• Sadik Acikel, Aylin Yildirir, Alp Aydinalp, Ugur Bal, Gamze Kaynar, Bulent Ozin, and Haldun Muderrisoglu.
• Faculty of Medicine, Department of Cardiology, Ministry of Health Dişkapi Yildirim Beyazit Research and Educational Hospital, Baskent University, Ankara, Turkey. sadik.acikel@tkd.org.tr
• Blood Coagul. Fibrinolysis. 2009 Sep 1;20(6):427-32.

AbstractIn this study, we aimed to assess the factors associated with laboratory-defined aspirin resistance and the relationship of this laboratory-defined aspirin resistance with thrombolysis in myocardial infarction risk score, markers of cardiac necrosis, and inflammatory and thrombotic risk factors in patients with unstable angina or non-ST elevation myocardial infarction. Ninety-seven patients who were under aspirin therapy and hospitalized with unstable angina/non-ST elevation myocardial infarction were included in the study. Laboratory-defined aspirin sensitive and resistant groups were determined by platelet function analyzer; aspirin resistance was defined as collagen/epinephrine closure time less than 165 s. Laboratory-defined aspirin resistance was noted in 29 patients (29.9%), and non-ST elevation myocardial infarction was observed in 46 patients (47.4%). Patients in the group with laboratory-defined aspirin resistance had significantly higher thrombolysis in myocardial infarction risk scores (P < 0.001). When the details of cardiac myonecrosis markers were compared, baseline and follow-up creatine kinase-myocardial band and troponin I values were higher in laboratory-defined aspirin-resistant group. Multivariate analyses revealed that laboratory-defined aspirin resistance was an independent predictor of non-ST elevation myocardial infarction (P = 0.022). Laboratory-defined aspirin resistance is associated with non-ST elevation myocardial infarction, higher markers of cardiac necrosis and thrombolysis in myocardial infarction risk score in patients hospitalized with unstable angina/non-ST elevation myocardial infarction.

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