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

Summary Background High P2Y 12 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. Aim To investigate the role of PR in the genesis of microvascular obstruction. Methods Patients with STEMI undergoing PPCI within 12 hours of symptoms onset were included prospectively. All patients received a 600 mg clopidogrel-loading dose before PPCI and 250 mg aspirin. PR was measured thereafter during PPCI while wiring the culprit lesion and before coronary dilatation, using the P2Y 12 VerifyNow ® assay. No-reflow was defined as ST-segment regression  Results Between January 2014 and November 2015, 140 STEMI patients were included, and divided into two groups: a low PR group (LPR) defined as PR  12 reaction units (PRU); and a high PR group (HPR) defined as PR ≥ 209 PRU. 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 ± 10.9 kg, respectively; P  = 0.55). Delay to revascularization was 270.1 ± 175.5 vs. 295.6 ± 206.2 minutes ( P  = 0.49) and time between clopidogrel-loading and PR measurement was 53 ± 37 vs 65 ± 54 minutes ( 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 254 PRU. Conclusion High PR level measured at PPCI is independently associated with no-reflow.