricuspid valve.B. Gross specimen shows aortic valve vegetations.

FIGURE 3.21. Aortic valve vegetation with abscess formation. The localized bounded echolucent area (A,B) is a large abscess communicating with the left ventricular outflow tract (LVOT) (arrow in C) and protruding into the left atrium (LA). AB, abscess; AO, aorta; AV, aortic valve; V, aortic valve vegetation. LV, left ventricle; RV, right ventricle. D.Torrential aortic regurgitation (AR). E. Associated moderate mitral regurgitation resulting from annular dilatation. The mitral valve was not infected. F. Diastolic noncoaptation of infected aortic valve leaflets in another patient. G. Fistulous communication with the right atrium and RV (arrows) in the same patient seen in F

FIGURE 3.22. Aortic valve abscess. Abscess cavity (arrows) at the mitral–aortic junction (A–C) extending into the right atrium (arrowheads in E and F). Color-flow examination(C,D) shows the abscess cavity communicating with the left ventricular outflow tract (arrow in D). AO, aorta; LA, left atrium; PA, pulmonary artery; PV, pulmonary valve; RPA, right pulmonary artery; RVOT, right ventricular outflow tract; SVC, superior vena cava.

FIGURE 3.23. Aortic and mitral valve vegetations. Vegetations involving both the aortic (open arrow) and the mitral (closed arrow) valves are shown. AV, aortic valve; LA, left atrium; LV, left ventricle; MV, mitral valve; RV, right ventricle.

FIGURE 3.24. Aortic and mitral vegetations. A–G. Prominent vegetations (V, arrows) involving both mitral and aortic valves are shown. This demonstrates that infection of one valve can lead to infection of the contiguous valve. Note the presence of a vegetation at the mitral–aortic junction (closed arrow in D). AO, aorta; LA, left atrium; RV, right ventricle.

FIGURE 3.25. Aortic and mitral vegetations. A–C. Another patient with mitral and aortic vegetations (V, arrow). AO, aorta; LA, left atrium; RVO, right ventricular outflow tract.

FIGURE 3.26. Ascending aortic aneurysm. The aneurysm measured 6 cm on echo and at surgery. A. Noncoaptation of the aortic valve leaflets (arrow) resulting from distortion by the aneurysm. B. Resulting severe aortic regurgitation with flow acceleration (FA). Note that the junction of the left ventricular outflow tract with the aortic root is not enlarged. C,D. Systolic frames. AO, aorta; LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RVOT, right ventricular outflow tract.

FIGURE 3.27. Ascending aortic aneurysm. Same patient seen in Figure 3.26, showing diastolic noncoaptation of the aortic valve leaflets (arrowheads in A) resulting in aortic regurgitation (red arrow in B). AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RVOT, right ventricular outflow tract.

FIGURE 3.28. Ascending aortic aneurysm. A–D. Another example of a huge aneurysm with severe aortic regurgitation (AR). D shows the aneurysm viewed in short axis with measurement of the anteroposterior (AP) and transverse (TR) diameters. AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 3.29. Ascending aortic aneurysm. A. The aneurysm of the ascending aorta in the short-axis view measures 5.1 cm in the anteroposterior (A) diameter and 5.3 cm in the transverse (B) diameter. B. The descending aorta is normal in size. AO, aorta; LA, left atrium; PA, pulmonary artery; LAD, left anterior descending coronary artery; LM, left main coronary artery.

FIGURE 3.30. Aortic arch aneurysm. A–C. A large aneurysm with a thrombus (TH). C, aneurysm cavity. AO, aorta; LPA, left pulmonary artery; RPA, right pulmonary artery.

