Left ventricular hypertrophy (LVH) is a response by the heart to haemodynamic overload. It is frequently observed in hypertension as a consequence of work overload secondary to an increased systemic resistance. This increase is not the only cause of LVH; there are other factors which can have a significant effect on its incidence. LVH in arterial hypertension acts initially as a useful compensatory mechanism against increased peripheral resistance. However after a certain amount of time it produces changes of variable intensity which have important consequences for the heart and some of them impair cardiac performance: 1. It affects both systolic and diastolic ventricular function; 2. It reduces coronary reserve; 3. It increases the incidence of angina and heart failure; 4. It increases the incidence of ventricular arrhythmias and sudden death. It therefore seems reasonable to include the reduction of LVH among the basic aims of antihypertensive treatment. Antisympathetic drugs (methyldopa, prazosin, urapidil), adrenergic beta-blockers, calcium antagonists and the converting enzyme inhibitors have proven to have a variable degree of efficacy in effecting a regression of LVH.