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Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking
Insights
Smoking acutely increases platelet thrombus formation on injured arteries, raising the risk of heart attack. This effect, linked to catecholamine release, is not prevented by aspirin and contributes to acute coronary events in smokers.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pharmacology
Background:
- Smoking is a major risk factor for myocardial infarction and sudden cardiac death.
- Platelet activation and thrombosis are key mechanisms in acute coronary events.
- Understanding smoking's acute effects on thrombosis is crucial for prevention.
Purpose of the Study:
- To investigate whether cigarette smoking acutely enhances platelet thrombus formation on injured arterial surfaces.
- To assess these effects at shear rates relevant to arterial stenosis.
Main Methods:
- Studied 12 smokers on aspirin before and after smoking two cigarettes.
- Measured ex vivo platelet thrombus formation on porcine arterial media at shear rates of 754 and 2546 s-1.
- Assessed plasma catecholamines, thromboxane B2, 6-keto-PGF1 alpha, and platelet aggregation responses.
Main Results:
- Platelet thrombus formation increased by 48% and 64% at 754 and 2546 s-1, respectively, after smoking (P=.014 at high shear).
- Plasma epinephrine levels more than doubled post-smoking (P=.026).
- Whole blood platelet aggregation to thrombin also increased (P ≤ .05).
Conclusions:
- Smoking acutely enhances platelet thrombosis, potentially contributing to acute coronary events in smokers.
- Aspirin treatment did not prevent smoking-induced increases in platelet thrombus formation.
- Increased catecholamines and heightened platelet aggregation may underlie smoking's prothrombotic effects.
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 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 B2, and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) 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 alpha levels did not change. Smoking also increased whole blood platelet aggregation to thrombin (P < or = .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.
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