FIGURE 3.31. Descending aortic aneurysm. A,B. Two examples of descending thoracic aortic aneurysm (DTA) with thrombus (TH). An associated left pleural effusion (EFF) is present in A

FIGURE 3.32. Transesophageal echocardiographic identification of descending aortic aneurysm rupture into left lung parenchyma. A–C. “To-and-fro” flow (arrowheads) with flow signals moving into the partially clotted aneurysm (AN) in systole and back into the descending aorta (DA) in diastole. D. Arrowheads on the right denote two separate sites of rupture of aneurysm into the lung parenchyma (L). Arrowhead on the left shows communication between DA and AN. E. Schematic. (Reproduced with permission from

Srinivasa R. Aaluri, Andrew Miller, Navin C. Nanda, Osman Mukhtar, Kamlesh Anskingkar, Wen Ying Huang, Virender Puri, Lincoln L. Berland, David C. McGiffin: Transesophageal Echocardiographic Identification of a Descending Aortic Aneurysm Rupture into the Left Lung. Echocardiography 2000;17:269–271.

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FIGURE 3.33. Transesophageal echocardiographic diagnosis of aortic arch-left innominate vein fistula. A. Arrow points to the fistulous connection between the aortic arch (ACH) and the left innominate vein (LIV). B. Color Doppler guided continuous-wave Doppler interrogation of the fistula shows very high velocity flow signals moving from the aortic arch into the LIV throughout the cardiac cycle. C,D. The arrow points to an interrupted linear echo in the LIV with flow signals moving across the interrupted area (arrowhead), suggesting LIV pseudoaneurysm or LIV dissection. E. Color Doppler guided pulsed-Doppler examination shows flow signals moving continuously throughout the cardiac cycle across the gap in the linear echo in the LIV. (Reproduced with permission from 

Srinivas Vengala, Navin C. Nanda, Maninder Singh Sidhu, Harvinder S. Dod, Gopal Agrawal, Vikramjit Singh, James K. Kirlin: Transesophageal Echocardiographic Diagnosis of Aortic Arch-Left Innominate Vein Fistula. Echocardiography 2005;22:43–45.

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FIGURE 3.34. Aortic dissection. A. The dissection flap is seen clearly in the ascending aorta, close to but not involving the aortic valve leaflets. B. In another patient, the flap (F, arrowhead) is seen impinging on the aortic leaflets and interfering with their motion. AV, aortic valve; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RA, right atrium; RV, right ventricle; RVO, right ventricular outflow tract; SVC, superior vena cava. C,D. Prolapse of a dissection flap (red arrow) into the left ventricular outflow tract and the resulting severe aortic regurgitation (AR) are shown in a different patient. E. Short-axis view shows a flap in the vicinity of the origin of the left main coronary artery (LMCA) but not involving it. F,G. On the other hand, in two other patients, the dissection flap can be seen extending into the lumen of the LMCA in F and into the right coronary artery (RCA) in G. H,I. Short-axis views at the level of the ascending aorta show a communication (C) between the true lumen (TL) and the false lumen (FL) as well as a thrombus (TH) in the false lumen. J–L. Long-axis views of the ascending aorta show prominent flow signals in both the TL and FL. Note the absence of flow signals in the FL following surgery in L (right panel). M–P. Short-axis and long-axis views of the descending thoracic aorta show dissection. Q,R. Communications (C) between the true or perfusing lumens (PL) and the false or nonperfusing lumens (NPL). Note the presence of two communications in R. S,T. Pulse Doppler demonstrates to-and-fro flow between the PL and NPL. U. Spontaneous contrast in the NPL in the descending aorta consistent with low flow state. V. Thrombus formation. CX, left circumflex artery; LAD, left anterior descending coronary artery; LPV, left pulmonary vein. (B, D, F–H, L–N, and R reproduced with permission from 

Ballal R, Nanda NC, Gatewood R, et al. Usefulness of transesophageal echocardiography in assessment of aortic dissection. Circulation 1991;84:1903–1914.

 C reproduced with permission from 

Nanda NC et al. Transesophageal Echocardiography. American Heart Association Council on Clinical Cardiology Newsletter 1990; Summer: 3–22.

)

FIGURE 3.35. Aortic dissection. A. Long-axis view of the ascending aorta shows a thin linear echo (arrowheads) in the aortic lumen located very close to the anterior aortic wall, mimicking intimal thickening. This echo was immobile. B. Color Doppler examination, in the short-axis view, shows no flow signals in the false lumen (FL). This is an example of intramural dissection. There is no communication with the aortic lumen. AO, aorta; LA, left atrium; RPA, right pulmonary artery; TL, true lumen. (Reproduced with permission from 

Mehta R, Nanda NC, Roychoudhury D, et al. Atypical aortic dissection diagnosed by transesophageal echocardiography. Echocardiography 1994;11:261–263.

