Left ventricular hypertrophy (LVH) in essential hypertension has been identified as a major and pressure independent risk factor for the occurrence of sudden death and other cardiovascular morbidity and mortality. Previous studies by our group have shown that patients with LVH exhibit more frequent and more severe ventricular ectopy than patients without LVH or normotensive subjects. These ventricular dysrhythmias are independent of the morphological form of LVH and occur in patients with normal coronary arteries. Most recent data from our laboratory documents that some calcium antagonists reduce LVH and, in parallel, suppress ventricular dysrhythmias. In contrast, antihypertensive therapy with a thiazide diuretic had no effect on ventricular dysrhythmias or LVH, despite the fact that blood pressure was lowered to the same extent as with the calcium channel blockers. What remains to be determined is whether or not the ominous prognosis of patients with LVH will be improved by specific antihypertensive therapy, that over and above lowering pressure, also improves hypertensive target organ disease, such as LVH and associated ventricular dysrhythmias.