Cigarettes, Coronary Occlusions, and Myocardial Infarction

There is now substantial evidence incriminating the cigarette habit in coronary heart disease. This evidence is broadly based, including not only prospective epidemiologic observations, but clinical and pathological correlations and laboratory and experimental findings. Since the original Surgeon General's report in 1964, a mass of information has accumulated that amply serves to clarify and strengthen the original observations and tentative conclusions.1 Mechanisms whereby cigarette smoking can both accelerate the rate of development of cardiovascular disease and provoke coronary attacks have been elucidated.2The chief components identified as noxious to the cardiovascular system are nicotine and carbon monoxide.2,3These have been shown to evoke multiple adverse effects through cardiodynamic influences, atherogenesis, hemostatic changes, and vasculotoxic and inflammatory influences. Nicotine stimulates catecholamine release, increases myocardial irritability and heart rate, and causes vascular constriction and a transient rise in pressure, while at the same time, platelets become more adherent. As