)

FIGURE 3.36. Left sinus of Valsalva dissection. A,B. Longitudinal plane examination of the aortic root. A depicts a sac-like dissection cavity (D) with a narrow neck (black arrow) connecting to the left sinus of Valsalva. B shows color Doppler flow signals entering the dissection cavity (D) as well as mosaic-colored signals filling the whole of the left ventricular outflow tract (LVO) in diastole, indicative of severe aortic regurgitation (AR). The left main coronary artery (LM) is not enlarged. LA, left atrium; LV, left ventricle;RV, right ventricle. C–F. Transverse plane examination of the aortic root. C. Systolic frame shows all three cusps of the aortic valve as well as the dissection cavity (D). D.Diastolic frame shows the dissection cavity (D) filled with color-flow signals as well as mosaic signals of AR. AV, aortic valve; E,F. The hematoma (H) lining the dissection cavity near the origin of the anterior mitral leaflet (MV). RVO, right ventricular outflow tract; LC, left coronary; NC, noncoronary; RC, right coronary. (Reproduced with permission from 

Maxted W, Sanyal R, Nanda NC, et al. Transesophageal echocardiographic detection of sinus of Valsalva dissection. Echocardiography 1995;12:99–102.

)

FIGURE 3.37. Proximal right coronary artery dissection extending into the aortic root. A. Coronary angiogram shows dissection (arrows) of the right coronary artery (RCA). B.Left ventriculogram shows the contrast dye (arrows) outside the lumen of the ascending aorta (AO). C. The aortic short-axis view demonstrates a dissection flap (solid arrow) in the lumen of the RCA as well as in the adjacent portion of the aortic root (open arrow). D,E. Longitudinal plane examination shows the dissection flap (open arrow, F) in the region of the right coronary sinus of the aortic root, viewed in oblique long-axis view. LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RA, right atrium;RVOT, right ventricular outflow tract. (Reproduced with permission from 

Varma V, Nanda NC, Soto B, et al. Transesophageal echocardiographic demonstration of proximal right coronary artery dissection extending into the aortic root. Am Heart J 1992;124:1055–1057.

)

FIGURE 3.38. Aortic dissection. A–D. The dissection flap (F, arrow), together with associated severe aortic regurgitation (AR), is well visualized. E. The dissection flap (arrow) can be clearly distinguished from the aortic valve (AV) leaflets (arrowheads). F. The dissection flap (F, arrow) appears to involve the origin of the left main coronary artery (LM). G,H. A thrombus (TH) is seen in the false lumen (FL). I–L. Dissection extending to involve the descending thoracic aorta. Communications between the true lumen (TL) and the FL are visualized in I and L. This patient underwent resuspension of the AV and resection of the ascending aorta with placement of a Hemashield interposition graft. LA, left atrium; LV, left ventricle; PA, pulmonary artery; MPA, main pulmonary artery; RA, right atrium; RV, right ventricle; RVO, right ventricular outflow tract.

FIGURE 3.39. Aortic dissection. A–C. Dissection flaps (arrowheads) are noted close to the aortic valve (AV) leaflets. There is severe aortic regurgitation (arrows in B). In D the dissection appears to involve the origin of the right coronary artery (RCA). FL, false lumen; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle; TL, true lumen.

FIGURE 3.40. Aortic dissection. A,B. Because of the aortic valve–like motion of the dissection flap, this patient was initially labeled as having a double aortic valve. C. One large communication between the true (TL) and false lumens (FL) is noted in the aortic arch. D. Reduplication of the dissection flap (F). E. Two communications (arrowheads) are present in the descending aorta. F. Thrombus (TH) formation and another communication (arrowhead) are noted more distally in the descending aorta. G. Flow signals confined only to the TL in the descending aorta imaged in long axis. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 3.41. Aortic dissection. A–J. The dissection flap (FL, F) appears to extend up to the origins of the right coronary artery (RCA) and left the main coronary artery (LM). Reduplication of the dissection flap is well seen in D. G–J shows extension of the dissection into the descending thoracic aorta imaged in long-axis and short-axis views. Collapse of the true lumen (TL) in diastole and expansion in systole, as shown in the short-axis view in G, result in a characteristic “help” sign when the descending aorta is viewed in real-time motion. AO, aorta; AV, aortic valve; FL, false lumen; LA, left atrium; LAA, left atrial appendage; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle.

