Pathophysiology of Cardiac Pain

ANGINA pectoris can be no better described than in Heberden's original discussion some 160 years ago.' Despite the enduring quality of his description, Heberden had no idea of the cause of angina pectoris, although he did appreciate its morbid quality. In the same era, Jenner, Parry, and Burns were among the first clinicians to associate angina pectoris with anatomic disease of the coronary arteries. This notion lost favor somewhat during the latter half of the nineteenth century when anginal pain was thought to originate in spasm of the coronary arteries or in disease of the aortic wall itself.2 The twentieth century witnessed the observations of Herrick,3 MacKenzie,4 Levine,5 Keefer and Resnik,6 and Blumg-art, Schlesinger, and Davis,7 culminating in the theory that angina pectoris came about as the result of myocardial ischemia, usually in the presence of intraluminal coronary artery disease or disease causing cardiac hypertrophy, and elicited by disturbance of the balance between coronary oxygen supply and myocardial oxygen demand. The purpose of this report is to indicate what new facts may be added to these masterful disser;tations. The discussion is divided into three parts: mechanism of pain excitation within the heart; myocardio-neuronal reception and transmission of pain impulses; clinico-physiologic factors in the development of angina pectoris.