Atlas of Transesophageal Echocardiography, 2nd Edition (2007)

Chapter 6. Ischemic Heart Disease

Careful transesophageal imaging can reveal a great deal of information about the anatomy of the coronary tree. The presence of stenosis is indicated by the compromise of the lumen. To be certain that what is being imaged is truly a stenosis rather than an artifact produced by an oblique section through the vessel, it is necessary to be able to see normal lumen on either side of the obstruction. Poststenotic dilatation may be present; it suggests a severe stenosis. Other markers of severe stenosis are an elevated pressure gradient across the stenosis by conventional Doppler and the presence of turbulence in the region of the stenosis on color-flow Doppler. The use of echocardiographic contrast may enhance flow visualization. Additional segments of the coronary vessels may be visualized and stenosis identified in these segments following contrast injection. The left main and proximal segments of the left anterior descending, left circumflex, and right coronary arteries, together with some of their branches, can be visualized by transesophageal echocardiography. With newer color Doppler equipment, smaller epicardial and intramyocardial vessels (e.g., septal perforators) can also be seen.

Wall motion abnormalities are also well visualized by transesophageal echocardiography, especially using the transgastric approach. Mitral regurgitation in ischemic heart disease can be recognized and its severity assessed. Mitral annular dilatation and dilatation of the left atrium and left ventricle imply long-standing, significant mitral regurgitation. When the head of the papillary muscle is ruptured, it can often be imaged prolapsing into the left atrium. In up to 30% of patients, however, the ruptured head may not prolapse into the left atrium. In these cases the diagnosis is made by observing the chaotic movement of the ruptured head in the left ventricle. Meticulous examination is important in these cases.

The term pseudoaneurysm refers to a rupture of the ventricle that is walled off by a clot before the patient experiences fatal tamponade. These lesions have a narrow neck (which distinguishes them from true aneurysms) that leads to a walled-off cavity. Pseudoaneurysms are inherently unstable in that they have a propensity to rupture. They should be resected even if discovered late after a myocardial infarction in an otherwise stable patient.

Other mechanical complications that can result from ischemic heart disease include ventricular septal rupture, which is easily seen on color-flow Doppler. Posterior ventricular septal defects are often best visualized using the transgastric approach.

FIGURE 6.1. Coronary lesions. A–G. A. A linear atherosclerotic plaque that produced a 33% stenosis of the left main (LM) lumen. A, width of nonstenotic lumen; B, width of stenosed lumen. B. An eccentric, highly reflectile atherosclerotic plaque (upper arrow) that produced >80% stenosis of the left main coronary artery (LMCA). The presence of normal-sized lumen beyond the stenosed area increases the diagnostic confidence, because it excludes the possibility of artificial narrowing produced by an oblique section through the coronary vessel. C. Another view of the coronary artery shown in B, demonstrating the atherosclerotic plaque (arrow) as well as bifurcation of the LMCA into the left circumflex (LCX) and left anterior descending (LAD) arteries. D,E. A patient with left main ostial stenosis. D. A very narrow color-flow jet (arrow) in the ostium with distal widening. E. Doppler interrogation demonstrates high-velocity (1.13 m/sec) diastolic (DS) flow, further confirming the presence of ostial stenosis. A lower velocity antegrade systolic flow (SF) is also noted. The ostial velocity in this patient is underestimated because of the nonperpendicular orientation of the ultrasound beam relative to the blood flow direction. SV, Doppler sample volume. F,G. Another patient with severe midleft main stenosis with turbulent flow seen beyond the lesion. Pulsed Doppler interrogation reveals a high diastolic velocity. H–J. LAD stenosis. The upper vertical arrows in H point to two atherosclerotic plaques, one located at the ostium and the other more distally, producing severe stenosis. Note the presence of a normal LAD lumen beyond the second lesion. I. Another patient in whom significant proximal LAD stenosis was identified because of flow acceleration and aliasing (arrow). J. Another patient in whom a localized flow acceleration and aliasing (red arrow) identified discrete stenosis at the origin of the LAD. K,L. LCX stenosis. Discrete severe stenosis (arrow), approximately 1 cm from its origin, with poststenotic dilatation in the circumflex (LCX) coronary artery. M,N. Right coronary artery stenosis. Two discrete areas of severe stenosis (arrows), one at the ostium and the other a little more distal, involving the right coronary artery (RCA). O–Q. Contrast echocardiography in assessing coronary stenosis. O. Left panel. Color-flow signals are seen filling the LMCA and the proximal LAD completely, following IV injection of 3 g of Levovist (an echo contrast agent). Right panel: Before injection hardly any flow signals are apparent. P. Left panel: Linear flow signals (arrows) are demonstrated in the LAD (without demonstrating the walls) following IV injection of Levovist. Right panel: This LAD segment could not be demonstrated without contrast injection. Q. Left panel: IV injection of Levovist not only demonstrated flow signals in the LAD but also showed an area of flow acceleration and aliasing corresponding to an area of severe stenosis in the proximal LAD on the coronary angiogram. Right panel: a smaller area of flow signals with a smaller flow acceleration persisting from a previous Levovist injection. Contrast enhancement is useful in demonstrating additional segments of the coronary arteries not visualized on routine examination and demonstrating stenoses in these segments. R–V. LAD stenosis. The arrowheads in R and S show narrowing and interruption of color-flow signals in the LAD (2), indicative of severe stenosis. Color Doppler–guided pulsed Doppler examination (T) in this patient demonstrates a high diastolic velocity of 1 m/sec, also consistent with stenosis. 1, left main coronary artery; 3, left circumflex artery; 4, left atrial branch. Aliased signals in another patient (U) suggest narrowing in the proximal LAD, which is supported by the presence of a high diastolic velocity of 1.3 m/sec obtained by pulsed Doppler examination (V). The red flow signals next to the aliased area in U represent antegrade flow in the anterior interventricular vein, which accompanies the LAD. LM, left main coronary artery. W–Y. Saphenous vein graft. The arrows in W–Y demonstrate a saphenous vein graft (G) originating from the medial aspect of the ascending aorta (AO). LA, left atrium; LAA, left atrial appendage; LV, left ventricle; PA, pulmonary artery; RCA, right coronary artery; RV, right ventricle;RVO, RVOT, right ventricular outflow tract. (C,D,H, and K reproduced with permission from 

