Abstract
For over 100 years there has been controversy about the role of coronary-artery spasm in the production of angina pectoris. In classic, effort-induced Heberden's angina, a number of observations, indirectly at least, suggest that coronary spasm may not have a role. Post-mortem studies1 and more recently arteriographic studies have shown that patients with classic angina have severe organic obstructive disease of at least one, but usually two or more major coronary arteries. In response to increased caridac work, augmentation of myocardial oxygen supply is dependent solely on increases in coronary blood flow, since the left ventricle extracts oxygen from blood . . .

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