Abstract

Introduction: Previous studies have demonstrated that β-adrenergic blocking agents improved neurologic function and the rate of survival. However, its negative inotrope effects that increased the severity of PRMD (post-resuscitation myocardial dysfunction). We studied whether ivabradine (IVA) improves PRMD in a cardiac arrest model. Hypothesis: we hypothesized that the rational use of IVA would improve severity of PRMD and prognosis in a porcine model of CA. Methods: Ventricular fibrillation was induced and untreated for 8 minutes in anesthetized domestic swine while defibrillation was attempted after 6 minutes of cardiopulmonary resuscitation. Hemodynamic parameters were monitored continuously after ROSC. Mitral E/A ratio and E/e′ velocity ratio were assessed by echocardiography at Baseline, PR 1, 2, 4, 8 and 24hours after ROSC. The levels of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured by ELISA method at Baseline, PR 1, 4 and 24hours. The animals were euthanized 24h after ROSC, and the cardiac tissue was removed for histopathological analysis. Results: Heart rate in the IVA group reduced significantly compared with the control group (all P < 0.05) at PR 1, 2, 4, 8hours. Animals subjected to IVA groups presented significantly better post-resuscitation relaxation function (E/A, E/e′) than those in the Placebo groups (all P < 0.05) (Figure1). IVA group had a lower cTnI and NT-proBNP levels than Placebo group at PR 1, 4 and 24hours (all P < 0.05) (Figure1). Biopsy score in the IVA group was significantly lower at PR 24hours when compared with the Placebo group (all P < 0.05) (Figure2). Conclusions: Heart rate reduction with IVA, improved left ventricular diastolic function and reduced myocardial injury.

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