In
essential hypertension ventricular function is determined primarily by the degree of
hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to
ischemia, because the coronary reserve is seriously limited even in the absence of
coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial
hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular
hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of
hypertrophy shows that the
hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Coronary reserve is reduced even in hypertensive
hypertrophy without evidence of
coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of
left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing
cardiac hypertrophy (
prazosin,
clonidine,
enalapril, and
nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of
cardiac hypertrophy, i.e. therapeutic intervention on a critical precursor of hypertensive
congestive heart failure, can be obtained by various
antihypertensive agents.
Prazosin,
calcium channel blockers and
angiotensin-converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with
diuretics and
vasodilators can all induce regression of
hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all
antihypertensive drugs seem equally effective in bringing about coronary regression of
left ventricular hypertrophy. No regression or little regression has been found with
diuretic monotherapy despite a satisfactory reduction in blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)