Pathologic physiology of angina pectoris and acute myocardial infarction. Symposium on coronary heart disease

T HE DISTRESS or pain of angina pee-toris and of acute myocardial infarction is consequent to ischemia. In angina pectoris the isehemia is transitory because of tempo-rary disproportion between the blood supply and the myocardial requirements; in acute myocardial infaretion the ischemia is pro-longed and leads to the irreversible changes of necrosis. The actual stimulus at the nerve end-organs that give rise to the pain has not been identified with certainty. Sir Thomas Lewis termed it the "P factor. " It has cer-tain characteristics in common with lactic acid: it is acid, is destroyed by alkali and by oxidation, and develops most rapidly un-der oxygen deprivation and carbon dioxide accumulation. The predisposing cause of these two con-ditions is coronary obstruction. Atherosclero-sis is the most prevalent lesion. Syphilitic aortitis distorting the coronary ostia and rheumatic arteritis are next in frequency. Rarely, periarteritis nodosa, seleroderma, amyloid, hemorrhagic diseases, vegetations of bacterial endocarditis or tumors impinging on the ostia, emboli, and the arteritis associ-ated with systemic infections may be respon-sible. Congenital malformations and trauma are sometimes encountered. The chief effect of these lesions is to interfere with coronary blood flow and to prevent an adequate blood supply to the myocardium. Various factors greatly influence the de-gree of ischemia. Among these are the ana-tomic distribution of the coronary arteries, the localization of the atheromatous lesion