The presence of left ventricular hypertrophy (LVH) is of poor prognosis in essential arterial hypertension, but it may regress under antihypertensive treatment. Angiotensin-converting enzyme inhibitors, calcium antagonists, centrally acting antihypertensive agents and beta-blockers with low intrinsic sympathomimetic activity constantly reduce the left ventricular mass. This stands in contrast with diuretics and vasodilators which induce stimulation of the sympathetic and/or renin-angiotensin systems and usually have no effect on LVH. Animal experiments have shown that regression of LHV has no adverse effect on the myocardial changes aimed at correcting the LVH-associated abnormalities (collagen content, changes in isomyosins, density of beta-adrenergic receptors, etc.) and that it improves the coronary haemodynamics disturbed by LVH. In clinical practice, reducing the ventricular mass does not modify the left ventricular systolic function, usually improves the diastolic function precociously altered by LVH and seems to reduce the LVH-induced ventricular hyperexcitability. The regression of LVH under antihypertensive treatment should result in a lesser cardiovascular risk in hypertensive patients.