Arrhythmia due to heart failure (HF) is one of the leading causes of cardiac death. Structural and electrical remodeling due to increased strain of the heart is some of the contributing factors in the proarrhythmic milieu seen in HF patients. Mapping the severity and timeframe of these changes may help discover new targets in treatment of HF and the consequent arrhythmia. Rabbits were implanted with pacemakers and telemetric equipment (n=7) and LV tachy-paced at 300bpm for 10½ weeks. The development of HF was monitored by echocardiography and following the 10½ weeks, the hearts were excised and hung in a Langendorff set-up, where hemodynamic and electrical properties were measured. The effects of the pacing protocol were assessed for IKs and IKr under conditions of both high (10mM) and low (2.5mM) potassium. During the 10½ weeks of tachy-pacing the QTc of the tachy-paced group increased from 216±10ms at baseline to 242±6ms at the end of the protocol (P<0.01). In comparison, the QTc of the sham-operated rabbits remained unchanged (220ms) during the entire period. Furthermore, a decrease in the unpaced HR was observed in the tachy-paced group (from approximately 230bpm at baseline to approximately 180bpm). The echocardiography showed a clear dilation of the left ventricular end-diastolic volume (LVEDV) when comparing baseline to 10½ weeks. The HW/BW ratio was greater in the tachy group (4.96±0.6g/kg) compared to the WT- (3.01±0.2g/kg) and the sham group (3.34g/kg). In conclusion, we have developed a model which induces end stage HF in rabbits following 10½ weeks of pacing at 300bpm. The echocardiography and telemetric data confirmed this, showing increased LVEDV and QTc at the end of the pacing protocol, and furthermore a large increase in the HW/BW ratio showing cardiac hypertrophy. In the Langendorff clear indications of reductions in the repolarizing currents, Iks and Ikr, as well as in the total repolarizing reserve was shown as consequences of the developed HF.