Identifying clopidogrel resistance during chronic therapy: The case for a biochemical approach

Thromb Haemost 2008; 100(04): 519-520
DOI: 10.1160/TH08-08-0544

Editorial Focus

Schattauer GmbH

Authors

John D. Horowitz

¹Cardiology Unit, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Australia
Yuliy Y. Chirkov

¹Cardiology Unit, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Australia

References
1 Wenaweser P, Dorffler-Melly J, Imboden K. et al. Stent thrombosis is associated with an impaired respose to antiplatelet therapy. J Am Coll Cardiol 2005; 45: 1748-1752.
2 Chirkov YY, Chirkova LP, Sage RE. et al. Impaired responsiveness of platelets from patients with stable angina pectoris to antiaggregating and cyclic AMP-elevating effects of prostaglandin E1. J Cardiovasc Pharmacol 1995; 25: 961-966.
3 Fontana P, Senouf D, Mach F. Biologic effect of increased maintenance dose of clopidogrel in cardiovascular outpatients and influence of the cytochrome P450 2C19*2 allele on clopidogrel responsiveness. Thromb Res 2008; 121: 463-468.
4 Schafer A, Weinberger S, Flierl U. et al. ADP-induced platelet aggregation frequently fails to detect impaired clopidogrel-responsiveness in patients with coronary artery disease compared to a P2Y₁₂-specific assay. Thromb Haemost 2008; 100: 618-625.
5 Bonello L, Camoin-Jau L, Arques S. et al. Adjusted clopidogrel loading doses according to vasodilator-stimulated phosphoprotein phosphorylation indexdecrease rate of major adverse cardiovascular events in patients with clopidogrel resistance: a multicenter randomized prospective study. J Am Coll Cardiol 2008; 51: 1404-1411.