Abstract

Introduction: Among adult patients with previous surgical correction for Tetralogy of Fallot or other repaired Congenital Heart Disease (rCHD) involving the RV, ventricular arrhythmias (VA) and sudden cardiac death (SCD) represent a late complication. The imparied haemodynamics that lead to RV dilatation and overload could also alterate its electroanatomic structure. Hypothesis: 3D electroanatomic mapping (EAM) of the RV could confirm the presence of myocardial electrical abnormalities, allowing to better identify patients at risk for life-threatening arrhythmias. Methods: 146 patients (age 19.2 ±7.0) with rCHD involving the RV were selected from a population undergoing routine post-surgical follow-up, according to the presence of VA or severe RV dilatation. These patients underwent 3D EAM of the RV. We tested the correlation between size of scar tissue (areas with voltage < 0.5 mV) and several parameters universally accepted by the literature as risk factors for VA in this particular patient population. Results: In 125 (85.6%) patients, EAM demonstrated areas of low voltage in the antero-lateral RVOT. In 20 of these (16%, 13.7% of the total) the scar extended to the septum. 72 (49.3%) had a peritricuspid scar, and in 20 (13.7%) other areas of the RV were interested. Total low-voltage area, expressed as % of total endocardial area, was significantly higher in patients with history of PVCs [3.2% (±2.6) vs 2.2% (±1.8), p<0.05], complex PVCs at 24h-Holter ECG (Lown class ≥2) [3.4 (±2.5) vs 2.6 (±2.3), p<0.05], exercise-inducible PVCs [3.8 (±2.4) vs 2.6 (±2.2), p=0.01] and history of previous shunt [4.0 (±2.7) vs 2.6 (±2.2), p=0.01]. Scar size was also positively correlated with age (p=0.01), age at correction (p=0.01) and QRS duration on surface ECG (p<0.05). Conclusions: In patients with rCHD involving the RV it is common to observe endocardial low-voltage areas with variable distribution, not always corresponding to the sites of surgical lesion. Morover, the size of the scar tissue area correlates with some of the parameters which have been already identified as risk factors for life-threatening arrhythmias and SCD in adult patients with CHD. We suggest that EAM should become part of the routine tests for the stratification of arrhythmic risk in this population.

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