Background Proton pump inhibitors (PPIs) are usually prescribed to patients undergoing dual antiplatelet therapy to decrease the risk of gastrointestinal bleeding. However, the proportion of patients increased incidence of major adverse cardiovascular event because of interaction of PPIs and clopidogrel. The aim of the study was to assess the effect of omeprazole and pantoprazole on platelet reactivity in acute coronary syndrome patients receiving clopidogrel.
Method From October 2012 to September 2013, a total of 620 consecutive acute coronary syndrome patients from Shenyang General Hospital were enrolled. All patients received clopidogrel loading dose 300 mg and aspirin 300 mg. Patients were randomised to two groups by the ratio of 1:1 and received routine dual anti-platelet treatment. The omeprazole group (aspirin 300 mg/d and clopidogrel 75 mg/d and omeprazole 20 mg/d, n = 310). The pantoprazole group (aspirin 300 mg/d and clopidogrel 75 mg/d and pantoprazole 20 mg/d, n = 310). The reversion rate of ADP which was defined as 20 μmol/L adenosine diphosphate induced platelet aggregation (by LTA) (on admission, three days and 30 days after dual antiplatelet therapy) and clinical events (stent thrombosis, MACEs, which included cardiac death, myocardial infarction or ischaemic symptoms driven target vessel revascularisation, all-cause death, TIMI) were observed.
Result All groups were generally well balanced with regard to baseline demographic, clinical, and proced-ural characteristics. There were no different on platelet response to clopidogrel at three days (52.8% ± 19.3% vs 50.2% ± 19.3%, respectively, p = 0.384) and 30 days (49.9% ± 14.9% vs 49.1% ± 14.7%, respectively, p = 0.559) between omeprazole group and pantoprazole group. 1 stent thrombosis in the omeprazole group and 0 stent thrombosis in pantoprazole group (p = 0.219). 2 patients in omeprazole group were suffered from MACE (0.6%), and 3 patients in pantoprazole group (0.97%, p = 0.359). In addition, there were no major or minor bleeding in the two groups, the minimal bleeding in omeprazole and pantoprazole groups were no significantly difference (2.1% vs 2.8%, respectively, p = 0.235). There was no significantly association between the two groups for all-cause death (p = 0.687), and 1 patient died due to the traumatic brain injury in the omeprazole group.
Conclusion These results suggest that the drug interaction between PPIs (omeprazole and pantoprazole)and clopidogrel does not result in ADP induced platelet aggregation. There was no apparent clinical events interaction between clopidogrel and omeprazole and pantoprazole in patients who received dual antiplatelet therapy. The clinic impact of this strategy needs to be proved by long term follow-up outcome studies.
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