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November 11, 2009Heart131 citations

The antiplatelet effect of aspirin is reduced by proton pump inhibitors in patients with coronary artery disease

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MWMorten WürtzEGErik Lerkevang GroveSKS. D. Kristensen

Key Result

Proton pump inhibitor use in CAD patients on aspirin was associated with significantly higher residual platelet aggregation (median 180 vs 152 aggregation units*min; p=0.003).

Study Design

Type

Case-Control (n=418)

Structured PICO

Does proton pump inhibitor use reduce the antiplatelet effect of aspirin in stable patients with coronary artery disease?

P
Population
418 stable patients with coronary artery disease treated with aspirin 75 mg/day, 54 of whom were taking proton pump inhibitors.
E
Exposure
Proton pump inhibitors (PPIs)
C
Comparator
No proton pump inhibitors
O
Outcome
Platelet aggregation measured by Multiplate whole blood aggregometry induced by arachidonic acid 1.0 mmol/lsurrogate

Concomitant use of PPIs in CAD patients on aspirin is associated with increased residual platelet aggregation and activation, suggesting a potential reduction in aspirin's cardiovascular protection.

Main Result

Absolute Event Rate: 180% vs 152%

p-value: p=0.003

Abstract

OBJECTIVE: To evaluate the effect of proton pump inhibitors (PPIs) on the platelet response to aspirin in patients with coronary artery disease (CAD). DESIGN: Case-control study. PATIENTS: 418 stable patients with CAD, 54 of whom were treated with PPIs. All patients were treated with non-enteric coated aspirin 75 mg/day and received no other antithrombotic drugs. MAIN OUTCOME MEASURES: Platelet aggregation was measured by Multiplate (Dynabyte, Munich, Germany) whole blood aggregometry induced by arachidonic acid 1.0 mmol/l and expressed as area under the aggregation curve (aggregation units*min). Platelet activation was assessed by soluble serum P-selectin. Compliance was confirmed by serum thromboxane B(2) levels. RESULTS: The distribution of age, sex, body mass index, blood pressure, family history of ischaemic heart disease, smoking, diabetes and the number of previous ischaemic events did not differ between groups. All patients were compliant with aspirin treatment according to serum thromboxane B(2) levels. Platelet aggregation (median 180 (interquartile range 119-312) vs 152 (84-226) aggregation units*min, p=0.003) and soluble serum P-selectin levels (88.5 (65.2-105.8) vs 75.4 (60.0-91.5) ng/ml, p=0.005) were significantly higher in patients treated with PPIs. Furthermore, these patients had significantly higher serum thromboxane B(2) levels (geometric mean 1.29 (95% CI 0.96 to 1.72) vs 0.92 (0.84 to 1.01) ng/ml, p=0.01). CONCLUSIONS: Patients with CAD treated with PPIs had a reduced platelet response to aspirin, as shown by increased residual platelet aggregation and platelet activation, compared with patients with CAD not taking PPIs. Concomitant use of aspirin and PPIs might reduce the cardiovascular protection by aspirin.

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Cite This Study

Würtz et al. (2009) conducted a case-control in coronary artery disease (n=418). Proton pump inhibitors (PPIs) vs. No proton pump inhibitors was evaluated on Platelet aggregation (aggregation units*min) (p=0.003). Proton pump inhibitor use in CAD patients on aspirin was associated with significantly higher residual platelet aggregation (median 180 vs 152 aggregation units*min; p=0.003).

synapsesocial.com/papers/6a626c34f72da4096ac1f366https://doi.org/10.1136/hrt.2009.181107
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