Left ventricular hypertrophy (LVH), a target-organ response to chronic pressure or volume overload, is associated with its own independent risks of death in patients with hypertension. Numerous studies have shown that LVH increases the risk of coronary heart disease, congestive heart failure, stroke or transient ischemic attack, all-cause deaths, and sudden death. Although the mechanisms by which LVH develops are incompletely understood, the renin-angiotensin system may play an important role. All major classes of antihypertensive agents (calcium channel blockers, diuretics, β-blockers, angiotensin-converting enzyme inhibitors) can cause LVH regression but not all to the same degree. Angiotensin-converting enzyme inhibitors may provide the most pronounced reduction in left ventricular mass per millimeter of mercury of blood pressure reduction. In addition, animal studies and human trials show promise for the regression of LVH with the use of angiotensin receptor blockers (ARBs). Because ARBs act specifically on the AT₁ receptor, angiotensin II can exert its favorable effects on cell growth inhibition through the AT₂ receptor. One small study that compared the ARB valsartan with atenolol found significant regression of LVH with the ARB by 8 months of treatment. (Am Heart J 2000;139:S9-S14.)