Samdarshi TE, Nanda NC, Gatewood RP Jr, et al. Usefulness and limitations of transesophageal echocardiography in the assessment of proximal coronary artery stenosis. J Am Coll Cardiol 1992;19:572–580.

)

FIGURE 6.2. Transesophageal echocardiographic examination of coronary arteries. A. The top arrow points to dilatation of the proximal left anterior descending coronary artery (LAD), whereas the bottom arrow demonstrates turbulent flow in mid-LAD. Pulsed Doppler examination of this area revealed a high diastolic velocity of 1.3 m/sec (arrowhead in the inset), consistent with significant stenosis. B. The top arrow points to turbulent flow in mid-LAD, whereas the bottom arrow shows turbulent flow in the more distal portion of LAD. C. Arrow demonstrates narrowing in the first diagonal branch (arrowhead) of LAD. Continuous-wave Doppler examination reveals a very high diastolic velocity of 3.0 m/sec (arrowhead in the inset), indicative of very severe stenosis. D. The arrows show large segments of proximal, mid, and distal segments of LAD visualized in this view. E. The arrow demonstrates the presence of turbulent flow in the proximal right coronary artery (RCA). F. Pulsed Doppler examination (arrowhead) of RCA demonstrates a high velocity of 1.3 m/sec (arrowhead in the inset), indicative of significant stenosis. G. The arrow points to the presence of turbulent flow in the left circumflex coronary artery. H. The arrow points to the origin of the left circumflex coronary, which appears normal. However, reversed flow (blue) with turbulent flow signals (arrowhead) is noted in the mid and distal portions of the circumflex vessel, consistent with filling from collaterals and significant stenosis. Doppler interrogation of this area shows a high diastolic velocity of 1.0 m/sec (arrowheads in the inset). I. The arrowhead demonstrates turbulent flow signals in the intramyocardial coronary arteries consistent with stenosis. J. The interventricular vein (V) is imaged next to the dilated LAD (arrow). Note that the flow in the interventricular vein is in the direction opposite to that of the LAD flow. K. Coronary angiogram. The top arrowhead demonstrates 90% stenosis at the origin of the diagonal branch. The proximal LAD is dilated, and beyond the dilation, the mid-LAD shows 50% stenosis (just beyond the bottom arrowhead). Note multiple areas of significant stenosis in the more distal segments of LAD. L. The arrow points to total occlusion of the proximal circumflex coronary artery. Retrograde filling of more distal portions of the circumflex vessel from collaterals was noted. M. Coronary angiogram. The arrow points to significant stenosis in the proximal RCA. Note significant stenosis in the mid and distal portions. AO, aorta; LA, left atrium; LAA, left atrial appendage; LAD, left anterior descending artery; LM, left main coronary artery; LV, left ventricle; LVO, left ventricular outflow tract; MV, mitral valve; PA, pulmonary artery; RA, right atrium; RV, right ventricle; RVO, right ventricular outflow tract. (Reproduced with permission from 

Nanda NC, Gomez C, Liu M, et al. Transesophageal echocardiographic diagnosis of coronary stenosis in a stroke patient. Echocardiography 1999;16:589–592.

