Background Ventricular arrhythmias are an important cause of mortality in the acute myocardial infarction (MI). Objective To elucidate effect of ivabradine, pure heart rate (HR) reducing drug, on ventricular arrhythmias within 24 hours after non‐reperfused MI in the rat. Methods ECG was recorded for 24 hours after MI in untreated and ivabradine treated rats and episodes of ventricular tachycardia/fibrillation (VT/VF) were identified. 45 minutes and 24 hours after MI epicardial monophasic action potentials (MAPs) were recorded, cardiomyocyte Ca2+ handling was assessed and expression and function of ion channels were studied. Results Ivabradine reduced average HR by 17%. Combined VT/VF incidence and arrhythmic mortality were higher in MI vs. MI + Ivabradine rats. MI resulted in (1) increase of Ca2+ sensitivity of ryanodine receptors 24 hours after MI; (2) increase of HCN4 expression in the left ventricle (LV) and funny current (IF) in LV cardiomyocytes 24 hours after MI, and (3) dispersion of MAP duration both 45 minutes and 24 hours after MI. Ivabradine partially prevented all these three potential proarrhythmic effects of MI. Conclusions Ivabradine is antiarrhythmic in the acute MI in the rat. Potential mechanisms include prevention of: diastolic Ca2+‐leak from sarcoplasmic reticulum, upregulation of IF current in LV and dispersion of cardiac repolarization. Ivabradine could be an attractive antiarrhythmic agent in the setting of acute MI. J. Cell. Physiol. © 2013 Wiley Periodicals, Inc.