Beneficial Effects of Ivabradine on Post-Resuscitation Myocardial Dysfunction In A Porcine Model of Cardiac Arrest Background: Ivabradine selectively inhibits the If current, reducing the heart rate and protecting against myocardial ischemia/reperfusion injury. We investigated the effects of ivabradine on post-resuscitation myocardial function in a porcine model of cardiopulmonary resuscitation. Methods and Results: Ventricular fibrillation was induced and untreated for 8 minutes while defibrillation was attempted after 6 minutes of cardiopulmonary resuscitation in anesthetized domestic swine. Then the animals were randomized into ivabradine and placebo groups (n = 5 each). Ivabradine and saline were administered at the same volume 5 minutes after ROSC (Return of Spontaneous Circulation), followed by continuous intravenous infusion at 0.5 mg/kg for 480 minutes. Hemodynamic parameters were continuously recorded. Myocardial function was assessed by echocardiography at baseline and at 60, 120, 240, 480 minutes and 24 hours after resuscitation. The serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) were measured by commercial enzyme-linked immunosorbent assay kits. Animals were killed 24 hours after resuscitation, and all myocardial tissue was removed for histopathological analysis. The heart rate was significantly reduced from 1 hour after resuscitation in the ivabradine group (all p < 0.05). The post-resuscitation mitral E/A and E/e′ velocity ratios and left ventricular ejection fraction were significantly better in the ivabradine than placebo group (p < 0.05). The serum levels of myocardial injury biomarkers (NT-proBNP, cTnI) and the myocardial biopsy scores were significantly lower in the ivabradine than placebo group (p < 0.05). Neurological deficit scores were lower in the IVA group at PR 24 hours (p < 0.05). Conclusions: Ivabradine improved post-resuscitation myocardial dysfunction, myocardial injury and post-resuscitation cerebral function, and also slowed the heart rate in this porcine model. Address reprint requests to Min Yang, MD, PhD, The 2nd Department of Intensive Care Unit, No. 2 Hospital Affiliated to Anhui Medical University, Furong Road 678, Hefei, China, 230032. E-mail: 512130761@qq.com Received 4 April, 2019 Revised 25 April, 2019 Accepted 27 June, 2019 Source of funding: This study was supported by the National Natural Science Foundation of China (No. 81601661), Natural Science Foundation of Anhui Province of China (No. 1608085MH195), and Science Foundation for Post-doctoral Researchers in Anhui Province of China (No. 2016B140). Disclosure: The authors have no conflicts of interest to declare. This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0 © 2019 by the Shock Society