Abstract

Historical background. Those of us who have been interested in the concept of coronary artery spasm and re• search on it have witnessed a remarkable pattern of oscil• lation. The pendulum has swung from the enthusiasm of Sir William Osler (1), who in 1910 stated, I do not know of any better explanation of anginal pain ... , to the skep• ticism of Keefer and Resnick (2), who in 1928 wondered how rigid atherosclerotic coronary arteries could possibly constrict or go into spasm. The pendulum could not be stopped by Danielopolu (3), Gallavardin (4) and Kohn (5), who between 1924 and 1926 suggested that both spasm and atherosclerosis were involved in the pathophysiology of an• gina pectoris. With the influence of Blumgart et al. (6), not only the role of spasm, but its existence, was questioned. However, Blumgart himself (7) seemed to recognize some role for spasm when he stated, ., Some episodes, particularly those occurring in the absence of effort, or increased cardiac work, are best understood as the expression of vasocon• striction or absence of vasodilation leading to relatively insufficient coronary blood flow. Recent historical perspective. The advent of coronary arteriography in the late 1950s and the failure to demonstrate spontaneous spasm in a significant number of patients with angina focused attention on atherosclerosis as the sole phe• nomenon underlying ischemic heart disease. However, in the early 1970s it became clear that spasm could produce clinical myocardial ischemia in workers after withdrawal from long-term industrial exposure to nitroglycerin (8) and, in patients with Prinzmetal' s variant angina, during episodes of chest pain at rest (9). These observations were followed by a flurry of studies and reports documenting some role for spasm in the broad spectrum of ischemic heart disease ( 10) or proposing it as the key mechanism underlying myo• cardial infarction (II). However, in the early 1980s coro• nary angiography, performed in the acute phases of infarc-

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