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Angina management rests on ischemia recognition; confirms early theories but leaves open additional mechanisms.
Heberden, by his classic description of angina pectoris, called attention to its importance. Hunter, Jenner, Parry and others early recognized the fact that fatal attacks of precordial pain were usually associated with arteriosclerosis of the coronary arteries. Later, Blackhall, See, and Huchard,1believing the pain of angina pectoris to be due to decreased blood supply to the heart muscle, advanced the theory of spasm of the coronary arteries to explain those cases in which no obvious arteriosclerotic changes were observed. By 1899, Huchard was able to collect eighty theories as to the cause of angina pectoris. Of these, only three are now recognized as possible causes of cardiac pain: Cardiac pain is due to decreased blood flow to a part or all of the myocardium, which is caused either by arteriosclerotic narrowing or by a temporary spasm of the coronary arteries. Cardiac pain is due to the stretching of
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Don C. Sutton (1931) studied this question.
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