Impact of platelet inhibition level on subsequent no-reflow in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction

Abstract

High P2Y12 platelet reactivity (PR) level after primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) affects prognosis and may induce the no-reflow phenomenon. To investigate the role of PR in the genesis of microvascular obstruction. Patients with STEMI undergoing PPCI within 12hours of symptoms onset were included prospectively. All patients received a 600mg clopidogrel-loading dose before PPCI and 250mg aspirin. PR was measured thereafter during PPCI while wiring the culprit lesion and before coronary dilatation, using the P2Y12 VerifyNow® assay. No-reflow was defined as ST-segment regression<50% observed 90minutes after PPCI. Between January 2014 and November 2015, 140 STEMI patients were included, and divided into two groups: a low PR group (LPR) defined as PR<209P2Y12 reaction units (PRU); and a high PR group (HPR) defined as PR≥209PRU. There were no differences in baseline characteristics between LPR and HPR groups, including age (57.8±11.9 vs. 59.4±13.2 years, respectively; P=0.44) and weight (76.1±15.1 vs. 74.8±10.9kg, respectively; P=0.55). Delay to revascularization was 270.1±175.5 vs. 295.6±206.2minutes (P=0.49) and time between clopidogrel-loading and PR measurement was 53±37 vs 65±54minutes (P=0.29) in the LPR and HPR groups, respectively. No-reflow was more frequent in the HPR group (44 [47.3%] vs. 9 [19.1%]; P=0.0012). Mean PR was higher in patients with no-reflow: 268.3±53 vs. 223.8±50.1 PRU (P=0.002). In multivariable analysis, HPR was an independent predictor of no-reflow. Area under the receiver operating characteristic curve was 0.745 (0.654, 0.835); the cut-off value predicting no-reflow was 254PRU. High PR level measured at PPCI is independently associated with no-reflow.