Pathogenesis of angina pectoris.
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 mechanisms by which myocardial ischemia produces the sensation of angina is discussed, along with the application of pathogenetic principles to medical therapy.
D000787:Angina Pectoris / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000473:pathology; D006339:Heart Rate; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D005082:Physical Exertion; D014664:Vasodilation