Differential effect of aspirin on platelet aggregation in patients with coronary artery disease in relation with associated risk factors.
Platelets play a key role in the pathogenesis of atherosclerosis and acute coronary syndromes and antiplatelet therapy offers a clinical benefit. Although aspirin is the most widely used agent, there are several conditions in which aspirin may fail to provide a full antithrombotic benefit. Furthermore, data concerning the relationship between platelet function, aspirin, and the associated risk factors are limited. In the present study. ADP and collagen-induced platelet aggregation of 200 consecutive patients with suspected coronary artery disease (CAD) who underwent coronary angiography were evaluated. The patients were classified into three groups according to the number of stenotic vessels. One hundred and eight patients were using 300 mg/day of aspirin. The associated cardiovascular risk factors were also considered. The collagen-induced platelet aggregation of smokers was significantly higher than non-smokers (P < 0.05). Although platelet aggregation was higher in diabetic and hypertensive patients, the difference was not statistically significant. No significant correlation was found between platelet aggregation and other risk factors. The collagen-induced platelet aggregation of the subjects with non-stenotic vessels was reduced by aspirin (P < 0.05). Aspirin did not sufficiently inhibit ADP and collagen-induced aggregation in patients with CAD. This finding supports the idea that the nonplatelet-mediated effects of aspirin could be more important than its antiplatelet effect in clinical use and the use of new potent antiplatelet drugs may complete its antiplatelet effect.
Ersöz
Gülriz
G
Faculty of Medicine, Department of Physiology, Ankara University, Ankara, Turkey.
Tikiz
Hakan
H
Yakaryilmaz
Ali
A
Tezcan
Kemal
K
Genç
Yasemin
Y
Korkmaz
Sule
S
D000328:Adult; D000368:Aged; D001241:Aspirin / Q000494:pharmacology*; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000188:drug therapy / Q000503:physiopathology; D004311:Double-Blind Method; D006801:Humans; D006949:Hyperlipidemias / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D012307:Risk Factors; D012907:Smoking / Q000503:physiopathology
D010975:Platelet Aggregation Inhibitors; D001241:Aspirin