Patients after repaired tetralogy of Fallot (TOF) frequently have right ventricular (RV) dysfunction and prolonged duration (QRSd), the latter is considered as a sudden death risk factor. It has been suggested that QRSd mainly reflects abnormalities of the RV outflow tract (RVOT) rather than the RV body itself. We aimed to better understand the RV electrical activation pattern in these patients using activation mapping.

63 adults (36,3±14 yo, median QRS duration 159ms IQR 142- 170) referred for either catheter ablation or pulmonary valve replacement late after TOF repair underwent a MRI, with fibrosis analysis, and an invasive RV activation mapping (201±32 sites per patient; Carto 3 – Biosense Webster). RV total activation time (RVTAT) was defined as the duration between the first and the last RV EGM.

The delay between QRS onset and earliest RV EGM was 28±23ms traducing the absence of RV purkinje activation and the left to right ventricle activation. We observed in all patients a single RV breakthrough (mid-septal in 86%, septo-basal in 7% and apico-septal in 7%) followed by 2 spreads of activation: a first wave from the septum to the RV anterior wall through the RVOT with fragmented EGM in the infundibulum; a second wave from the septum to the RV free wall through the apex with slow conduction. The RV free wall was the latest activated in all the patients (Figure). RVTAT (145±20ms) was correlated to QRS duration (r=0,72 ; p<0,001) and to RVOT scar surface area in MRI (r=0,62 ; p<0,001). These activation parameters were correlated with fibrosis revealed by MRI.

RV delayed activation in patients with repaired TOF traduces a homogeneous activation pattern that is not only the consequence of an infundibular disease but also reflects a slow conduction in the RV free wall.

The author hereby declares no conflict of interest