Effects of cigarette smoke and nicotine on platelets and experimental coronary artery thrombosis

Abstract

The causal link between smoking, atherosclerosis and an increased risk for acute platelet mediated coronary events such as acute platelet thrombus formation, myocardial infarction, and sudden coronary death is not clear. Our studies suggest that there may be a transient increase in in vivo platelet activity with each exposure to cigarette smoke or elevated plasma nicotine. It is thought that platelets may contribute to the acceleration of the atherosclerotic process by several mechanisms (5). Thus it may be that each time a person increases their platelet activity, by smoking or some other means, and given other predisposing conditions such as elevated lipids and/or acute intimal damage, such as rupture of an atherosclerotic placque, the atherosclerotic process may be enhanced. In addition it appears that cigarette smoke makes a developing thrombus more adherent and less likely to embolize distally, although the effect is transient. Finally, cigarette smoke may provide the final stimulus for an occlusive coronary thrombus in a stenosed coronary artery already predisposed to thrombosis by other risk factors. This may account for the fact that the risk of coronary occlusion and myocardial infarction decreases markedly in the first year after quitting (65). It may be that smoking has a greater likelihood of precipitating a fatal thrombus than it does of accelerating the altherosclerotic process. This would be reflected in the inability of aspirin to prevent the smoking induced enhancement of CFR's in our model (23) or the enhancement of platelet function in men with coronary artery disease (66).