Intensified P2Y12 inhibition for high-on treatment platelet reactivity

摘要: High on treatment platelet reactivity (HPR) during 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 HPR measured by the VerifyNow (VN) assay. Prasugrel and ticagrelor are more potent inhibitors than commonly substituted when is documented, however benefit of VN guided intensified antiplatelet therapy uncertain. We identified patients who had undergone testing PCI pretreatment (n = 252) in a single center observational analysis. Patients defined as PRU > 208 were switched alternate inhibitors. Primary clinical endpoint was 1-year post combined cardiovascular death, myocardial infarction (MI), stent thrombosis. One hundred eight (43%) subjects prasugrel (n = 60) (n = 48). Risk primary remained higher either or compared low (n = 144) (LPR) [Hazard Ratio: 3.5 (95% CI 1.1–11.1); p = 0.036)]. Propensity score matched analysis demonstrated event rates inhibitor LPR (log-rank: p = 0.044). The increased associated not completely attenuated switching Non-P2Y12 mediated pathways likely contribute incidence thrombotic HPR.