Effect of carbon monoxide on cardiovascular disease

Abstract

Carbon monoxide exposure from heavy smoking or heavy atmospheric carbon monoxide pollution depresses myocardial function in patients with coronary heart disease, aggravates angina pectoris, aggravates intermittent claudication of the calf or thigh, increases myocardial ischemia in patients with clinical and subclinical coronary heart disease, and contributes to an increased incidence of nonfatal and fatal myocardial infarction and sudden death from coronary heart disease. Carbon monoxide contributes to the increase in nonfatal and fatal myocardial infarction and in sudden death from coronary heart disease in cigarette smokers by (a) carboxyhemoglobin interfering with myocardial oxygen delivery at the time nicotine has caused an increase in myocardial oxygen demand, aggravating an episode of myocardial ischemia, (b) the negative inotropic effect of carboxyhemoglobin aggravating an attack of myocardial ischemia, (c) carboxyhemoglobin reducing the threshold for ventricular fibrillation during an episode of myocardial ischemia, and (d) carboxyhemoglobin increasing platelet stickiness, thereby, increasing a thrombotic tendency. Furthermore, experimental data indicate that exposure to carbon monoxide in concentrations found in heavy tobacco smokers or in persons with heavy occupational exposure to carbon monoxide plays a role in the pathogenesis of cardiovascular disease.