Abstract

Large clinical trials have demonstrated that dual antiplatelet therapy (aspirin plus clopidog‑ rel) reduces the risk of recurrent cardiovascular events in patients with coronary artery disease. Dual antiplatelet therapy is the standard of care in patients with acute coronary syndromes undergoing stent implantation (1). Aspirin irreversibly acetylates the serine resi‑ due (ser529) in COX‑1 preventing the binding of arachidonic acid to the catalytic site. Controversy exists regarding the clinical relevance of non ‑ COX‑1 ‑ mediated antiplatelet effects of aspirin. Clopidogrel is a second ‑ generation thienopyri‑ dine that is converted to an active metabolite by the hepatic cytochrome P450 pathway. The active thiol metabolite of clopidogrel forms a covalent disulfide bond with cys17 and cys270 residues present in the extracellular domains of P2Y12 and inhibits ADP binding. High on-treatment platelet reactivity: beyond the concept

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