The atrioventricular node (AVN) is the only pathway for the propagation of the action potential from the atria to the ventricles. It is known that heart failure (HF) causes dysfunction of the AVN and the aim of the study was to determine if left ventricular heart failure (LVHF) causes remodelling of the AVN and the closely related right atrioventricular ring (RAVR) tissue (located around the tricuspid valve and made of nodal-like myocytes). The study was conducted in accordance with Guide for the Care and Use of Laboratory Animals (US National Institutes of Health Publication No. 85-23, revised 1996). LVHF was induced in 4 male Wistar rats (12 weeks old) by ligation of the proximal left coronary artery, which resulted in a large infarct of the left ventricle. Rats for myocardial infarction induction and Sham operated were anaesthetized with ketamine HCl and xylazine (100 mg and 5 mg/kg body weight, intrapertioneal). 4 sham operated rats were used as controls. 8 weeks after surgery, animals were anaesthetised ((ketamine HCl and xylazine, 75 mg and 3.5 mg/kg body weight, intraperitoneal), the ECG was recorded and left ventricular end diastolic pressure (LVEDP) was measured by left ventricular catheterisation. In the LVHF rats (but not the controls), the LVEDP was increased from 7±2 to 20±5 mm Hg, indicative of heart failure. In the LVHF rats (but not the controls), the PR interval was also increased (from 49±2 to 59±2 ms), indicative of AVN dysfunction. The hearts were retrieved and frozen in liquid nitrogen. Cryosections were cut from different regions of the heart: the right atrium (RA), left atrium (LA), right ventricle (RV), left ventricle (LV), AVN and RAVR. The tissues were studied using histology (Masson’s trichrome and picrosirius red), immunohistochemistry and TUNEL assay (in situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling), and image analysis software (Velocity and Image J) was used to quantify the results. Immunolabelling of caveolin3 (cell membrane marker for cardiac myocytes) showed that there was hypertrophy in HF; the cell diameter was significantly increased in the AVN, RAVR and working myocardium. Picrosirius red staining showed that there was fibrosis in HF: the collagen content was significantly increased in the AVN, RAVR and working myocardium (RA, RV and LV). Immunolabelling showed that in HF: expression of HCN4 (a major pacemaker channel in the cardiac conduction system) was significantly decreased in the AVN and RAVR; expression of Cx43 (a major gap junction channel in the working myocardium) was significantly decreased in the RA, LA, RV and LV; and there was a redistribution of RYR2 (a Ca2+-handing protein) in the ventricular muscle. The TUNEL assay suggests that in HF animals the cardiac myocytes of the AVN, RAVR and working myocardium undergo apoptotic cell death. We conclude that in this model of HF there is a remodelling of the AVN and RAVR (as well as the working myocardium) and this remodelling may contribute to the AVN dysfunction.