Beta blockers and left ventricular hypertrophy in hypertension

Abstract

It is now generally accepted that hypertension-induced left ventricular hypertrophy (LVH) represents a phenomenon of multifactorial origin. Antihypertensive therapy with beta-blocking drugs influences most of the factors involved in the control of left ventricular mass. Therefore, although initial animal experiments yielded conflicting results, it is not surprising that a great deal of evidence has been accumulated in clinical studies showing that successful long-term antihypertensive treatment with beta blockers induces regression of LVH in hypertensive subjects. Differences in molecular structure among various beta-blocking agents do not seem to influence this property. On the contrary, the question of whether reversal of LVH represents a beneficial or harmful byproduct of antihypertensive treatment with beta blockers is still unanswered. Animal and clinical studies suggest that left ventricular systolic function is unchanged or even improved after regression of LVH, whereas the ability of the heart to withstand recurrence of hypertension is slightly reduced. Furthermore, development of LVH in hypertensive subjects is associated with abnormalities in diastolic function which are not reduced by reversal of LVH induced by antihypertensive treatment with beta blockers.