EVALUATION OF THE CARDIAC EFFECTS OF ANTIHYPERTENSIVE AGENTS

Left ventricular hypertrophy (LVH) in hypertension is initially a usef ul compensatory process, but it can also represent the first step towa rd a pathologic process that leads to the development of congestive he art failure. In fact, epidemiologic studies have documented that LVH i n essential hypertension represents an independent risk factor for car diovascular morbidity and mortality. Reversing or even preventing LVH, through a reduction of elevated blood pressure values and modificatio n of some other pathogenetic factors, should represent a major therape utic goal for the treatment of hypertensive patients. It has been demo nstrated that different classes of antihypertensive drugs do not have the same effect in reducing left ventricular mass, probably because, b eyond the control of blood pressure, their pharmacologic interference with the adrenergic system, the renin-angiotensin-aldosterone system, or other growth factors can influence the development and the reductio n of cardiac hypertrophy. Two recent meta-analyses of the principal re gression studies have indicated that angiotensin-converting enzyme (AC E) inhibitors and calcium antagonists, followed by drugs capable of re ducing sympathetic nervous system activity, are most effective in decr easing LV mass. The results of experimental and clinical studies have demonstrated that the reversal of cardiac hypertrophy is associated wi th an improvement of the functional consequences of increased LV mass. Further studies are needed to verify whether the reversal of LVH per se increases survival rate in patients with essential hypertension.