)

FIGURE 6.3. Left ventricular dysfunction. A. Marked hypokinesis of the anterior septum (arrowheads) is seen in this patient with ischemic heart disease. The inferior wall is also hypokinetic. B. M-mode image from the same patient shows hypokinesis of anterior (ANT) and inferior walls (POST). C. Color Doppler examination in this patient demonstrates two mitral regurgitation (MR) jets resulting from left ventricle (LV) dysfunction. D. Another patient with moderate MR resulting from ischemic heart disease. E,F.Two other patients with mild (E) and severe (F) MR. Because the mitral valve (MV) leaflets appear to be structurally normal, the MR is presumed to be ischemic in origin. In both patients the LV and the mitral annulus were enlarged. G. Dyskinesis of the LV anterior free wall (black arrow) in this transgastric systolic frame in another patient. IW, LV inferior wall. IVS, ventricular septum. LA, left atrium; LAA, left atrial appendage; LUPV, left upper pulmonary vein; RA, right atrium; RV, right ventricle.

FIGURE 6.4. Left ventricular apical aneurysm. A. A bright, fibrotic scar (arrowhead) in the aneurysmal apex. B. A huge left ventricular (LV) apical aneurysm (arrowheads). C.Gross specimen of LV apical aneurysm caused by an acute myocardial infarction. D–F. Another patient with a large apical aneurysm containing a thrombus (arrowheads). F.Color Doppler examination shows the presence of associated mitral regurgitation (MR). G,H. Gross specimens of LV aneurysm with mural thrombus. I. Aneurysmal proximal inferior wall (arrowheads) is seen in the two-chamber view. Note the myocardial thinning, which is well seen. LA, left atrium; LAA, left atrial appendage, LVO, left ventricular outflow tract; MV, mitral valve; RV, right ventricle.

FIGURE 6.5. Left ventricular pseudoaneurysm. The arrows in A and B show the communication of the left ventricle (LV) with a large pseudoaneurysm (PSA). In B and C the pseudoaneurysm appears to be larger than the LV cavity. D. Color Doppler examination reveals flow signals moving from the LV into the PSA through the relatively narrow neck (arrowheads). Pseudoaneurysms are differentiated from true aneurysms by their narrow necks; in pseudoaneurysms the neck or mouth is smaller than the aneurysm cavity, whereas in true aneurysms the mouth or neck is much larger, often as large as or larger than the cavity. RV, right ventricle.

FIGURE 6.6. Contained slit-like cardiac rupture following acute myocardial infarction. A–E. Transgastric views (A,B) show a large and narrow color jet (arrow) within the left ventricle (LV) posterior wall. B also shows color-flow signals partially filling the pseudoaneurysm cavity (PAN). In C, the color Doppler was turned off, revealing an echo-free space (arrow), which corresponded to the site of the color jet seen in A; however, it could not otherwise be distinguished from an artifactual echo “dropout.” Associated moderate mitral regurgitation (MR) is noted in D. E. Postoperative image shows absence of color-flow signals within the myocardial wall. F. Gross specimen from another patient shows a contained LV rupture. LA, left atrium; RA, right atrium; RV, right ventricle. (A–E reproduced with permission from 

Rao A, Garimella S, Nanda NC, et al. Transesophageal color Doppler echocardiographic diagnosis of cardiac rupture following acute myocardial infarction. Echocardiography 1996;13:309–312.

)

FIGURE 6.7. Ventricular septal rupture. A–C. Ventricular septal rupture (R) with an apical aneurysm (AN). D,E. Color Doppler examination shows shunting of flow across the ruptured interventricular septum into the right ventricle (RV) (arrows). F. Gross specimen from another patient shows a probe passing through a ruptured ventricular septum (VS). LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle.

