Clopidogrel resistance / Clopidogrel-Resistenz
2006
Geisler, Tobias | Gawaz, Meinrad
Clopidogrel as a thienopyridine is a potent antiplatelet drug blocking the P2Y₁₂ ADP receptor. Clopidogrel resistance can be regarded as missing pharmacological effect or as the incidence of atherothrombotic events despite antiplatelet therapy. However, clear definitions are still lacking. The incidence is dependent on the type of platelet function assay. ADP-induced aggregation, flow cytometric quantification of platelet activation markers, the degree of phosphorylization of vasodilator-stimulated phosphoprotein, or even bedside tests are used to measure the pharmacological effect of clopidogrel. Current data show that 4 to 30% of patients treated by coronary stenting do not adequately respond to clopidogrel treatment and are therefore at increased risk for subacute stent-thrombosis. Variants of cytochrome P3A5 and ADP receptor P2Y₁₂ genotype may influence the response to clopidogrel. As first clinical studies demonstrated, low response to clopidogrel is indeed associated with future cardiovascular events. A promising approach to overcome clopidogrel resistance could be a higher loading dose, an increased maintenance dose, or the application of alternative thienopyridines such as CD-747 (Prasugrel) or non-thienopyridine P2Y₁₂ antagonists.
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