Abstract
IntroductionDelivery of crushed ticagrelor via a nasogastric tube is a widely spread off-label use in unconscious patients following out-of-hospital cardiac arrest (OHCA). Notwithstanding the importance of a potent dual antiplatelet therapy in these patients, the efficacy of crushed ticagrelor after OHCA has not been established yet.MethodsIn a prospective, single-center, observational trial, 38 consecutive MI patients after OHCA were included. 27 patients (71.1 %) underwent mild induced hypothermia. The primary outcome was platelet inhibition at 24h measured by impedance aggregometry.ResultsThere was sufficient platelet inhibition in most patients after OHCA. In all hypothermic patients, there was an adequate platelet inhibition by ticagrelor at 24 h (p < 0.001). 15 patients (39.5 %) had significant gastroesophageal reflux and one patient with significant reflux had inadequate platelet inhibition at 24 h. There were no stent thrombosis or recurrent atherothrombotic events in these patients.ConclusionAdministration of crushed ticagrelor via a nasogastric tube reliably inhibited platelet function in vitro and in vivo regardless of the presence of hypothermia in MI patients. Thus, platelet inhibition can be reliably achieved in MI patients during neuroprotective hypothermia following OHCA.
Highlights
Delivery of crushed ticagrelor via a nasogastric tube is a widely spread off-label use in unconscious patients following out-of-hospital cardiac arrest (OHCA)
Of these primary OHCA survivors, about a third died despite maximum intensive care treatment. 24 patients could be discharged from hospital
Most deaths were attributed to fatal hypoxic brain damage, while other patients died despite maximum intensive care treatment in a catecholamine refractory cardiogenic shock
Summary
Delivery of crushed ticagrelor via a nasogastric tube is a widely spread off-label use in unconscious patients following out-of-hospital cardiac arrest (OHCA). Cardiac diseases such as acute myocardial infarction (MI) are the leading cause for out-of-hospital cardiac arrest (OHCA) [1]. The post-cardiac arrest phase is a complex combination of various processes, including myocardial dysfunction, systemic ischemia/reperfusion response and brain injury [3,4,5]. These effects lead to an activation of endogenous coagulation and anticoagulation, acidosis, and pro-inflammatory mechanisms, which can alter platelet count and function [6,7,8,9]. Ticagrelor does not require cytochrome p450 (CYP) conversion and there are no genetic polymorphisms known that may result in a loss of function, and be of disadvantage in patients after OHCA [19]
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