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Decreased Platelet Inhibition by Thienopyridines in Hyperuricemia
Silvia Lee1, Patricia P Wadowski1, Timothy Hoberstorfer1
1Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Insights
High uric acid levels reduce the effectiveness of clopidogrel and prasugrel antiplatelet therapy in patients with acute coronary syndrome. However, ticagrelor effectiveness remains unaffected by hyperuricemia.
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis
Background:
- Hyperuricemia is linked to increased atherothrombotic events in acute coronary syndrome (ACS) patients post-percutaneous coronary intervention (PCI).
- Inadequate P2Y12 inhibition may contribute to this increased risk.
- This study investigates the relationship between hyperuricemia and P2Y12 antagonist efficacy.
Purpose of the Study:
- To prospectively assess the association between hyperuricemia and platelet inhibition in patients treated with P2Y12 antagonists.
- To compare the effect of hyperuricemia on clopidogrel, prasugrel, and ticagrelor in ACS patients.
Main Methods:
- Assessed uric acid levels and on-treatment residual platelet reactivity to adenosine diphosphate (ADP).
- Studied 301 clopidogrel-treated patients and 206 ACS patients treated with prasugrel or ticagrelor post-PCI.
- Defined high on-treatment residual platelet reactivity (HRPR) based on established cut-off values.
Main Results:
- Hyperuricemia correlated with increased residual platelet reactivity in clopidogrel and prasugrel users.
- Ticagrelor-treated patients showed similar platelet reactivity regardless of uric acid levels.
- HRPR was more common in hyperuricemic patients on clopidogrel or prasugrel compared to those with normal uric acid levels.
Conclusions:
- Hyperuricemia impairs platelet inhibition with thienopyridines (clopidogrel, prasugrel) but not ticagrelor.
- Further research is needed to determine if lowering uric acid can improve antiplatelet effects of clopidogrel and prasugrel in hyperuricemic patients.
Purpose:
Hyperuricemia carries an increased risk of atherothrombotic events in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI). This may at least in part be due to inadequate P2Y12 inhibition. The aim of this study was to prospectively investigate the potential association between hyperuricemia and decreased platelet inhibition by P2Y12 antagonists.
Methods:
Levels of uric acid as well as on-treatment residual platelet reactivity in response to adenosine diphosphate (ADP) were assessed in 301 clopidogrel-treated patients undergoing elective angioplasty and stenting, and in 206 prasugrel- (n = 118) or ticagrelor-treated (n = 88) ACS patients following acute PCI. Cut-off values for high on-treatment residual ADP-inducible platelet reactivity (HRPR) were based on previous studies showing an association of test results with clinical outcomes.
Results:
Hyperuricemia was significantly associated with increased on-treatment residual ADP-inducible platelet reactivity in clopidogrel- and prasugrel-treated patients in univariate analyses and after adjustment for differences in patient characteristics by multivariate regression analyses. In contrast, ticagrelor-treated patients without and with hyperuricemia showed similar levels of on-treatment residual platelet reactivity to ADP. HRPR occurred more frequently in clopidogrel- and prasugrel-treated patients with hyperuricemia than in those with normal uric acid levels. In contrast, hyperuricemic patients receiving ticagrelor did not have a higher risk of HRPR compared with those with normal uric acid levels.
Conclusion:
Hyperuricemia is associated with decreased platelet inhibition by thienopyridines but a normal response to ticagrelor. It remains to be established if lowering uric acid increases the antiplatelet effects of clopidogrel and prasugrel in hyperuricemic patients with HRPR.
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