Ventricular arrhythmias are frequent in patients with repaired tetralogy of Fallot but their underlying mechanisms remain unclear. In this study, ventricular electrical and structural remodelling was assessed in an animal model that mimics postoperative tetralogy of Fallot. Piglets underwent a tetralogy of Fallot repair-like surgery (rTOF N=6) or were sham-operated (Sham N=5). Following cardiac function assessment in vivo by MRI 3-4 months after surgery, pigs were euthanized and their hearts rapidly excised. Electrophysiological properties of right (RV) and left ventricles (LV) were obtained by optical mapping. Fibrosis was assessed histologically. RV dysfunction was evident while LV function remained unaltered in rTOF pigs. LV action potential duration (APD) was significantly longer on the epicardium (Sham 280±50ms; rTOF 390±76ms) and endocardium (Sham 301±20ms; rTOF 403±34ms) of rTOF animals (P<0.05). RV epicardial and endocardial APD were not different between rTOF and Sham RVs. LV conduction velocity (CV) was significantly reduced in the longitudinal direction in rTOF pigs (65.37 ±6.76cm/s vs 51.27±0.57cm/s; P<0.05) but remained unchanged in the transverse direction compared to Sham animals (27.34±3.08cm/s vs 30.19±1.97cm/s). In the RV both longitudinal and transverse CVs were significantly in rTOF compared to Sham (P<0.05). An elevated collagen content was found in both the LV and RV of rTOF pigs (P<0.05). A trend for a lateralization of Connexin43 was found in the LV of rTOFs which, together with the increased fibrosis, may account for the reduced longitudinal conduction velocity in this ventricle. Altogether, these findings highlight the presence of an arrhytmic substrate in the ventricles of rTOF pigs. Interestingly, the remodeling in LV is reminiscent to that observed in LV failure, despite no functional alterations, and is likely to contribute to ventricular arrhythmias in patients with rTOF.