 |
| 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.
2004
