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Volume 157, Issue 1, Pages 148.e1-148.e5 (January 2009)


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Effects of pantoprazole and esomeprazole on platelet inhibition by clopidogrel

Jolanta M. Siller-Matula, MDa, Alexander O. Spiel, MDa, Irene M. Lang, MDb, Gerhard Kreiner, MDb, Guenter Christ, MDb, Bernd Jilma, MDaCorresponding Author Informationemail address

Received 24 August 2008; accepted 25 September 2008. published online 07 November 2008.

Background

Clopidogrel is activated by CYP2C19, which also metabolizes proton pump inhibitors (PPI). As proton pump inhibitors are metabolized to varying degrees by CYP2C19, we hypothesized that the reported negative omeprazole-clopidogrel drug interaction may not be a class effect.

Methods

Responsiveness to clopidogrel was assessed by the vasodilator-stimulated phosphoprotein phosphorylation (VASP) assay and aggregometry (Multiplate Analyzer) in 300 patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI).

Results

The mean platelet reactivity index (PRI, assessed by the VASP assay) was nearly the same in patients with (n = 226; PRI = 51%) or without PPI treatment (n = 74; PRI = 49%; P = .724). Likewise, the adenosine diphosphate–induced platelet aggregation did not differ significantly between patients with or without PPI treatment (45 vs. 41 U; P = .619). Similarly, there was no difference in the PRI or the adenosine diphosphate–induced platelet aggregation between patients with pantoprazole (n = 152; PRI = 50%; aggregation = 47 U), esomeprazole (n = 74; PRI = 54%; aggregation = 42 U), or without PPI (n = 74; PRI = 49%; aggregation = 41 U; P = .382).

Conclusion

In contrast to the reported negative omeprazole-clopidogrel drug interaction, the intake of pantoprazole or esomeprazole is not associated with impaired response to clopidogrel.

a Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria

b Department of Cardiology, Medical University of Vienna, Vienna, Austria

Corresponding Author InformationReprint requests: Bernd Jilma, MD, Department of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria.

 This study was supported by a grant from the Jubiläumsfond of the Austrian National Bank (Nr. 12565).

PII: S0002-8703(08)00822-3

doi:10.1016/j.ahj.2008.09.017


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