Decreased Platelet Inhibition by Thienopyridines in Hyperuricemia
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ORIGINAL ARTICLE
Decreased Platelet Inhibition by Thienopyridines in Hyperuricemia Silvia Lee 1 & Patricia P. Wadowski 1 & Timothy Hoberstorfer 1 & Constantin Weikert 1 & Joseph Pultar 1 & Christoph W. Kopp 1 & Simon Panzer 2 & Thomas Gremmel 1,3 Accepted: 17 August 2020 # The Author(s) 2020
Abstract 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. Keywords Hyperuricemia . Clopidogrel . Prasugrel . Ticagrelor . Platelet reactivity
Introduction Uric acid is generated through oxidation of hypoxanthine to xanthine and further degradation of xanthine by xanthine oxidase and constitutes the final product of purine catabolism. Levels of uric acid are associated with chronic kidney disease, diabetes, arterial hypertension, and metabolic syndrome [1–3]. Moreover, by enhancing intracellular oxidative stress, * Thomas Gremmel [email protected] 1
Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
2
Department of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Vienna, Austria
3
Department of Internal Medicine I, Landesklinikum Mistelbach-Gänserndorf, Mistelbach, Austria
endothelial dysfunction, and vascular inflammation[4–7], high lev
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