Key result
Cigarette smoking is linked to ~30% higher urinary 11-dehydrothromboxane B2 excretion versus non-smokers.
Why the study?
Risk factors that activate platelets to develop carotid atherosclerosis were not fully understood.
Is platelet activation associated with cardiovascular risk factors and the severity of carotid atherosclerosis?
Population
Healthy subjects including smokers and non-smokers, patients evaluated for carotid atherosclerosis, and patients on chronic aspirin treatment
Comparison
Smokers vs non-smokers; aspirin treatment vs no aspirin
Design
Observational study measuring urinary 11-dehydrothromboxane B2 and carotid plaque score
Authors
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Smoking associated with platelet activation; hypothesis-generating for carotid atherosclerosis link, needs prospective confirmation before practice implications.
Observational
Is platelet activation associated with cardiovascular risk factors and the severity of carotid atherosclerosis?
Absolute Event Rate: 1063% vs 815%
p-value: p=< 0.01
Cardiovascular risk factors such as smoking, age, and hypercholesterolemia are associated with increased in vivo platelet activation, which correlates with the severity of carotid atherosclerosis.
Uyama et al. (1994) conducted an observational in Carotid atherosclerosis. Cigarette smoking vs. Non-smokers was evaluated on Urinary excretion of 11-dehydrothromboxane B2 (ng/g creatinine) (p=< 0.01). Cigarette smoking was associated with higher urinary excretion of 11-dehydrothromboxane B2 compared to non-smokers (1063 vs 815 ng/g creatinine; P<0.01).
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