FIGURE 6.8. Ventricular septal rupture after acute anterior myocardial infarction. A. Apical five-chamber view. Flow signals are seen moving from the left ventricle (LV) into the right ventricle (RV) through the large apical defect (arrows). B. The patch (solid arrow) used to close the defect. C. Transgastric views (transverse plane imaging) from the same patient show marked enlargement and widening of the ventricular septum (VS), with large areas of echolucency consistent with dissection (horizontal open arrows in C). Color Doppler imaging shows prominent color-flow signals (maximal width 10 mm) moving from the LV into the ventricular septum (VS) (vertical open arrow in C) and occupying the large echolucent areas seen on the non-color Doppler image. The prominent area of localized relatively high-velocity signals (flow acceleration) noted in the LV measured 9 mm at the site of the defect. No corresponding defect at the same level is seen on the right ventricular aspect, but two smaller sites of rupture, both 5 mm in size, are noted on the right side further posteriorly (solid arrows in C). These are associated with smaller areas of flow acceleration (1.5 to 2 mm). These defects are not delineated on the two-dimensional image, but are visualized only during color Doppler examination. Therefore, the patient has four defects in the VS, one very large and located in the apical region, and the other three much smaller and located more posteriorly. None of the findings noted in C were demonstrated by transthoracic echocardiography. VSD, ventricular septal defect. LA, left atrium. (Reproduced with permission from 

Ballal RS, Sanyal RS, Nanda NC, et al. Usefulness of transesophageal echocardiography in the diagnosis of ventricular septal rupture secondary to acute myocardial infarction. Am J Cardiol 1993;71:367–370.

)

FIGURE 6.9. Ventricular septal rupture after acute inferior myocardial infarction. Transgastric views. A. Transverse plane imaging demonstrates mosaic color signals indicative of turbulent blood flow moving from the left ventricle (LV) through the posterior ventricular septum (P) into the right ventricle (RV). The arrow indicates a localized area of increased velocity with aliasing (flow acceleration) on the left ventricular side of the defect. Note that the defect is not identified on the non-color Doppler two-dimensional image. Top A, ascitic fluid; bottom A, anterior ventricular septum. B,C. Longitudinal plane imaging demonstrates mosaic signals moving from the LV into the RV through the inferior portion of the ventricular septum during systole (left panel in B and C). The diastolic frame (right panel in B) reveals right-to-left shunt (red flow signals) through a large area of ventricular septal defect (VSD, arrowheads). With the use of both transverse and longitudinal plane imaging, the site of rupture was correctly identified in the inferior aspect of the posterior septum. L, liver; C, Swan-Ganz catheter. D. Color M-mode examination shows flow signals moving from the RV into the LV during diastole (open arrow). Mosaic-colored signals in the RV during systole are denoted by solid arrows. LA, left atrium; MV, mitral valve; PA, pulmonary artery; RA, right atrium. (Reproduced with permission from 

Ballal RS, Sanyal RS, Nanda NC, et al. Usefulness of transesophageal echocardiography in the diagnosis of ventricular septal rupture secondary to acute myocardial infarction. Am J Cardiol 1993;71:367–370.

)

FIGURE 6.10. Ventricular septal rupture after acute inferior myocardial infarction. A. Four-chamber view shows an irregular defect that extends from the middle of the ventricular septum (VS) on the left side to the apical region on the right side (arrows). In addition, a large echo density (arrowhead) is seen attached to a tricuspid valve (TV) leaflet or chord, which demonstrates marked prolapse into the right atrium (RA). At surgery, the patient was found to have right ventricular (RV) papillary muscle rupture in addition to VS rupture. B. Another four-chamber view from the same patient demonstrates localized widening (arrows) of the apical portion of the ventricular septum consistent with dissection. C. The same defect (solid arrow) viewed from the transgastric approach (transverse plane imaging). Color Doppler examination shows complete filling of the markedly enlarged RA with aliased flow signals during systole, indicative of severe tricuspid regurgitation (TR). Aliased flow signals also are seen moving from the left ventricle (LV) into the RV through the defect. The open arrow points to the moderator band in the RV. L, liver; PM, posteromedial papillary muscle. LA, left atrium; VSD, ventricular septal defect. (Reproduced with permission from 

Ballal RS, Sanyal RS, Nanda NC, et al. Usefulness of transesophageal echocardiography in the diagnosis of ventricular septal rupture secondary to acute myocardial infarction. Am J Cardiol 1993;71:367–370.

)

FIGURE 6.11. Left ventricular papillary muscle rupture. A,B. Classic findings of prolapse (arrows) of the ruptured papillary muscle head into the left atrium LA in two patients. A. The ruptured head involved the anterior papillary muscle. B. In this case it involved the posterior muscle. AO, aorta; LV, left ventricle; RV, right ventricle; RVO, right ventricular outflow tract. (Reproduced with permission from 

Moursi MH, Bhatnagar SK, Vilacosta I, et al. Transesophageal echocardiographic assessment of papillary muscle rupture. Circulation 1996;94:1003–1009.

