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In chronic stable angina, the efficacy of nifedipine stems from an interplay of direct and reflex effects. A decrease in systemic vascular resistance, and thus, in myocardial oxygen demand, is considered the most important effect. Although this is partially offset by baroreceptor\u2010mediated reflex increases in blood pressure and heart rate, the net effect is a decrease in myocardial oxygen consumption. The importance of nifedipine\u2010induced increases in coronary blood flow in relieving stable angina remains controversial. Numerous clinical trials in patients with chronic angina have demonstrated that nifedipine increases exercise tolerance by lowering the heart rate\u2010blood pressure product (an approximation of myocardial oxygen consumption). The maximal double product during exercise, however, does not increase, suggesting that the drug does not importantly improve myocardial oxygen supply. Nifedipine may also be of value in the therapy of unstable angina, acute myocardial infarction, and hypertension, as well as in the protection of the myocardium at risk during open heart surgery. However, definite recommendations on the use of the drug for these indications must await results of ongoing randomized studies. The effects of nifedipine are dose\u2010related. Larger doses have been shown more effective than smaller doses, as long as an appropriate blood pressure is maintained. 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