Effect of Remote Ischemic Post-conditioning on Out-of-hospital Cardiac Arrest

Chonnam National University Hospital58 enrolled

Overview

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.

Study Type

INTERVENTIONAL

Allocation

RANDOMIZED

Purpose

TREATMENT

Masking

SINGLE

Enrollment

Conditions

Out-Of-Hospital Cardiac Arrest

Eligibility

Sex: ALLMin age: 19 Years

Medical Language ↔ Plain English

Inclusion Criteria: * Adult (19 years and older) * comatose out-of-hospital cardiac arrest with sustained restoration of spontaneous circulation * Undergoing targeted temperature management * Time of enrollment ≤ 6hrs from restoration of spontaneous circulation * cardiac arrest from medical cause (cardiac or other medical cause) Exclusion Criteria: * Pre-existing dementia, brain injury, or dependence on others (cerebral performance category scale greater than 3) * Traumatic etiology for cardiac arrest * Protected population (pregnant, prisoner) * in-hospital cardiac arrest * Known bleeding diathesis * suspected or confirmed acute intracranial hemorrhage * suspected or confirmed acute ischemic stroke * Known limitations in therapy and do-not-resuscitate order * known disease making 180-day survival unlikely * \>6 hours from restoration of spontaneous circulation to randomization * cardiac arrest from asphyxia (hanging, foreign body airway obstruction), drowning, drug overdose, or electrocution * peripheral vascular disease (Deep vein thrombosis, arteriosclerosis obliterans) * systolic blood pressure \< 80 mmHg in spite of fluid loading/vasopressor and/or inotropic medication

Outcomes

Primary Outcomes

neuron specific enolase

expressed in ng/ml

Time frame: at 48 hour after restoration of spontaneous circulation

Secondary Outcomes

change over troponin-I

troponin-I will be expressed in ng/ml

Time frame: at 24 hour and 48 hour after restoration of spontaneous circulation

change over creatinin kinase-MB

CK-MB will be expressed in ng/ml

Time frame: at 24 hour and 48 hour after restoration of spontaneous circulation

neurologic outcome

cerebral performance category scale 1, 2, 3, 4, 5

Time frame: an average of 3 weeks after restoration of spontaneous circulation