Atlas of Transesophageal Echocardiography, 2nd Edition (2007)

Chapter 7. Left Ventricular Function Cardiomyopathy

Systolic Function

There is considerable literature devoted to load-independent measures of contractility, but the venerable ejection fraction, for all its load dependence and the well-known and well-described vagaries of measuring it, remains a useful tool for the assessment of ventricular function. Where edges are well defined (with the use of contrast as necessary to visualize endocardium), echocardiography can provide a reasonable estimate of left ventricular ejection fraction.

An advantage of transesophageal echocardiography (TEE) over transthoracic echocardiography (TTE) in the assessment of systolic left ventricular function is its excellent resolution of the endocardium. However, the foreshortening of the four- and two-chamber views of the left ventricle (LV) limits TEE in its capacity to calculate LVEF accurately and so, in practice, TTE is the usual approach to left ventricular ejection fraction (LVEF) calculation. On the other hand, regional wall motion can be effectively assessed, assigning a wall motion score (normal = 1; hypokinetic = 2; akinetic = 3; dyskinetic = 4; aneurysmal = 5) to each of the 17 segments as recommended by the American Society of Echocardiography. The normal myocardium thickens by approximately 30% to 50% and this can be used as a quantitative approach to scoring. In practice, scores for each segment are most often assigned on the basis of visual inspection. The segments correspond, in general, to the distribution of the different coronary arteries, but of course, individual anatomy varies. For instance, the inferior wall would be served by different arteries depending on whether the posterior descending artery arises from the right coronary artery or the left circumflex artery. The segmental scores can be added and divided by the number of segments scored to give an index of global function. An average score of 1.0 with all segments visualized would indicate a completely normal ventricle. A substantial advantage of TEE is the ability to routinely visualize the endocardium well.

Because the left ventricle contracts not only in an inward or radial fashion, but also longitudinally, attempts have been made to assess longitudinal shortening, using Doppler tissue imaging (DTI). A pulsed Doppler sample volume is placed on the mitral annulus on either the septal or the lateral aspect and the flow velocity measured. A peak velocity of 9 cm/sec is consistent with normal longitudinal left ventricular function; decreased velocities indicate diminished function.

Diastolic Function

Unlike TTE, not much work has been done on the assessment of LV diastolic function by TEE, using either Doppler mitral inflow velocities or DTI. In contrast to mitral inflow velocities, the movement of the mitral annulus in diastole has relatively limited load dependence. As a result, the peak early diastolic annular velocity measured by DTI has attained popularity for the assessment of diastolic function. An Em <8 cm/sec, when measured on the septal side, or <13 cm/sec, when measured on the lateral aspect, suggests diastolic dysfunction. Some authors have also used the Em/Am ratio (abnormal <1) but restriction of diastolic filling of the LV or loss of atrial function limits the usefulness of this ratio. Although either the septal or lateral aspect of the mitral annulus can be used, it has been suggested that the septal aspect is less error prone. On the other hand, the septal velocities may be affected by right ventricular function.

A reduced mitral inflow velocity ratio (E/A) is a classical measure of diastolic dysfunction (diagnosed when E/A <1) but is limited by pseudonormalization of the ratio as diastolic function worsens. A Valsalva maneuver can be used to unmask abnormal function, although it is difficult to get some patients to perform a proper Valsalva. Another parameter found useful in assessing LV diastolic function is a ratio of the peak early diastolic velocities obtained from the mitral inflow (E) by regular Doppler imaging and from the mitral annulus by DTI. When the ratio is >15 the left atrial filling pressure is usually elevated and when it is <10 it is usually normal. Values between these are not of diagnostic significance. Percent change in the shortening or relaxation (strain) or the rate of change of deformation (strain rate) between two adjacent points of myocardial tissue has been utilized to assess systolic and diastolic LV longitudinal function. This methodology has been developed to reduce errors introduced by twisting and rotation of the heart during the cardiac cycle when assessing velocities using the standard DTI approach. However, this newer methodology is fraught with significant intra- and interobserver variabilities, which reduce its clinical utility.

It must be added that there is considerable controversy surrounding the diagnosis of heart failure with preserved systolic function and even about the presence of diastolic dysfunction-based heart failure as assessed by the above parameters. Indeed, some authors have advocated the use of a dilated left atrium as a very sensitive measure of elevated filling pressures, which, in the absence of systolic dysfunction, is consistent with a diagnosis of heart failure with preserved systolic function.

DTI is also useful in assessing LV dyssynchrony in patients with cardiomyopathy with markedly reduced LV systolic function (LV ejection fraction <35%) and left bundle branch block. Marked delay in peak annular systolic velocity observed in the LV lateral wall as compared to the septum is an indication of biventricular pacing (resynchronization therapy) in these patients. This shortens the delay, reducing or abolishing dyssynchrony with consequent improvement in LV function.

