Abstract
Transition from cangrelor to oral P2Y12 inhibitors after PCI carries the risk of platelet function recovery and acute stent thrombosis. Whether the recommended transition regimen is appropriate for hypothermic cardiac arrest survivors is unknown. We assessed the rate of high platelet reactivity (HPR) after transition from cangrelor to ticagrelor in hypothermic cardiac arrest survivors. Adult survivors of out-of-hospital cardiac arrest with ST-segment elevation myocardial infarction (STEMI), who were treated for hypothermia (33 °C ± 1) and received intravenous cangrelor during PCI and subsequent oral loading with 180mg ticagrelor were enrolled in this prospective observational cohort study. Platelet function was assessed using whole blood aggregometry. HPR was defined as AUC > 46U. The primary endpoint was the rate of HPR (%) at predefined time points during the first 24 h after cangrelor cessation. Poisson regression was used to estimate the relationship between the overlap time of cangrelor and ticagrelor co-administration and the number of subsequent HPR episodes, expressed as incidence rate ratio (IRR) with 95% confidence interval (95%CI). Between December 2017 and October 2019 16 patients (81% male, 58 years) were enrolled. On average, ticagrelor was administered 39 min (IQR 5–50) before the end of cangrelor infusion. The rate of HPR was highest 90 min after cangrelor cessation and was present in 44% (7/16) of patients. The number of HPR episodes increased significantly with decreasing overlap time of cangrelor and ticagrelor co-administration (IRR 1.03, 95%CI 1.01–1.05; p = 0.005). In this selected cohort of hypothermic cardiac arrest survivors who received cangrelor during PCI, ticagrelor loading within the recommended time frame before cangrelor cessation resulted in a substantial amount of patients with HPR.
Highlights
Acute coronary occlusion is a leading cause of cardiac arrest requiring immediate antiplatelet treatment and percutaneous coronary intervention (PCI) [1]
In a meta-analysis of three large phase III trials (CHAMPION PCI, PLATFORM and PHOENIX) consisting of patients undergoing PCI, cangrelor has been shown to reduce the rate of death, myocardial infarction, ischemia-driven revascularization, or stent thrombosis at 48 h and 30 days compared with clopidogrel, without increase in major bleeding [10]
This transition regimen, might be inappropriate for resuscitated patients treated with hypothermia, as it may pose the risk of early platelet function recovery and stent thrombosis, which carries a 40% mortality at 30 days [13]
Summary
Acute coronary occlusion is a leading cause of cardiac arrest requiring immediate antiplatelet treatment and percutaneous coronary intervention (PCI) [1]. Hypothermia, morphine treatment and hemodynamic compromise, may impair oral P2Y12 inhibitor uptake and metabolism, resulting in delayed and insufficient platelet inhibition after coronary stenting [4,5,6,7] Both cardiac arrest and absence of P2Y12 inhibition are independent risk factors for acute stent thrombosis, a potentially fatal complication following successful PCI [8,9]. In accordance with cangrelor’s product characteristics, oral P2Y12 inhibitors should be administered a maximum of 30 min prior to cangrelor cessation, or immediately thereafter [12] This transition regimen, might be inappropriate for resuscitated patients treated with hypothermia, as it may pose the risk of early platelet function recovery and stent thrombosis, which carries a 40% mortality at 30 days [13]
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