FIGURE 3.42. Aortic dissection. A prominent atherosclerotic plaque (arrowhead) in the true lumen (TL) could have predisposed this patient to dissection. FL, false lumen.

FIGURE 3.43. Aortic dissection. A–C. The dissection flap (F) is noted in the aortic root and ascending aorta (ASC AO), and there is severe aortic regurgitation (AR). Because there was no involvement of the descending thoracic aorta, this dissection was classified as DeBakey type II. AO, aorta; LA, left atrium; LV, left ventricle; MV, mitral valve; RV,right ventricle.

FIGURE 3.44. Aortic dissection. A–C. The dissection in this patient involves only the descending thoracic aorta, which is imaged in the long and short axes (DeBakey type Ill or Stanford type B dissection). There is associated left pleural effusion (PLE). F, dissection flap; FL, false lumen; L, lung echoes; PV, pulmonary valve; TL, true lumen.

FIGURE 3.45. Traumatic rupture of atherosclerotic plaque producing aortic isthmus dissection. Multiplane transesophageal echocardiographic examination. A. The arrowhead indicates the site of rupture in the atherosclerotic plaque (white arrow). Black arrow shows resulting dissection. The site of rupture is at the junction of a relatively less calcified and a heavily calcified area of the plaque. B. Color Doppler examination showing flow signals moving from the aorta (AO) into the false lumen (black arrow) through the site of rupture (arrowhead). C. Circumferential extent of the aortic dissection (arrow). Note the relationship of the left subclavian artery (LSA) to the dissection. D.The intravenous injection of normal saline results in opacification of the pulmonary artery (PA). Black arrowhead points to left pleural effusion, and the echo density within it represents the lung tissue. E. The arrowhead shows a large heavily calcified atherosclerotic plaque protruding prominently into the lumen of the proximal descending thoracic aorta (AO). This plaque is intact. F. The arrowhead points to an atherosclerotic plaque lining the proximal segment of the LSA visualized in both short- and long-axis views. TL, true lumen. (Reproduced with permission from 

Aditya K. Samal, Navin C. Nanda, Robert W. Biederman, Joan B. de Sousa Jr., Abraham S. John, Anil Nanda, Anita Nanda, David McGiffin: Traumatic Rupture of Atherosclerotic Plaque Producing Aortic Isthmus Dissection. Echocardiography 1998;695–701.

)

FIGURE 3.46. Aortic dissection. A,B. Compression of the true lumen. The ascending aortic (AA, ASC, AO) true lumen (TL) appears in this patient to be compressed (arrow in B) by the thrombosed (T, TH) false lumen (FL). F, dissection flap. C,D. Rupture into the mediastinum (another patient). The arrow in C points to the site of a contained rupture in the ascending aorta with the development of false aneurysm and hematoma (H) in the mediastinum. The hematoma extends around the pulmonary arteries and the left atrium (D). Constrast echoes are seen in the main and right pulmonary arteries; these resulted from an intravenous injection of normal saline. (Reproduced with permission from 

Ballal R, Nanda NC, Gatewood R, et al. Usefulness of transesophageal echocardiography in assessment of aortic dissection. Circulation 1991;84:1903–1914.

)

FIGURE 3.47. Aortic dissection. Rupture into the right ventricle. A–D. In addition to the typical dissection flap (F, DIFP) in the aortic root, an abnormal linear echo is seen in the right ventricle (RV). E,F. Color Doppler demonstrates turbulent flow (arrows) in the RV originating in the region of the linear echo, consistent with dissection rupture into the RV. G,H. Communication (arrows) between the aorta (AO) and RV is demonstrated. AV, aortic valve; AR, aortic regurgitation; MV, mitral valve; LA, left atrium; LV, left ventricle; PAN, PANY, pseudoaneurysm; RA, right atrium; RPA, right pulmonary artery; VS, ventricular septum.

