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Randomized Controlled Trial
Dose-related effect of aspirin on laboratory-defined platelet aggregation and clinical outcome after coronary stenting.
- Javad Kojuri, Yadollah Mahmoody, Bardia Zangbar Sabegh, Mansoor Jannati, Ali Mahboodi, and Andia Khalili.
- Cardiology Department, Shiraz University of Medical Sciences, Shiraz, Iran. kojurij@yahoo.com
- Cardiovasc Ther. 2010 Jun 1;28(3):147-52.
BackgroundAcetylsalicylic acid (aspirin) is widely used in the secondary prevention of coronary artery disease. There is controversy regarding the prevalence of aspirin resistance in patients with coronary artery disease and the effect of dose on resistance. Our primary aims were to determine the degree of platelet responsiveness to aspirin, and to study the influence of dose on platelet inhibition and clinical outcomes after coronary stenting.Methods And ResultsWe prospectively studied the effect of aspirin on platelet function in 106 stable outpatients 6 months after successful percutaneous coronary angioplasty. Participants were randomized in a double-blind, double-crossover study (80 or 500 mg per day for 6 months). The platelet response to aspirin was determined by 10 micromol/L adenosine-5-diphosphate-induced aggregation with light transmission aggregometry. The clinical outcome was determined by single photon emission computed tomography with Tc-99m, and major adverse cardiac events were recorded (myocardial infarction, death, unstable angina or need for revascularization). In both groups 30.2% of the participants were resistant to aspirin. There was no significant difference between the dose of 80 mg compared to 500 mg aspirin in the incidence of aspirin resistance (P= 0.3). No correlation was found between aspirin resistance and clinical outcome (P= 0.4). Female sex and smoking were strongly associated with aspirin resistance.ConclusionThe frequency of aspirin resistance is not dependent on the dose of aspirin. Female sex and smoking were the strongest predictors of aspirin resistance. Aspirin resistance is not a predictor of poor clinical outcome in patients who received double antiplatelet therapy.
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