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September 17, 1982

Smoking, Propranolol, and Myocardial Infarction

JAMA. 1982;248(11):1309. doi:10.1001/jama.1982.03330110017011

To the Editor.—  The β-Blocker Heart Attack Trial (BHAT) (1982;247:1707) was carried out in groups using propranolol hydrochloride and placebo, each of which contained 57% current smokers. It is important to examine the reported reduction in mortality in smokers and nonsmokers separately. Cigarette smoking is thought to have a role not only in the pathogenesis of coronary atherosclerosis, but also in aggravating angina, left ventricular dysfunction, and rhythm disturbances predisposing to sudden death.1 Epidemiologic studies have shown reduction in mortality from coronary disease after smoking cessation.2 While smoking exposes the body to numerous chemical agents, carbon monoxide and nicotine have been more often incriminated. The former affects oxygen transport. Nicotine from smoking cigarettes or from an intravenous bolus increased heart rate and BP.1,3 Propranolol hydrochloride abolishes these adrenergically mediated hemodynamic effects attendant on smoking.4 Until an analysis of the nonsmoking subjects of the BHAT demonstrates significant reduction in