“…Thus, in the presence of coronary athero sclerosis and/or intramural arteriolar sclerosis (16), the metabolic vulnerability of the heart muscle to hypoxiating sympalhogenic catecholamine action becomes extreme, and any catecholamineliberating sympathetic reflex stimulation, as during physical effort or emotional stress, can suffice to provoke potentially fatal myo cardial injury; this all the more if oxygen-preserving sympathoinhibitory and cholinergic counterregulation happens to be insuf ficient. The syndrome of angina pectoris, and probably a large number of non-occlusive myocardial infarctions are, in all likeli hood, caused by the hypoxiating and ultimately necrotizing effect of acute sympathogenic and adrenal medullary catecholamine in fluxes into poorly vascularized areas of the myocardium (25). It is significant that in patients with angina pectoris, one of the most common "diseases of civilization", the physiological, exer cise-, emotion-, and nicotine-induced discharges of catecholamines and corresponding free fatty acids into the blood circulation have been found abnormally exaggerated (8, 14a, 27, 35, 36).…”