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(Circulation. 1995;92:2432-2436.)
© 1995 American Heart Association, Inc.
Articles |
Cigarette Smoking Acutely Increases Platelet Thrombus Formation in Patients With Coronary Artery Disease Taking Aspirin
From the Laboratory of Thrombosis and Atherosclerosis, the Department of Medicine, the Montreal Heart Institute and the University of Montreal, Canada.
Correspondence to Dr Jules Y.T. Lam, MD, Department of Medicine, Montreal Heart Institute, 5000 Belanger St, Montreal, Quebec H1T 1C8, Canada.
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 flow chambers at 37°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
B2, and 6-ketoprostaglandin
F1
(6-keto-PGF1) levels and whole
blood platelet 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 B2 and
6-keto-PGF1 levels did not change. Smoking also
increased whole blood platelet aggregation to thrombin
(P
.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.
Key Words: smoking • platelets • thrombosis • aspirin • coronary disease
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