Echocardiography, in general, is a critically useful tool in the workup for heart failure and dyspnea (and also hypotension). Indeed, one of the most common clinical issues for which echocardiography is ordered is the assessment of the physiology underlying a presentation in heart failure or deciding whether shortness of breath is caused by the heart. The clinical syndrome of heart failure can result from systolic or diastolic dysfunction, valvular disease (including endocarditis), constrictive pericarditis, and even pericardial effusion. All of these are also part of the differential diagnosis of dyspnea. The assessment of diastolic dysfunction has gained increased currency with the recognition that 30% to 50% of patients with heart failure have preserved systolic function.

Generally, TTE is sufficient to make the diagnoses mentioned in the preceding text and to guide therapy. However, TEE offers an effective alternative when TTE is inadequate.

Dilated cardiomyopathy (DCM) is recognized by dilatation of the cardiac chambers and poor ventricular function. The sluggish flow that occurs in these patients may result in thrombus formation that is visible with echocardiography. Ventricular assist devices have been used to support the left and right ventricles. Some examples of imaging of the conduits that are placed in these patients are shown in this chapter.

Hypertrophic cardiomyopathy is characterized by inappropriate hypertrophy of the left ventricle. Although asymmetric septal hypertrophy is the classical presentation, any wall or even the entire ventricle may be involved. Systolic anterior motion of the mitral valve occurs, leading to outflow obstruction. The result is mitral regurgitation and a subvalvular gradient across the left ventricular outflow tract (LVOT). The obstruction of the LVOT results in turbulence that can be recognized on a color flow Doppler. The velocity waveform obtained from conventional Doppler examination of the outflow tract shows a high peak velocity, reflecting the increased pressure gradient. The location of obstruction within the ventricle can be determined. Additionally, there is a slow upslope of the velocity waveform and a more rapid downslope. This differentiates it from fixed LVOT obstruction in which the velocity waveform is symmetric. Midsystolic notching of the aortic valve is another common finding. There is often evidence of reduced diastolic function.

The surgical treatment of this lesion is myomyectomy of the ventricular septum. The resection appears as a “scooped-out” area with echocardiography.

FIGURE 7.1. Hypertrophic cardiomyopathy. A. Prominent systolic anterior motion (SAM) (arrowhead) of the anterior mitral leaflet touching the ventricular septum (VS). B. SAM of both the anterior and posterior mitral leaflets with noncoaptation. The resulting eccentric mitral regurgitation (MR) jet (arrowheads) is demonstrated in C. D,E. M-mode studies demonstrate midsystolic preclosure of the aortic valve (AV; arrowhead in D) and coarse systolic fluttering (arrowheads in the second beat in E). AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 7.2. Hypertrophic cardiomyopathy. A–I. Serial frames demonstrate the closing motion of the mitral leaflets and the development of systolic anterior motion of both anterior and posterior leaflets. LA, left atrium; LV, left ventricle.

FIGURE 7.3. Hypertrophic cardiomyopathy: mitral regurgitation. Serial frames demonstrate changing severity of mitral regurgitation (MR). A. MR appears to be severe. B.There is no MR, or only traces of MR. C–E. The MR is eccentric. F. Mild MR. G. Aliased left ventricle (LV) inflow is noted with the leaflets open in diastole. LA, left atrium; MV, mitral valve.

FIGURE 7.4. Hypertrophic cardiomyopathy. A. Prominent systolic anterior motion (SAM) of the anterior mitral leaflet touching the ventricular septum (VS) is seen. B.Prominent systolic turbulent flow in the narrowed left ventricular outflow tract (LVOT) as well as significant eccentric mitral regurgitation (MR). C. A schematic shows asymmetric VS hypertrophy (ASH), narrow LVOT with turbulent flow, SAM of anterior mitral leaflet and MR. LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle.

FIGURE 7.5. Hypertrophic cardiomyopathy. A,B. Turbulent systolic flow in the narrowed left ventricular outflow tract (LVOT) and eccentric mitral regurgitation (MR) jet. C.Color flow-directed continuous wave Doppler demonstrates a high velocity of 3 m/sec in the LVOT. The slope of the upstroke of the Doppler velocity waveform is less (slower) than the downslope, typical of hypertrophic cardiomyopathy. LA, left atrium; LV, left ventricle; LVO, left ventricular outflow tract; MV, mitral valve; RV, right ventricle; VS, ventricular septum.

