Intensified P2Y12 inhibition for high-on treatment platelet reactivity
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Intensified P2Y12 inhibition for high‑on treatment platelet reactivity Fakilahyel S. Mshelbwala1 · Daniel W. Hugenberg1 · Rolf P. Kreutz1
© Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract High on treatment platelet reactivity (HPR) during treatment with clopidogrel has been consistently found to be strong risk factor for recurrent ischemic events after percutaneous coronary intervention (PCI). Insufficient P2Y12 receptor inhibition contributes to HPR measured by the VerifyNow (VN) assay. Prasugrel and ticagrelor are more potent P2Y12 inhibitors than clopidogrel and commonly substituted for clopidogrel when HPR is documented, however benefit of VN guided intensified antiplatelet therapy is uncertain. We identified patients who had undergone platelet reactivity testing after PCI with VN after pretreatment with clopidogrel (n = 252) in a single center observational analysis. Patients who had HPR defined as PRU > 208 were switched to alternate P2Y12 inhibitors. Primary clinical endpoint was 1-year post PCI combined cardiovascular death, myocardial infarction (MI), and stent thrombosis. One hundred and eight (43%) subjects had HPR and were switched to prasugrel (n = 60) and ticagrelor (n = 48). Risk of recurrent 1-year primary endpoint remained higher for HPR patients switched to either ticagrelor or prasugrel as compared to subjects who had low on treatment platelet reactivity (n = 144) (LPR) on clopidogrel [Hazard Ratio: 3.5 (95% CI 1.1–11.1); p = 0.036)]. Propensity score matched analysis demonstrated higher event rates in patients with HPR on alternate P2Y12 inhibitor as compared to patients with LPR (logrank: p = 0.044). The increased risk of recurrent events associated with HPR measured by VN is not completely attenuated by switching to more potent P2Y12 inhibitors. Non-P2Y12 mediated pathways likely contribute to increased incidence of thrombotic events after PCI in subjects with HPR. Keywords Clopidogrel · Prasugrel · Ticagrelor · Myocardial infarction
Highlights • Prasugrel and ticagrelor are commonly substituted for
clopidogrel when high on treatment platelet reactivity (HPR) is documented, however benefit of VerifyNow platelet assay guided therapy is uncertain. • Patients who had HPR defined as PRU>208 on clopidogrel were switched to prasugrel or ticagrelor. • Risk of recurrent 1-year ischemic events remained higher for HPR patients who were switched to ticagrelor or prasElectronic supplementary material The online version of this article (https://doi.org/10.1007/s11239-020-02075-x) contains supplementary material, which is available to authorized users. * Rolf P. Kreutz [email protected] 1
Department of Medicine, Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
ugrel, as compared to subjects who had low on treatment platelet reactivity on clopidogrel. • Non-P2Y12 mediated pathways likely contribute to increased incidence of thrombotic events after PCI in subjects with HPR.
Introduction Dual antiplatelet therapy (DAPT)
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