The left ventricle increases its mass and wall thickness in hypertension as a result of the progressive increase in hemodynamic overload offered by increasing arterial blood pressure and total peripheral resistance. However, evidence is increasing that nonhemodynamic factors may also be important in the development of left ventricular hypertrophy (LVH). This LVH resulting from hypertensive disease conveys an independent risk of premature cardiovascular morbidity and mortality. The specific mechanisms accounting for this increased risk are not known with assurance, although several mechanisms are under active study; they include more prominently ventricular dysrhythmias and myocardial ischemia. It is possible to diminish the increased left ventricular mass with pharmacological agents, although currently it is not known whether this reversal also diminishes the risk associated with LVH. Therefore, at the present time the best means for preventing the risk of LVH is to prevent its development in the first place, and this seems to be preventable through control of arterial blood pressure at the earliest stages of hypertension. Risk may also be diminished in patients with existing LVH who are receiving digitalis or diuretics or who have chronic fluid- and electrolyte-disturbing diseases. Under these circumstances, the careful use and selection of antihypertensive therapy and control of electrolyte balance no doubt will prevent unnecessary morbidity and mortality.