Left ventricular hypertrophy and antihypertensive therapy.

Cardiac adaptation to long-standing arterial hypertension consists of left ventricular hypertrophy (LVH), usually of the concentric type, i.e. an increase in wall thickness at the expense of chamber volume. LVH can no longer be considered only as a simple adaptive myocardial process; it drastically increases the risk of sudden death and cardiovascular morbidity and mortality, irrespective of the levels of arterial pressure. Patients with LVH have more premature ventricular contractions than patients without LVH or normotensive subjects, which indicates that LVH per se increases ventricular ectopic activity. Antihypertensive therapy should not only lower blood pressure, but also prevent or improve end-organ damage and therefore allow left ventricular mass to regress. Although they lower blood pressure, certain antihypertensive agents such as the thiazide diuretics and arteriolar dilators (hydralazine, minoxidil) have little or even a detrimental effect on LVH. In contrast, other agents such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, antiadrenergic drugs, and certain calcium antagonists decrease left ventricular mass in parallel with arterial pressure. Recent evidence has shown that a decrease in left ventricular mass induced by certain antihypertensive drugs suppresses ventricular ectopic activity by 85%. In contrast, left ventricular mass and ventricular ectopic activity remain unchanged or may even increase in patients treated with diuretics. It is not known whether the risk of sudden death can be decreased and the ominous prognosis of LVH altered by such specific antihypertensive therapy.