Aim: We tested the hypothesis that heart rate (HR) reduction induced by the selective If current inhibitor ivabradine (IVA) might improve left ventricular (LV) function, structure and electrical remodeling in severe post-myocardial infarction (MI) chronic heart failure (HF). Methods: MI was produced in adult male Wistar rats. After 2 months, echocardiography was performed before randomization into MI and MI+IVA (10 mg/kg/d) groups. After 3 months of treatment, echocardiography and 24-hour telemetry were recorded. Cardiac interstitial collagen, mRNA expressions of ACE and AT-1 receptor were quantified. Results: Two months post-MI, all rats displayed severe CHF signs (EF<30%). Five months post-MI, body and heart weights were similar in MI and MI+IVA groups. LVEF and LVEDP were worsened in MI group, while were improved on IVA. IVA reduced HR by 10.4% (p<0.03 vs. MI), VPC by 89% (p<0.03), and improved HR variability (sdRR) by 22% (p<0.05). There were no effects of IVA on PR, QRS and QT durations. Fibrosis in MI remote LV was markedly reduced by IVA (4.0±0.1 vs 1.8±0.1%, p<0.005). Increases in ventricular gene expression of ACE and AT-1 receptor in MI were completely blunted by IVA. Conclusion: These data indicated that HR reduction by IVA prevents worsening of LV dysfunction and remodeling that may be related to a down-regulation of cardiac RAAS transcripts. Such beneficial effects of IVA on cardiac remodeling open new clinical perspectives for the treatment of severe HF.