FIGURE 3.48. Aortic dissection. The side lobe (SL) artifact from a prosthetic aortic valve (P) can be distinguished from the dissection flap by its arc-like appearance and its extension to nonaortic structures such as the left atrium (LA). FL, false lumen; LV, left ventricle; TH, thrombus in false lumen; TL, true lumen.

FIGURE 3.49. Aortic dissection. Graft replacement of the proximal aorta following aortic dissection. In this transgastric view, the graft can be identified by its serrated appearance. AV, aortic valve; AML, anterior mitral leaflet; LV, left ventricle; RA, right atrium.

FIGURE 3.50. Aortic dissection. A,B. Graft to left main coronary artery (LMCA). Transverse plane examination. Short-axis view of ascending aorta (AO) in the postcardiopulmonary bypass period demonstrates a Cabrol graft (G) and its attachment to the LMCA. Closely packed, short linear echoes in the graft wall represent corrugations in the Dacron graft. LA, left atrium. (Reproduced with permission from 

Ballal R, Nanda NC, Gatewood R, et al. Usefulness of transesophageal echocardiography in assessment of aortic dissection. Circulation 1991;84:1903–1914.

)

FIGURE 3.51. Aortic dissection. Intraluminal tube graft dehiscence. A–H. The large space between the graft (G) and the native aortic aneurysm walls (arrows in A) indicate graft dehiscence, which is definitively identified by the presence of flow signals moving from the graft into the space (arrows in C,G). Graft dehiscence is also suggested by the discontinuity of the graft wall (arrow in E). Therefore, the graft dehiscence in this patient occurred in its proximal attachment to the aortic aneurysm. D shows severe aortic regurgitation and a dissection flap (F) beyond the graft. F shows a portion of the dehisced graft (arrowhead) protruding into the native lumen. AO, aorta; FL, false lumen; LA, left atrium; LM, left main coronary artery; LV, left ventricle; PA, pulmonary artery; RV, right ventricle; RVO, right ventricular outflow tract; TL, true lumen.

FIGURE 3.52. Aortic dissection. Intraluminal graft dehiscence at coronary anastomoses and pseudoaneurysm rupture into right atrium (RA). A–C. Multiplane images at plane angles of 144°, 153°, and 51° demonstrate the aortic tube graft (G). Color Doppler flow imaging shows prominent signals within the tube graft, as well as in the aortic wrap-around/aortic pseudoaneurysm (open arrow) in B and C. Localized kinking of the graft is also noted posteriorly in A (closed arrow). D–I. Two discrete areas of graft dehiscence with flow signals moving from the graft into the aortic pseudoaneurysm (AO) are noted in the regions of right (RCA, open arrow) and left main (LM, closed arrow) coronary anastomoses, visualized at various plane angulations. Ostia and proximal portions of both coronary arteries are patent and show good flow signals. J,K. Mosaic-colored signals (arrow) indicative of turbulent flow are noted in the right atrial appendage (RAA). LA, left atrium; LV, left ventricle; RA, right atrium; RCA, right coronary artery; RV, right ventricle; RVO, right ventricular outflow tract. (Reproduced with permission from 

Roychoudhury D, Nanda NC, Kim KS, et al. Transesophageal echocardiographic diagnosis of aortic graft dehiscence at coronary anastomoses and pseudoaneurysm rupture into right atrium. Echocardiography 1995;12:495–499.