FIGURE 7.6. Hypertrophic cardiomyopathy. A–C. Systolic anterior motion (SAM) of anterior mitral leaflet touching the ventricular septum (VS), with turbulent systolic flow in left ventricular outflow tract (LVOT) and mitral regurgitation (MR). This patient underwent a myectomy. D. The site of myectomy (scooped-out portion of the VS). AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 7.7. Hypertrophic cardiomyopathy. A–C. Systolic anterior motion (SAM) of mitral valve, turbulent systolic flow in the left ventricular outflow tract (LVOT), and a large mitral regurgitation (MR) jet with a large zone of flow acceleration and systolic backflow (SBF) in the left upper pulmonary vein (LUPV), indicative of severe MR. D. This patient also underwent myectomy; the arrow shows the scooped-out site. Note the presence of residual SAM. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; PV, pulmonary valve; RV, right ventricle; VS, ventricular septum.

FIGURE 7.8. Hypertrophic cardiomyopathy. A,B. Systolic anterior motion (SAM) of anterior mitral valve (MV) leaflet is well seen. C. A transgastric view shows marked left ventricular hypertrophy (LVH). D. Turbulent systolic flow in left ventricular outflow tract (LVOT) and mild mitral regurgitation (MR). E. Following myectomy, the LVOT has widened and the SAM has practically disappeared. The arrow shows the characteristic scooped-out appearance of the ventricular septum (VS) after myectomy. AO, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 7.9. Hypertrophic cardiomyopathy. A. The scooped-out area (arrow) of myectomy following surgery. Inset: the preoperative image demonstrates mitral systolic anterior motion (SAM) (arrowheads) and a narrow left ventricular outflow tract (LVOT). B. The left upper pulmonary vein (PV) and mitral inflow tracings from another patient with hypertrophic cardiomyopathy are shown. Note the presence of a small E and a large A wave on the mitral tracing and a large S wave, a small D wave, and a prominent biphasic A wave on the pulmonary vein flow tracing. The increased duration of pulmonary vein A wave compared to the mitral A wave is indicative of increased left ventricle (LV) end-diastolic pressure. C–E. Gross specimens from three other patients show hypertrophic cardiomyopathy. D,E. Right ventricular (RV) hypertrophy, often associated with this entity, is seen. AO, aorta; LA, left atrium; MV, mitral valve; RA, right atrium; RVO, right ventricular outflow tract.

FIGURE 7.10. Apical hypertrophic cardiomyopathy. A–C. The arrow shows marked hypertrophy in the left ventricle (LV) apical region. The proximal ventricular septum (VS), seen well in A, is only mildly hypertophied. D,E. Postoperative images; the arrowheads show the area of muscle resection. F. A short-axis view of the LV shows marked hypertrophy of the LV free wall (open arrow) and mild hypertrophy of the ventricular septum (VS) (closed arrow) and inferior wall. AO, aorta; LA, left atrium; RA, right atrium;RV, right ventricle; RVO, right ventricular outflow tract.

FIGURE 7.11. Dilated cardiomyopathy. Diastolic (A) and systolic (B) frames show poor left ventricle (LV) function. C. Midsystolic notching of the aortic valve (AV) is seen on M-mode examination, consistent with low cardiac output and significant mitral regurgitation (MR). D. A thrombus in the left atrial appendage (LAA) imaged from the transgastic approach. E. Diminished systolic S wave in the left upper pulmonary vein (PV) Doppler tracing is consistent with poor LV function and moderate MR. F. Dilated right atrium (RA), right ventricle (RV), and coronary sinus (CS), also typical of dilated cardiomyopathy. G. Prominent trabeculation (arrowheads) in the RA free wall resulting from hypertrophy. These should not be confused with thrombi. H. RA free wall hypertrophy. I. Four-chamber view from a patient with dilated cardiomyopathy shows dilatation of all four cardiac chambers. J. Another patient with dilated cardiomyopathy demonstrating a thrombus (arrowhead) located in the LV adjacent to the posterior mitral leaflet. K,L. Gross specimens show dilated LV and RV. LAA, left atrial appendage; LCX, left circumflex; LPA, left pulmonary artery; LUPV, left upper pulmonary vein; MV, mitral valve; RAA, right atrial appendage; RPA, right pulmonary artery; RVO, right ventricular outflow tract; SVC, superior vena cava; TV, tricuspid valve.

FIGURE 7.12. Dilated cardiomyopathy: right ventricular assist device. A,B. A right ventricular (RV) assist device (arrows) placed in this patient with dilated cardiomyopathy. The arrowheads demonstrate acoustic shadowing produced by the metallic device. LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium.

FIGURE 7.13. Mechanical biventricular assist device. The arrangement of a biventricular assist device, with the right-sided device pumping blood from the right atrium to the pulmonary artery and the left-sided device pumping blood from the left atrium to the aorta. (Reproduced with permission from 

Holman W. VAD approved as a bridge to transplantation. Birmingham, AL: UAB Insight, 1989; Vol. 1, No. 2.


