Pressure or volume overload of the myocardium increases the wall stress, particularly of the subendocardium, and leads to hypertrophy. Even though cardiac hypertrophy is viewed as a beneficial compensatory process that normalizes wall stress, the increased muscle mass carries with it the need of increased blood supply. Overall flow per unit mass is similar at rest in hypertrophic and normal hearts but a reduction of flow to the subendocardium and an increase in minimal coronary vascular resistance have been described. Thus, the potential exists for a vasodilator-induced steal mechanism shunting blood away from potentially ischemic areas. Angiotensin-converting enzyme inhibitors reduced myocardial oxygen consumption and coronary blood flow in parallel manner in some studies, indicating preserved coronary autoregulation, but there is also some evidence of a coronary vasodilator effect. Calcium antagonists reduce coronary vascular resistance and improve the myocardial demand-supply ratio, but the clinical usefulness of the newer compounds with supposedly little or no negative inotropic effects remains to be established. Hydralazine improved the myocardial oxygen demand-supply ratio in patients with dilated cardiomyopathy, but metabolic function may deteriorate more often after hydralazine than after angiotensin-converting enzyme inhibitors in patients with coronary heart disease. Similar observations have been made using alpha-adrenergic blockers. Although progress has been made in the understanding of the coronary circulation and the influence of vasodilators in congestive heart failure, many questions await clarification using refined or new methodology.