Clinical Aspects of Atherosclerosis. Role of Coronary Artery Spasm

Abstract

Over the past several years, pathological and pathophysiological studies suggested that fixed coronary artery stenosis due to atherosclerosis were responsible for myocardial ischemia and infarction. Most physicians had been taught in medical school that the coronary narrowing was the cause of angina and that pain occured as a result of an imbalance of myocardial oxygen supply and demand. However in the 18’s many authors have postulated that spasm was the likely cause of angina. In fact, like many concepts in medicine the idea of spasm, once popular, was subsequently rejected and is now being rediscovered. In 1959 Prinzmetal (1) revived interest in coronary artery spasm when he described a group of patients with “variant angina” and postulated that this clinical syndrome could be related to an increased vascular tonus superimposed on fixed proximal atherosclerotic narrowing. In 1962 Gensini (2) was able to document the appearance of spontaneous coronary artery spasm. Subsequent developments including coronary arteriography, hemodynamic and electrocardiographic monitoring, isotope studies provided important evidence concerning the existence of coronary artery spasm in man. Maseri and colleagues (3) have provided very elegant physiopathologic investigations in patients with angina at rest These developments have implicated coronary artery spasm in the pathophysiology of many other ischemic syndromes in addition to Prinzmetal’s variant angina, More recently provocative testing (4–7) provided some more lights on the possible role of coronary spasm in heart disease in general.