Left ventricular hypertrophy (LVH) is an important independent cardiovascular risk factor. Angiotensin II and aldosterone, the effectors of the renin-angiotensin-aldosterone system (RAAS), have been found to increase LVH in a blood-pressure– independent fashion in several animal models of RAAS activation and in observational studies in humans. Pharmacological interventions interacting with the RAAS, namely, angiotensin-converting enzyme inhibition, blockade of the angiotensin II type 1 receptor, and antagonism at the mineralocorticoid receptor, have been shown to reduce LVH. These beneficial effects are in addition to, and independent from, their blood pressure–lowering properties and improve cardiovascular prognosis. The main question to be answered in the future is which combination of drugs interfering with the RAAS will prove to be most beneficial...