RISK FACTORS FOR CAROTID ATHEROSCLEROSIS AND PLATELET ACTIVATION

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Thromboxane A₂ biosynthesis was studied in healthy subjects, in patients in whom the extent of carotid atherosclerosis was determined, and in patients receiving chronic aspirin treatment, to determine what factors activate platelets to develop carotid atherosclerosis. Urinary 11-dehydrothromboxane B₂, a major metabolite of thromboxane A₂, was measured by radioimmunoassay after purification by reverse-phase HPLC. The extent of carotid atherosclerosis was determined by real-time B-mode ultra-sonography. The severity of carotid atherosclerosis in each subject was evaluated by plaque score, which was computed by summing the maximum thickness of plaque measured in millimeters. Urinary excretion of 11-dehydrothromboxane B₂ in healthy subjects was higher (P<0.01) in cigarette smokers (1063±244 ng/g creatinine) than in non-smokers (815±183 ng/g creatinine). Aspirin significantly suppressed 11-dehydrothrom-boxane B₂ excretion (266±114 ng/g creatinine). In the 24 patients in whom the plaque score was measured, multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B₂ and plaque score, age, smoking and hypercholesteremia. Our results indicate that risk factors such as age, hypercholesteremia, atherosclerosis and smoking activate platelets in vivo to develop carotid atherosclerosis.