CIGARETTE-SMOKING ACUTELY INCREASES PLATELET THROMBUS FORMATION IN PATIENTS WITH CORONARY-ARTERY DISEASE TAKING ASPIRIN

Background Smoking is associated with an increased risk of myocardial infarction and sudden death. Platelet activation and thrombosis at sites of vessel stenosis and injury or plaque disruption play a crucial role in these acute coronary events. Thus, the aim of this study was to determine whether cigarette smoking acutely increases platelet thrombus formation on an injured arterial surface at local shear rates typical of a stenotic artery. Methods and Results Twelve habitual smokers with stable coronary disease, on aspirin 325 mg/d, were studied immediately before and 5 minutes after smoking two cigarettes each. Ex vivo platelet thrombus formation on porcine arterial media (simulating deep arterial injury) was measured after exposure to the patient's circulating venous blood for 3 minutes in cylindrical how chambers at 37 degrees C. The flow chambers were designed to produce shear rates of 754 or 2546 s(-1), the latter being typical of the high shear rates produced by Vessel stenosis. Plasma catecholamine, thromboxane B-2, and 6-keto-prostaglandin F-1 alpha (6-keto-PGF(1 alpha)) levels and whole blood plate-aggregation responses to thrombin were also measured before and after smoking. Compared with before smoking, morphometrically measured platelet thrombus formation on arterial media at shear rates of 754 and 2546 s(-1) increased by an average of 48% (P=.19) and 64% (P=.014), respectively, after smoking. Plasma epinephrine increased by more than twofold after smoking (P=.026). Plasma thromboxane BI and 6-keto-PGF(1 alpha) levels did not change. Smoking also increased whole blood platelet aggregation to thrombin (P less than or equal to.05). Conclusions These results suggest that smoking-enhanced platelet thrombosis may be an important contributory mechanism for acute coronary events in smokers that is not prevented by aspirin treatment. Catecholamine release and heightened platelet aggregation response to in vivo agonists may contribute to the prothrombotic effects of smoking.