)

FIGURE 3.53. Aortic dissection. Graft dehiscence. A–C. Both the transverse (T) and longitudinal (L) planes demonstrate a large area (8 mm in maximum size) of posterior aortic (AO) graft (G) dehiscence (solid arrow) at the level of the aortic annulus. Prominent flow signals are noted to move in and out of the pseudoaneurysm (open arrow) during the cardiac cycle. The dehisced left main coronary artery (LMCA) arises from the pseudoaneurysm. D,E. Color M-mode and pulsed-Doppler interrogation of the ascending aorta (AO) demonstrate prominent retrograde flow signals (arrow) during diastole, indicative of significant aortic regurgitation (AR). F. Longitudinal (L) plane examination demonstrates a 5-mm dehiscence (closed arrow) in the posterior graft (G) at the level of the aortic annulus. In both longitudinal (F) and transverse plane views (G,H) flow signals are noted in the pseudoaneurysm (open arrow) posteriorly but not anterior to the graft, most likely caused by the attenuation of flow signal intensity by the graft walls. I,J. Transverse (T) plane examination shows a large clot (C) in the pseudoaneurysm (open arrow) compressing (solid black arrow) the aortic graft (G) and the flow signals moving through a localized area of the graft wall posteriorly into the pseudoaneurysm, consistent with dehiscence (solid yellow arrow). The site of dehiscence is located approximately 1.8 cm cephalad from the aortic annulus. K. Transverse (T) plane examination shows prolapse (arrow) of the noncoronary cusp of the aortic valve as well as flow signals filling approximately half of the proximal left ventricular outflow tract, consistent with moderately severe AR. L. Intact attachment of the graft (G) with the distal ascending aorta (A). M,N. Longitudinal (L) plane examination shows dehiscence (solid arrow) of the aortic graft (G) approximately 2 cm above the annulus with flow signals moving in and out of the localized pseudoaneurysm (open arrow) during the cardiac cycle. The left main coronary artery (LMCA) is dehisced and arises from the pseudoaneurysm. O. The distal portion of the aortic graft (G) viewed in short axis during transverse (T) plane examination demonstrates a large space (arrow) anteriorly filled with flow signals, consistent with distal graft dehiscence. P. Longitudinal (L) plane examination shows mosaic flow signals completely filling the proximal left ventricular outflow tract in diastole, indicative of severe AR. In addition, flow signals are noted moving from the region of the aortic prosthesis (P) into the right ventricle (RV), denoting the presence of an aortic–right ventricular fistula (solid arrow). Pulsed-Doppler examination of the fistula reveals continuous flow throughout the cardiac cycle (open arrow). A–E, F–H, I–L, and M–P are four different patients. AO, aorta; AML, anterior mitral leaflet; LA, left atrium; LV, left ventricle; MPA, main pulmonary artery; RPA, right pulmonary artery; (Reproduced with permission from 

Ballal RJ, Gatewood RP, Nanda NC, et al. Usefulness of transesophageal echocardiography in the assessment of aortic graft dehiscence. Am J Cardiol 1997;80:372–376

)

FIGURE 3.54. Aortic dissection. A patient with Marfan's syndrome who had an earlier graft repair of descending thoracic aortic dissection is shown. A,B. The junction of the graft (G) with the native descending aorta (DA) is well visualized. Also note the presence of the dissection flap (F) in the DA beyond the graft junction and the communication (arrow) between the true lumen (TL) and the false lumen (FL). In addition, a hematoma (H) is visualized posteriorly between the aorta and the esophagus, indicative of a contained rupture, for which this patient underwent reoperation. C,D. Communication (arrow) between the TL and FL imaged in short axis. E. Reduplication of the dissection flap. F. A linear, mobile echo (arrowhead) in the false lumen that could represent a fibrin plug, which helped contain the rupture, preventing exsanguination. The arrow points to the dissection flap (F). The patient also underwent aortic valve replacement because of severe aortic regurgitation (arrowhead in H) resulting from dilatation of the aortic root (AO) and sinuses (arrowheads in G). There was no evidence of dissection in the ascending aorta or the arch. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 3.55. Aortic dissection. Graft replacement of abdominal aortic aneurysm. A. Transverse plane imaging of the descending thoracic aorta demonstrates a communication (arrow) in the dissection flap with prominent flow signals moving from the true lumen (TL) into the false lumen (FL) in systole (left) and from the false lumen into the true lumen in diastole (right). B,C. Transgastric views. B. Left panel: Longitudinal plane imaging demonstrates intact anastomosis (arrows) between the lower abdominal aorta (AO) and the graft (G). Right panel: transverse plane imaging views the graft in short axis. C. Schematic representation. In this patient who underwent graft replacement of abdominal aortic aneurysm, transesophageal echocardiography was requested in the immediate postoperative period because of clinical suspicion of graft suture dehiscence. It was not possible to do a surface abdominal ultrasound study because of the dressings covering a fresh abdominal incision. The subsequent clinical course of the patient supported the transesophageal echocardiographic finding that the graft was intact. IN, intestines; LRV, left renal vein; ST, stomach. (Reproduced with permission from

