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September 1982

Pathogenesis of Angina Pectoris

Author Affiliations

From the Cardiology Division, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore. Dr Fuchs was a fellow of the American Heart Association-Maryland Affiliate and is now with the Department of Medicine, New York Hospital-Cornell Medical Center.

Arch Intern Med. 1982;142(9):1685-1692. doi:10.1001/archinte.1982.00340220105018

• There are two broad classes of angina pectoris, related to two fundamentally different pathogenetic mechanisms: in classic angina, atherosclerotic narrowings limit the ability of the coronary arteries to augment myocardial blood flow in response to increases in demand, and in variant angina, a primary reduction in coronary blood flow occurs, unrelated to changes in demand. Over the last decade, major advances have been made in our understanding of the factors that control coronary blood flow and how they interact in each of the major classes of angina. The present review examines these advances, as well as their relation to the syndromes of rest angina, postprandial angina, and exertional coronary artery spasm. Current knowledge about the mechanism by which myocardial ischemia produces the sensation of angina is discussed, along with the application of pathogenetic principles to medical therapy.

(Arch Intern Med 1982;142:1685-1692)

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