RA is safe and effective, with high rate of procedural success and relatively low incidence of MACE. PVD, DM, ACS presentation and SYNTAX score were significant predictors for MACE. © 2016 Wiley Periodicals, Inc.

Background Oral P2Y12 inhibitors take more than 2 hours to achieve full effect in healthy subjects and this action is further delayed in patients with acute myocardial infarction. Intravenous P2Y12 inhibition might lead to more timely and potent anti-platelet effect in the context of emergency primary angioplasty, improving myocardial recovery. Objectives This article compares the efficacy of intravenous cangrelor versus ticagrelor in a ST-elevation myocardial infarction (STEMI) population treated with primary percutaneous coronary intervention (PPCI). Materials and Methods In an open-label, prospective, randomized controlled trial, 100 subjects with STEMI were assigned 1:1 to intravenous cangrelor or oral ticagrelor. The co-primary endpoints were platelet P2Y12 inhibition at infarct vessel balloon inflation time, 4 and 24 hours. Secondary endpoints included indices of coronary microcirculatory function: index of microvascular resistance (IMR), initial infarct size (troponin at 24 hours) and final infarct size at 12 weeks (cardiac magnetic resonance). Secondary endpoints included indices of coronary microcirculatory function (index of microvascular resistance [IMR]), initial infarct size (troponin at 24 hours), final infarct size at 12 weeks (cardiac magnetic resonance), corrected thrombolysis in myocardial infarction (TIMI) frame count, TIMI flow grade, myocardial perfusion grade, and ST-segment resolution (ClinicalTrials.gov NCT02733341). Results P2Y12 inhibition at first balloon inflation time was significantly greater in cangrelor-treated patients (cangrelor P2Y12 reaction unit [PRU] 145.2 ± 50.6 vs. ticagrelor 248.3 ± 55.1). There was no difference in mean PRU at 4 and 24 to 36 hours post-dosing. IMR, final infarct size, angiographic and electrocardiographic measures of reperfusion were all similar between groups. Conclusion Cangrelor produces more potent P2Y12 inhibition at the time of first coronary balloon inflation time compared with ticagrelor. Despite this enhanced P2Y12 inhibition, coronary microvascular function and final infarct size did not differ between groups.

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BackgroundOral P2Y12 inhibitors have a delayed onset of action in ST-segment elevation myocardial infarction (STEMI) patients. We describe the first randomised controlled trial comparing Cangrelor with Ticagrelor in the context of primary percutaneous coronary intervention (PPCI).Methods100 subjects with first acute STEMI were randomised on arrival to Ticagrelor (180 mg then 90 mg bd) or Cangrelor (bolus then infusion). Cangrelor treated subjects received Ticagrelor 30 min prior to infusion end. All patients received Aspirin 300 mg.Platelet P2Y12 inhibition was assessed using VerifyNow at first coronary balloon inflation, 4 and 24 hours post drug initiation. Coronary microcirculation was assessed after PPCI by calculating the index of microvascular resistance (IMR). ST-segment resolution at 90 min was measured and the corrected TIMI frame count, flow grade and myocardial perfusion grade were calculated. Peak Troponin level at 24 hours and infarct size at 12 weeks were measured by cardiac magnetic resonance imaging (CMRI) (ClinicalTrials.gov NCT02733341).ResultsP2Y12 inhibition was markedly greater in the Cangrelor group (PRU 145.2 vs 248.3 p<0.0001) at balloon inflation. At 4 hours (158.1 vs 131.2 p=ns) and 24 hours (61.0 vs 60.1 p=ns) readings were similar. Despite this early more potent antiplatelet effect, no difference was seen in terms of IMR, ST-segment resolution, and angiographic measures of improved reperfusion or final infarct size.ConclusionEarly, more potent P2Y12 inhibition with Cangrelor does not translate into improved measures of microcirculatory function or infarct size.