This article reviews the management of stable angina, emphasizing risk factor reduction and the goals of antianginal therapy.
Reinforces risk factor reduction in stable angina; leaves open optimal antianginal strategies for prospective trials.
THE mechanism of the production of angina pectoris remains unclear.1 However, angina pectoris due to coronary-artery disease is generally considered to be chest pain due to myocardial ischemia that occurs because the myocardial oxygen demand exceeds the myocardial oxygen supply.The most sensible approach to the problem of coronary heart disease is the reduction, when possible, of the many risk factors that predispose to the development of the disease. However, once angina pectoris develops, the physician is faced with the problem of providing pain relief to the patient. In addition to relief of pain, an ideal antianginal drug would also . . .
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Wilbert S. Aronow (1973) studied this question.
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