Carbon monoxide may contribute to cardiovascular disease through several accepted and potential mechanisms including binding to hemoglobin, and reducing oxygen dissociation at the tissue level by shifting the oxygen-hemoglobin dissociation curve. Carbon monoxide in experimental animals also increases platelet stickiness which may contribute to atherogenesis, and accelerates atherosclerosis either through altered lipid metabolism or increasing vessel permeability to cholesterol. Carbon monoxide in experimental studies contributes to sudden death by reducing the cardiac threshold for ventricular fibrillation. Some of these mechanisms, such as those that would lead to transient hypoxia of the myocardium, would lead to increased risk of myocardial ischemia only when exposure is current, while other mechanisms, such as acceleration of atherogenesis, may lead to long standing elevation of risk for cardiovascular disease.