Abstract

Introduction: There are conflicting data on the optimal timing of platelet reactivity (PR) measurements to identify patients at risk of major adverse cardiovascular events (MACE) and bleeding. Hypothesis: We hypothesized that significant changes in PR occur peri-PCI Methods: We studied 395 patients undergoing PCI for NSTEMI/UA. Patients received, in the emergency room, aspirin (300 mg loading dose followed by 100 mg maintenance dose) and one of two P2Y 12 antagonists: clopidogrel (300 mg/ 75 mg OM) or ticagrelor (180 mg/ 90 mg BD). Adenosine diphosphate-induced multiple electrode aggregometry (Multiplate ®) was performed to analyze PR at the time of PCI and post-PCI (24 hours). In-hospital and 30-day MACE, defined as cardiovascular death, recurrent MI, stroke or stent thrombosis, and bleeding, defined as bleeding academic research consortium (BARC) type 2 or greater bleeding, were assessed in all patients. Results: Patients were treated with clopidogrel [N=356 (89%)] or ticagrelor [N=39 (11%)] (Table1). The mean pre and post PCI PR was consistently higher with clopidogrel than ticagrelor. However, the mean reduction in pre-post PCI PR was 3-fold greater for clopidogrel than ticagrelor (P<0.01 by Kruskall-Wallis test). In-hospital and 30-day post-discharge MACE and bleeding events corresponded closely with the frequency of pre and post PCI hyporesponders, defined as PR >468 AU*min, and hyperresponders, defined as PR > 300 AU* min, respectively. Conclusion: Large differential reductions in PR were observed within 24 hours post-PCI. PR measurements tracked well with inhospital and post-discharge MACE and bleeding events. Among patients with only pre-PCI measurement, consideration should be given to repeating PR measurements within 24 hours post-PCI.

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