Background: Right ventricular (RV) dysfunction remains a problem long term after repair of tetralogy of Fallot (TOF). Investigation of new therapies is needed. Objectives: to establish an animal model reproducing repaired TOF, usable for therapeutic investigation. Methods: 2-month-old piglets were divided in 2 groups: (1) RV tract enlargement by patch across pulmonary valve and light pulmonary band (n=6), (2) aged-matched control animals (n=6). Evaluation of RV function was done at baseline, 3 and 4 months of FU, by hemodynamic study, electrophysiology and histology. Results: At 4 m, RV was dilated in operated animals, as showed by increased normalized end diastolic volume(281.5±58.2 vs 103.8±7.6mL, p=.03)and stroke volume (91.6±9.8 vs 47.7±11.8mL,p=.01); end systolic RV pressure increased (47.6±9.5 vs 10±1 mmHg (p=.008) secondary to the pulmonary artery banding (mean gradient=23.7±6.3vs1.3±.2mmHg, p=.03). Pulmonary valve regurgitation significantly increased with time in operated animals, from 4.8±4.1 at baseline to 26.8±5.3% at 4m (p=.01). In operated animals, end systolic pressure-volume relationship significantly increased from baseline to 3m,then decreased at 4m (respective values: .28±.05;.77±1;.34±.07, p=.01) but stroke work increased with time (respective values: 419±38; 2941±816; 3903±750mL.mmHg, p=.03). QRS duration increased with time in operated animals and was longer at 4m: 81.8±3.9vs66±2.3ms (p=.01), as well as duration of action potential: 294.9±4.8 vs 260.5±3.1ms (p=.001). Percentage of fibrosis was higher in operated animals: 20.7±10.3 vs 13.4±5.5%, p<.0001. Conclusion: this model reproduces hemodynamic, electrophysiological and histological diseases of RV dysfunction secondary to chronic volumetric and barometric overload, as observed in repaired TOF. New therapies may be tested on this model.