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

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

John D. Horowitz
1   Cardiology Unit, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Australia
,
Yuliy Y. Chirkov
1   Cardiology Unit, Basil Hetzel Institute, Queen Elizabeth Hospital, University of Adelaide, Australia
› Author Affiliations
Further Information

Publication History

Received 25 August 2008

Accepted 25 August 2008

Publication Date:
22 November 2017 (online)

 

 
  • References

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  • 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.