Out-Of-Hospital Cardiac Arrest Clinical Trial
Official title:
Effect of Remote Ischemic Post-conditioning on Neurologic and Cardiac Recovery in Out-of-hospital Cardiac Arrest
Ischemia-reperfusion leads to mitochondrial injury, ion-pump injury, cell membrane damage, cytotoxic edema, and excessive oxygen free radical formation, and eventually destroys cells. Cardiac arrest is an example of global ischemia; after spontaneous circulation is restored, ischemia-reperfusion injury develops in cardiac arrest survivors. Remote ischemic postconditioning (RIPoC) involves the application of brief, reversible episodes of ischemia and reperfusion to a vascular bed or tissue, rendering remote tissues and organs resistant to ischemia-reperfusion injury. Accordingly, RIPoC has been suggested as adjunctive therapy to mitigate ischemia-reperfusion injury. RIPoC applied by repeated brief inflation-deflation of a blood pressure cuff protects against myocardial injury, and has been proven effective in acute myocardial infarction. This study aims to perform a randomized controlled trial to determine whether RIPoC has a neuroprotective effect and aids in myocardial recovery in out-of-hospital cardiac arrest patients after restoration of spontaneous circulation. Neuron-specific enolase (NSE) at 48 hours after restoration of spontaneous circulation will be measured as a primary outcome.
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