Agabiti-Rosei E
Department of Medical Sciences, University of Brescia, Italy.
J Cardiovasc Pharmacol. 1994;23 Suppl 5:S42-8. doi: 10.1097/00005344-199423005-00009.
Left ventricular hypertrophy (LVH) in hypertension is initially a useful compensatory process, but it can also represent the first step toward a pathologic process that leads to the development of congestive heart failure. In fact, epidemiologic studies have documented that LVH in essential hypertension represents an independent risk factor for cardiovascular morbidity and mortality. Reversing or even preventing LVH, through a reduction of elevated blood pressure values and modification of some other pathogenetic factors, should represent a major therapeutic goal for the treatment of hypertensive patients. It has been demonstrated that different classes of antihypertensive drugs do not have the same effect in reducing left ventricular mass, probably because, beyond 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 reduction of cardiac hypertrophy. Two recent meta-analyses of the principal regression studies have indicated that angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists, followed by drugs capable of reducing sympathetic nervous system activity, are most effective in decreasing LV mass. The results of experimental and clinical studies have demonstrated that the reversal of cardiac hypertrophy is associated with 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.
