Thromb Haemost 2009; 101(04): 714-719
DOI: 10.1160/TH08-12-0808
Platelets and Blood Cells
Schattauer GmbH

Impact of proton pump inhibitors on the antiplatelet effects of clopidogrel

Dirk Sibbing
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Tanja Morath
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Julia Stegherr
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Siegmund Braun
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Wolfgang Vogt
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Martin Hadamitzky
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Albert Schömig
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Adnan Kastrati
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
,
Nicolas von Beckerath
1   Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany
› Author Affiliations
Financial support:Material for platelet function analysis on the Multiplate device were provided free of charge from Dynabyte. The sponsors had no role in the design and conduct of the study; collection, management, analysis and interpretation of the data; or preparation, review or approval of the manuscript.
Further Information

Publication History

Received: 11 December 2008

Accepted after minor revision: 11 January 2009

Publication Date:
23 November 2017 (online)

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Summary

Patients receiving dual antiplatelet treatment with aspirin and clopidogrel are commonly treated with proton pump inhibitors (PPIs). Attenuating effects on platelet response to clopidogrel have been reported solely for the PPI omeprazole. PPIs differ in their metabolisation properties as well as their potential for drug-drug interactions. The aim of this study was to investigate the impact of different PPIs (pantoprazole, omeprazole, esomeprazole) on platelet response to clopidogrel in patients with previous coronary stent placement under chronic clopidogrel treatment. In a cross-sectional observational study, consecutive patients under clopidogrel maintenance treatment (n=1,000) scheduled for a control coronary angiography were enrolled. Adenosine diphosphate (ADP)-induced platelet aggregation (in AU*min) was measured with multiple electrode platelet aggregometry (MEA). From the entire study population, 268 (26.8%) patients were under PPI treatment at the time point of platelet function testing (pantoprazole, n=162; omeprazole, n=64; esomeprazole, n=42). Platelet aggregation (median [interquar-tile range]) was significantly higher in patients with omeprazole treatment (295.5 [193.5–571.2] AU*min) compared to patients without PPI treatment (220.0 [143.8–388.8] AU*min; p=0.001). Platelet aggregation was similar in patients with pantoprazole (226.0 [150.0–401.5] AU*min) or esomeprazole (209.0 [134.8–384.8] AU*min) treatment compared to patients without PPI treatment (p=0.69 and p=0.88, respectively). Attenuating effects of concomitant PPI treatment on platelet response to clopidogrel were restricted to the use of omeprazole. No attenuating effects on platelet response to clopidogrel were observed for pantoprazole or esomeprazole. Specifically designed and randomized clinical studies are needed to define the impact of concomitant PPI treatment on adverse events after percutaneous coronary intervention.