Extracorporeal membrane oxygenation mitigates myocardial injury and improves survival in porcine model of ventricular fibrillation cardiac arrest.

INTRODUCTION

Despite decades of improved strategy in conventional cardiopulmonary resuscitation (CCPR), survival rates of favorable neurological outcome after cardiac arrest (CA) remains poor. It is indicated that the survival rate of successful resuscitation of extracorporeal membrane oxygenation (ECMO) is superior to that of CCPR. But the effect of ECMO in heart is unclear. We aimed to investigate whether ECMO produces cardiac protection by ameliorating post-ischemia reperfusion myocardial injury and myocardial apoptosis.

METHODS

After undergoing 8-min untreated ventricle fibrillation (VF) and 6-min basic life support, 20 male pigs were ultimately used in this study and randomly divided into two groups: CCPR group (n = 10) and extracorporeal CPR (ECPR) group (n = 10). Hemodynamics and blood samples were obtained at baseline and 1, 2, 4, and 6 h during resuscitation. The successfully resuscitated pigs were sacrificed at 6 h after return of spontaneous circulation (ROSC), and the hearts were removed and analyzed under electron microscopy, and immunohistochemistry, quantitative real-time polymerase chain reaction, and immunofluorescence staining assay were performed to evaluate myocardial injury and myocardial apoptosis.

RESULTS

There were no significant differences at basic hemodynamic status between the two groups. The survival rate of ECPR was significantly higher than CCPR group (10/10 [100%] vs. 4/10 [40%], P = 0.04). Compared to CCPR group, ECPR group exhibited a better outcome in hemodynamic function. Cardiac function was significantly impaired after ROSC in both groups, but left ventricular ejection fraction (LVEF) was significantly elevated in ECPR group than CCPR group. The expression of myocardial injury biomarkers (CK-MB, cTNI, H-FABP), endothelial injury biomarker (sP-selectin), and cardiac function biomarker (BNP) were remarkably increased after ROSC in both groups, but low levels in ECPR group than in CCPR group. Cardiomyocytes injury was attenuated in ECPR group under transmission electron microscopy (TEM). Typical apoptotic nuclei of cardiomyocytes were significantly reduced and oxidative damage were attenuated in ECPR group.

CONCLUSIONS

During prolonged VF-induced CA, ECPR contributes to improving hemodynamics, attenuating myocardial ischemia-reperfusion injury, ameliorating myocardial ultra structure, improving cardiac function, and elevating survival rate by preventing oxidative damage, regulating energy metabolism, inhibiting cardiomyocyte apoptosis.