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TELECONFRENCES
2004
The Changing Left Ventricle

2003
Aortic Valve Disease: New Dimensions in Evaluation and Management

2002
Heart Failure: Echo's Role in and Emerging Health Crisis

2001
Chest Pain in Children & Adults: The Role of Echo

2000
Mitral Regurgitation: New Concept

1998
The Falling Left Ventricle: Diastolic & Systolic Function

1997
Changing the Outcome of Coronary Artery Disease
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Chest Pain in Children and Adults

Mitral Regurgitation: New Concepts

Diastolic and Systolic Function

Changing the Outcome of CAD

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2000 MV
2001 Chest Pain
2002 Heart Failure



Left Ventricular Hypertrophy
Fig. 1

Chronic elevation of myocardial stress due to pressure overload, as in hypertension or aortic stenosis, causes cardiac muscle to hypertrophy with a resulting increase in myocardial thickness. There is normally little or no change in overall cardiac size, so the wall thickening occurs at the expense of the cavity (Fig. 1 and Fig. 2).

Fig. 2

In the case of mitral regurgitation, on the other hand, ventricular volume increases with little or no change in maximum developed pressure; wall thickness does not alter significantly but total myocardial mass increases because of the ventricular enlargement. Except in the case of neonates, increase of mass does not alter the number of myocardial cells; the primary histological changes are intracellular, involving changes in the number and arrangement of the sarcomeres. In chronic cases widespread interstitial fibrosis occurs.

Fig. 3

Echocardiography represents the method of choice for in vivo assessment of left ventricular hypertrophy. In particular, it is superior to both precordial palpation and ECG. These alternative approaches are relatively insensitive and subject to differences in observer skill and patient body habitus.

Fig. 4

A typical M-mode echocardiogram of left ventricular hypertrophy is shown in (Fig. 3). Note the range marks are 1 cm, making the septum and the posterior wall of the left ventricle nearly 2 cm in thickness.

Fig. 5

A parasternal long axis (Fig. 4) and short axis (Fig. 5) from a patient with left ventricular hypertrophy show marked wall thickening in diastole. There is symmetrical thickening of both the septum and the free wall of the ventricle, The prominent papillary muscles are evident on the two-dimensional image. In systole, there may be virtual cavity obliteration due to the symmetric hypertrophy (Fig. 6).

Fig. 6

In the majority of instances, left ventricular hypertrophy causes equal thickening of both the septum and the posterior wall. In perhaps 10% of cases, left ventricular hypertrophy may manifest on echocardiograms in an asymmetric form with the septum thicker than the posterior wall but without other stigmata of hypertrophic cardiomyopathy.

Echocardiography can be used to estimate left ventricular volume and mass. Since the two-dimensional images contain cross-sectional data, volume may be estimated from the short and long axes in systole or diastole. There are many mathematical approaches to the estimation of volume, the simplest based on the assumption that the geometric shape of the left ventricle roughly approximates a cylinder (for the base of the heart) placed on an ellipse (for the apical portions). The formula for such a volume would be 5/6 the area of the short axis multiplied by the length of the ventricle (obtained from the long axis). Thus, the formula for estimation of volume is:

Volume = 5/6 Area x Length

Mass may also be approximated. The principle method is to estimate the total volume of the ventricle including the myocardium, and to subtract from this the volume of the cavity. This gives the volume of the myocardium, which is converted to mass by multiplying by the specific gravity of muscle (usually taken as 1.05). If the hypertrophy is symmetrical, and providing no regional wall motion abnormalities, these estimates show reasonable correlation with actual excised left ventricular weights measured at necropsy. Serial estimations of left ventricular mass can be used to monitor the efficacy of antihypertensive therapy or to determine the degree of myocardial recovery following aortic valve surgery. It should be noted, however, that such estimates require high quality two-dimensional images. In addition, these calculations are time consuming and not routinely performed in most laboratories.

Systolic function tends to remain normal in the presence of hypertrophy, but diastolic filling patterns are altered. Using M-mode studies with simultaneous apexcardiograms and phonocardiograms to delineate precisely the phases of the cardiac cycle, it has been shown that the protodiastolic isovolumic relaxation period is short and the ventricle fills slowly, peak filling rates of 5 cm.s-1 or less being not uncommon (normal > 10 cm.s-1). Diastolic hemodynamics are thus very similar to those of mitral stenosis, but the cause is the abnormal myocardium, whose relaxation is analogous to a stiff spring which exerts a powerful initial force but has a very limited range of motion. Now that Doppler echocardiography is available, such analyses of diastolic abnormalities are more readily derived from the diastolic flow patterns into the left ventricle through the mitral valve.

Severe pressure overload eventually leads to impairment of systolic function and finally to left ventricular failure. As systolic function deteriorates, the cavity enlarges, but the walls tend to remain thick. This is in contrast to the dilated cardiomyopathy of ischemic or idiopathic origin as discussed later.

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