Aspirin resistance and glycoprotein llla pla1/a2 polymorphism in asymptomatic and symptomatic patients with vascular risk factors

Aspirin, a widely used drug for prevention from vascular diseases, may not reveal the desired effect in all patients and recurrent ischemic events may occur despite aspirin therapy. Defined as "aspirin resistance", this entity is reported in 5–45% of high risk patients and various mechanisms have been proposed for its development. This study is planned to determine whether there is a relationship between aspirin resistance and aspirin dosage, preparation type and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. 208 patients with vascular risk factors, using aspirin for primary or secodary prevention were included.in the study. Patients were classified according to their clinical presentations and aspirin usage. Seventy-five patients, with acute ischemic stroke presentation were grouped as symptomatic and the remaining 133 patients were grouped as asymptomatic. Symptomatic group was further classified into two groups, according to the aspirin usage status at the time of stroke. Aspirin resistance was measured by PFA-100 system (Col/Epi cartridge) and glycoprotein IIIa P1A1/A2 polymorphism were determined by PCR. The overall prevalance of aspirin resistance was 32,2%. The mean age of patients with aspirin resistance were significantly higher (p=0,009). The prevalance of aspirin resistance were similar for both "symptomatic under aspirin therapy" and asymptomatic groups. The resistance rate was found to be highest with 100 mg enteric coated preparation usage (39,3%). Increasing the aspirin dosage and/or shifting to non-enteric coated preparations revealed aspirin sensitivity change between 36% and 60%. Repeated measurements revealed aspirin resistance development in time course in 14% of patients shown to be aspirin sensitive before. No significant relationship between glycoprotein IIIa P1A1/A2 polymorphism and aspirin resistance and atherotrombotic stroke development is found. In conclusion, the effect of aspirin can change by time, dosage and preparation.type used. A relationship between glycoprotein IIIa P1A1/A2 polymorphism and aspirin resistance and atherotrombotic stroke development cannot be found.