Chouinard M, Pinheiro L, Nanda NC, et al. Transgastric ultrasonography: a new approach for imaging the abdominal structures and vessels. Echocardiography 1991;8:397–403.

)

FIGURE 3.56. Aortic atherosclerosis. A,B. The descending aorta (DA), imaged in the transverse (T) plane, shows multiple mobile linear echoes (arrows) representing atherosclerotic plaques protruding from the aortic wall into the lumen. C,D. Multiple toes with necrotic areas from peripheral systemic embolization, which developed following cardiac catheterization. E. Microscopic section of the punch biopsy taken from the sole of the left foot demonstrates clefts within the lumen of a vessel that represent cholesterol crystals dissolved on histologic processing. (Reproduced with permission from 

Koppang J, Nanda NC, Coghlan C, Sanyal R. Histologically confirmed cholesterol atheroemboli with identification of the source by transesophageal echocardiography. Echocardiography 1992;9:379–383.

)

FIGURE 3.57. Aortic atherosclerosis. A–E. The arrows point to multiple, prominent mobile atherosclerotic plaques in the ascending aorta (AO)

FIGURE 3.58. Aortic atherosclerosis. A. Three different types of atherosclerotic plaques are seen in the aortic arch: a linear plaque (upper solid arrow); a thick, rounded immobile plaque (lower solid arrow); and uniform intimal atherosclerotic thickening (lower open arrow). B,C. M-mode studies demonstrate plaque (PL) mobility. AO, aorta.

FIGURE 3.59. Aortic atherosclerosis. A. Multiple mobile and immobile plaques (arrows) are shown in the aortic arch. B. In another patient a shallow plaque ulceration (arrow) and a much deeper ulceration (arrowhead), which is more clearly identified because of flow signals in it, are seen. C,D. Other plaque ulcerations in the aortic arch in this patient are identified by color Doppler. E–H. Flow signals (arrows) outline deep penetrating ulcerations in the atherosclerotic plaques in the same patient shown in AAO, aorta,DA, descending aorta.

FIGURE 3.60. Aortic atherosclerosis. A. Uniform atherosclerotic intimal thickening (arrowheads) in the ascending aorta (AA) and arch (ACH). B. Shadowing (arrowheads) produced by a heavily calcified plaque (CA) present in the proximal ascending aorta in the same patient. C. A hematoma (H) is also present anteriorly behind the ascending aorta and arch. This patient had a contained aortic rupture, the presumed cause being atherosclerosis. AV, aortic valve; LA, left atrium; RPA, right pulmonary artery; RV, right ventricle.

FIGURE 3.61. Aortic atherosclerosis. Descending aorta. A–C. Prominent atherosclerotic plaques (arrows) in the descending aorta (DA, DES AO) in two different patients.

FIGURE 3.62. A–E. Transesophageal echocardiographic identification of left subclavian artery stenosis with steal phenomenon. A. Arrow demonstrates the long stenotic segment of the left subclavian artery (LSA) at a short distance after its origin from the aorta. B. Arrowheads denote large atherosclerotic plaque as the cause of stenosis. C.Color Doppler–guided continuous-wave interrogation of the stenotic segment shows a high peak velocity of 3.5 m/sec (equivalent to a gradient of 49 mm Hg), indicative of severe stenosis. D,E. Reversal of flow is noted in the left vertebral artery (VA), consistent with steal phenomenon. R, artifactual reverberations. (Reproduced with permission from 

Osman M. Mukhtar, Andrew P. Miller, Navin C. Nanda, Anthon R. Fuisz, Virender K. Puri, Srinivasa R. Aaluri, Dilek Yesilbursa, Wen Ying Huang, Kamlesh Ansingkar, Paula Ross: Transesophageal Echocardiographic Identification of Left Subclavian Artery Stenosis with Steal Phenomenon. Echocardiography 2000;17:197–200.