)

FIGURE 6.12. Left ventricular papillary muscle rupture. A–C and D–G represent transgastric views in two different patients, both of whom demonstrated erratic motion of the ruptured papillary muscle head (arrows) in the left ventricle (LV). The ruptured head, which involved the posterior papillary muscle in both patients, did not prolapse into the left atrium (LA) in either case. RV, right ventricle. (Reproduced with permission from 

Moursi MH, Bhatnagar SK, Vilacosta I, et al. Transesophageal echocardiographic assessment of papillary muscle rupture. Circulation 1996;94:1003–1009.

)

FIGURE 6.13. Left ventricular papillary muscle rupture. A. Five-chamber view shows a flail anterior mitral leaflet (arrowhead) prolapsing into the left atrium (LA), but the ruptured papillary muscle head (arrow) remains in the left ventricle (LV) just beneath the posterior leaflet. B. Transgastric view demonstrates the anterior position of the ruptured head (arrow), which involved the anterior papillary muscle. AO, aorta; MV, mitral valve; RV, right ventricle. (Reproduced with permission from 

Moursi MH, Bhatnagar SK, Vilacosta I, et al. Transesophageal echocardiographic assessment of papillary muscle rupture. Circulation 1996;94:1003–1009.

)

FIGURE 6.14. Left ventricular papillary muscle rupture. A–C. The ruptured posterior papillary muscle head (arrows) moving back and forth between left ventricle (LV) and left atrium (LA). AO, aorta; RVO, right ventricular outflow tract.

FIGURE 6.15. Left ventricular papillary muscle rupture. Color M-mode examination in another patient with papillary muscle rupture shows systolic backflow (arrows) extending deep into the right upper pulmonary vein (RUPV), indicative of torrential mitral regurgitation (MR). LA, left atrium.

FIGURE 6.16. Left ventricular papillary muscle rupture. A,B. The ruptured papillary muscle head is not visualized in left atrium (LA), and the findings resemble chordae (CH) rupture (arrow in B). C–G. Careful examination, however, clearly shows the ruptured papillary muscle head (arrow) moving back and forth between the left ventricle (LV) and the LA. D. The site of rupture of the papillary muscle (PM) is clear; the shape of the ruptured head (arrow) matches that of the PM still attached to the LV wall. F,G. Chordae (arrowheads) in the LV. H,I. Color Doppler examination shows an unimpressive small eccentric mitral regurgitation (MR) jet. However, the zone of flow acceleration (arrowheads in H) is large, and color Doppler–guided pulsed Doppler examination (J) shows prominent aliased systolic backflow (SBF) in the left upper pulmonary vein (LUPV), indicative of severe MR. Note the presence of associated mild tricuspid regurgitation (TR) in I. D, A, diastolic, and atrial systolic waves in the pulmonary vein tracing. AO, aorta; AV, aortic valve; LAA, left atrial appendage; MV, mitral valve; RA, right atrium; RV, right ventricle; TV, tricuspid valve.

FIGURE 6.17. Left ventricular papillary muscle rupture. A. Diastolic frame. B,C. A small ruptured head (arrows) prolapsing into the left atrium (LA). AO, aorta; LV, left ventricle; RV, right ventricle; MV, mitral valve.

FIGURE 6.18. Left ventricular papillary muscle rupture. A. The ruptured head (arrow), which remains in the left ventricle (LV) in systole and does not prolapse into the left atrium (LA). In our experience, in approximately 30% of patients, the ruptured head does not prolapse into the LA and the diagnosis is made by observing its chaotic motion in LV. B. Gross specimen from another patient shows a ruptured papillary muscle (PM)

FIGURE 6.19. Right ventricular papillary muscle rupture. A,B. Transgastric views. A. The ruptured posterior right ventricular papillary muscle (M) is seen in the region of the posterior tricuspid leaflet (P) in systole. B. Anterior (A) and posterior (P) leaflets in the open position in diastole. C. The ruptured M in the right atrium (RA). The arrow points to an associated ventricular septal rupture. D. Associated severe tricuspid regurgitation (TR). LA, left atrium; LV, left ventricle; RV, right ventricle; S, septal tricuspid leaflet. (Reproduced with permission from 

Maxted W, Nanda NC, Kim KS, et al. Transesophageal echocardiographic identification and validation of individual tricuspid valve leaflets. Echocardiography 1994;11:585–591.

)

 

 

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