Comparison of Triflusal and Clopidogrel in Secondary Prevention of Stroke Based on the Genotyping

Clopidogrel has anti-platelet activity by irreversible inhibition of the P2Y12 platelet receptor. Clopidogrel must be converted into an active metabolite in order to show anti-platelet activity. Hepatic CYP2C19 enzyme is one of the key hepatic enzymes which convert clopidogrel into active metabolite and its genetic polymorphism is related to clopidogrel resistance. CYP2C19 poor or intermediate metabolizer groups show reduced anti-platelet activity of clopidogrel compared to extensive metabolizer group.

This study is designed to prove the superiority of the triflusal in preventing recurrent stroke over the clopidogrel in ischemic stroke patient with poor or intermediate metabolizer of CYP2C19 polymorphism. Also we plan to prove that clopidogrel resistance is related to CYP2C19 polymorphism by comparing the ischemic preventive effect of clopidogrel between groups of different CYP2C19 polymorphism.

Inclusion criteria

• Patients who have non-cardiogenic ischemic stroke of TOAST classification within 30 days prior to screening
• ≥ 20 years of age; adult, at the date of signing the informed consent
• Written informed consent

Exclusion criteria

• History for bleeding tendency or recent major bleeding within 2 weeks
• Chronic liver disease (ALT > 100 IU/L or AST > 100 IU/L) or renal dysfunction (creatinine > 4.0 mg/dl)
• Thrombocytopenia (platelet < 100,000mm3)
• Any contraindication of antiplatelet agent
• Severe congestive heart failure
• Patients who need to take anticoagulants or two or more antiplatelet agents
• Severe concomitant disease with the expected survival less than 2 years
• Pregnant or nursing
• Any drug clinical trials within 30 days of signing the informed consent