Pathologic Physiology of Angina Pectoris and Acute Myocardial Infarction

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Abstract
Some of the unique physiologic characteristics of the coronary circulation have been pointed out. In the normal heart, the coronary arteries are functionally end arteries. Watery injections, however, reveal anatomic fine anastomotic communications between the coronary arteries measuring less than 40 µ. But they are of limited functional significance in obviating the untoward effects of sudden coronary narrowing or occlusion. Complete occlusion or considerable narrowing of one or more coronary arteries may exist without giving rise to any clinical signs or symptoms and without having produced myocardial damage. The apparent inconsistency between the presence of long-standing obstructive arterial lesions and the absence of significant pathologic or clinical evidence of myocardial damage is dispelled by the demonstration of a collateral circulation which serves as a bypass in relation to the obstruction in each of these hearts. The pathologic and physiologic substrates of angina pectoris, coronary failure, and acute myocardial infarction have been discussed.