Abstract
PurposeHyperuricemia 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.MethodsLevels 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.ResultsHyperuricemia 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.ConclusionHyperuricemia 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.
Highlights
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
To investigate whether or not current state-of-the-art P2Y12 receptor inhibition is able to adequately suppress platelet aggregation in hyperuricemic patients, we studied on-treatment residual adenosine diphosphate (ADP)-inducible platelet
In group 2, there was a trend towards higher levels of uric acid in patients on ticagrelor compared with those on prasugrel (5.8 mg/dL (5.1–7 mg/dL) vs. 5.6 mg/dL (4.5–6.5 mg/dL), p = 0.05)
Summary
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 [1,2,3]. By enhancing intracellular oxidative stress, Cardiovasc Drugs Ther (2021) 35:51–60 reactivity by various platelet function tests in patients without standardized protocols. Hyperuricemia was defined as uric and with hyperuricemia following elective and acute PCI. Acid > 6 mg/dL in women and > 7 mg/dL in men, respectively
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