Abstract
Our concepts of the pathophysiology of myocardial ischemia have oscillated over the years like a pendulum. For more than a century since Allan Burns in 1809 [1] suspected coronary artery spasm as a cause of angina pectoris, until Sir William Osier in 1910 stated that he could not think of a better explanation of anginal pain [2], coronary artery spasm was believed to be the primary mechanism underlying acute myocardial ischemia. The pendulum began to swing away from spasm under the influence of Keefer and Resnik, who in the 1920s questioned the ability of rigid atherosclerotic coronary arteries to constrict or go into spasm [3]. Shortly after, Blumgart and co-workers focused attention on the association between the clinical history of angina and the finding of coronary atherosclerosis at autopsy [4]. Subsequently, the failure to find coronary artery spasm with any significant frequency during the first decade of coronary arteriography helped to shift thinking further away from spasm.
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Chahine, R.A. (1985). The Role of Coronary Artery Spasm in Acute Ischemic Syndromes. In: Califf, R.M., Wagner, G.S. (eds) Acute Coronary Care. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3828-4_5
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