)

FIGURE 3.63. Transesophageal echocardigoraphic identification of bilateral vertebral artery stenosis. A,B. The arrow points to stenosis at origin of the left vertebral artery (LVA) that arises from the left subclavian artery (LSA). Color Doppler–guided continuous-wave Doppler interrogation of the LVA demonstrates high peak systolic and peak end-diastolic velocities of 3.8 m/sec and 1.7 m/sec, respectively, indicative of severe ostial stenosis (bottom left inset in A). The bottom right inset in A demonstrates normal flow velocities obtained from the LSA. The inset in B reveals normal flow velocities from the more distal precervical LVA segment. C. The arrow points to stenosis at the origin of the right vertebral artery (RVA), which arises from the right subclavian artery (RSA). Color Doppler–guided continuous-wave Doppler interrogation of the RVA demonstrates high peak systolic and peak end-diastolic velocities of 3.7 m/sec and approximately 1.2 m/sec, respectively, indicative of severe ostial stenosis (inset in C). D,E. Cerebral angiogram. The arrow points to severe stenosis at the origin of both LVA and RVA. FA, flow acceleration. (Reproduced with permission from 

Sujood Ahmed, Rajasekhar Nekkanti, Navin C. Nanda, Camilo R. Gomez: Transesophageal Echocardiographic Identification of Bilateral Vertebral Artery Ostial Stenosis. Echocardiography 2003;20:395–398.

)

FIGURE 3.64. Bronchial artery dilatation in a patient with chronic obstructive pulmonary disease. A. A long segment of a dilated bronchial artery (BA) is seen adjacent to the aortic arch (AO). B. Color Doppler–directed pulsed-Doppler interrogation of the bronchial artery shows anterograde flow in both systole and diastole. The peak systolic velocity was 1.2 m/sec and the peak diastolic velocity was 0.6 m/sec. (Reproduced with permission from 

Seung-Wan Kang, Rajasekhar Nekkanti, Navin C. Nanda, David Z. Lan: Transesophageal Echocardiographic Finding of Bronchial Artery Dilatation in Chronic Obstructive Pulmonary Disease. Am J Geriatric Cardiol 2002;11:193–194.

)

FIGURE 3.65. Transesophageal echocardiographic identification of posterior intercostal artery stenosis. A. The arrowhead indicates a very narrow color Doppler jet width at the ostium of the posterior intercostal artery (PICA) followed by marked poststenotic dilatation. Color Doppler–guided continuous-wave Doppler interrogation of PICA reveals a very high peak systolic flow velocity of 3.2 m/sec. B. Another patient with PICA stenosis. The arrowheads indicate the atheromatous plaques encroaching and narrowing the ostium of the PICA imaged in transverse (left) and longitudinal (right) examination planes. Color Doppler–guided continuous-wave Doppler interrogation of the PICA (left inset) reveals a high peak systolic flow velocity of 2.23 m/sec. DA, descending aorta. Orientation symbols: A, anterior; I, inferior; L, left; P, posterior; R, right; S, superior. (Reproduced with permission from 

Barugur S. Ravi, Navin C. Nanda, Thein Htay, Harvinder S. Dod, Gopal Agrawal: Transesophageal Echocardiographic Identification of Normal and Stenosed Posterior Intercostal Arteries. Echocardiography 2003;20:609–615.

)

 

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Aaluri S, Miller AP, Nanda NC, et al. Transesophageal echocardiographic detection of left vertebral artery origin stenosis. Echocardiography 2002;19:695–697.

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Ahmed S, Nanda NC, Manchikalapudi P, et al. Transesophageal echocardiographic identification of right vertebral artery. Echocardiography 2002;19:527–530.

Ahmed S, Nekkanti R, Nanda NC, et al. Transesophageal echocardiographic identification of bilateral vertebral artery ostial stenosis. Echocardiography 2003;20:395–398.

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