FIGURE 7.14. Mechanical biventricular assist device. A. Using biplane imaging, the Teflon conduit (arrows) is identified by the transverse serrations in its walls, and its attachment to the ascending aorta (AO) is well delineated. The main pulmonary artery (PA) is imaged posterior to the aorta. B. Mosaic-colored signals indicative of turbulent flow are noted moving through the conduit into the ascending aorta. Similar flow signals are also noted in the main pulmonary artery. C. Pulsed Doppler examination of the conduit reveals prominent phasic flow signals. The electrocardiogram here and in A shows ventricular fibrillation. D. Using the standard single plane technique, the communication between the conduit and the aorta could not be delineated, even on extensive exploration of this region. E. Examination of the left ventricle (LV) shows a large thrombus occupying the apical region. LA, left atrium. (Reproduced with permission from 

Parks J, Nanda NC, Bourge RC, et al. Transesophageal echocardiographic evaluation of mechanical biventricular assist device. Echocardiography 1990;7:561–566.


FIGURE 7.15. Malpositioned Thoratec right ventricular assist device. A. The four-chamber view shows the Thoratec cannula (T) lodged in the left atrium (LA). B,C. Color Doppler examination shows a prominent right-to-left atrial shunt (arrowhead). LV, left ventricle; RA, right atrium; RV, right ventricle. (Reproduced with permission from 

Snoddy BD, Nanda NC, Holman WL, et al. Usefulness of transesophageal echocardiography in diagnosing and guiding correct placement of a right ventricular assist device malpositioned in the left atrium. Echocardiography 1996;13:159–163.


FIGURE 7.16. Malpositioned right ventricular assist device. Same patient as in Fig. 7.15. A,B. As the cannula (T) was being withdrawn into the right atrium (RA), a large left-to-right atrial shunt (arrowhead) developed. Note the distortion of the atrial septum in the fossa ovalis region. LA, left atrium; LV, left ventricle; RV, right ventricle. (Reproduced with permission from 

Snoddy BD, Nanda NC, Holman WL, et al. Usefulness of transesophageal echocardiography in diagnosing and guiding correct placement of a right ventricular assist device malpositioned in the left atrium. Echocardiography 1996;13:159–163.


FIGURE 7.17. Malpositioned right ventricular assist device. Same patient as in Figs. 7.15 and 7.16. A,B. When the cannula (T) was securely placed in the right atrium (RA), the left-to-right atrial shunt (arrowhead) became very small. C. The four-chamber view demonstrates tricuspid regurgitation (TR) and mitral regurgitation (MR) and a small left-to-right atrial shunt (arrowhead). The cannula was in the RA. D. Descending thoracic aorta (AO) shows a dissection flap (F). SC, spinal canal; VB, vertebral body. LA, left atrium;LV, left ventricle; RV, right ventricle. (Reproduced with permission from 

Snoddy BD, Nanda NC, Holman WL, et al. Usefulness of transesophageal echocardiography in diagnosing and guiding correct placement of a right ventricular assist device malpositioned in the left atrium. Echocardiography 1996;13:159–163.




Suggested Readings

Bashir JG, Frank G, Tyers O, et al. Combined use of transesophageal ECHO and fluoroscopy for the placement of left ventricular pacing leads via the coronary sinus. Pacing Clin Electrophysiol 2003;26:1951–1954.

Das AK, Wilson GM, Furnary AP. Coincidence of true and false left ventricular aneurysm. Ann Thorac Surg 1997;64:831–834.

Gummert JF, Rahmel A, Bucerius J, et al. Mitral valve repair in patients with end stage cardiomyopathy: who benefits? Eur J Cardiothorac Surg 2003;23:1017–1022; discussion 1022.

Moloney ED, Egan JJ, Kelly P, et al. Transplantation for myocarditis: a controversy revisited. J Heart Lung Transplant 2005; 24:1103–1110.

Posma JL, van der Wall EE, Blanksma PK, et al. New diagnostic options in hypertrophic cardiomyopathy. Am Heart J 1996;132:1031–1041.

Rice MJ, McDonald RW, Li X, et al. New technology and methodologies for intraoperative, perioperative, and intraprocedural monitoring of surgical and catheter interventions for congenital heart disease. Echocardiography 2002;19:725–734.

Smallhorn JF. Intraoperative transesophageal echocardiography in congenital heart disease. Echocardiography 2002;19:709–723.

Thakur AC, Nanda NC, Malhotra S, et al. Combined interatrial and intrapulmonary shunting in orthodeoxia detected by transesophageal echocardiography. Echocardiography 1998;15:101–104.

Vitarelli A, Gheorghiade M. Transthoracic and transesophageal echocardiography in the hemodynamic assessment of patients with congestive heart failure. Am J Cardiol 2000;86:36G–40G.

If you find an error or have any questions, please email us at Thank you!