BACKGROUND: Ablation of ventricular tachycardias in arrhythmogenic right ventricular dysplasia (ARVD-VTs) still remains a clinical challenge. We reported the value of abnormal electrophysiological substrate mapping for guiding ablation of ARVD-VTs using a non-contact mapping system. METHODS AND RESULTS: Dynamic substrate mapping was performed in three male ARVD patients during sinus rhythm. The sites of earliest activation, exit point and activation sequence were mapped for each induced VT. Three different patterns of substrates were determined in 3 patients and located in right ventricular outflow tract, anterior right ventricular wall, and anterolateral right ventricular wall, respectively. Five different clinical VTs (mean CL, 348 +/- 65 ms) were induced. Of 5 VTs, three originated from or near the boundary of substrate, and two had a remote origin. One VT conducted through the substrate. Linear ablations were created between the sites of the earliest ventricular activation and the VT exit point, or across the critical isthmus. The five clinical VTs were successfully ablated with a median of 17 radiofrequency applications. One patient was treated with amiodarone for a VT not clinically observed. There were no VT recurrences during 8.6 months of follow-up. CONCLUSIONS: Defining the abnormal anatomical VT substrates is useful for understanding the mechanisms of ARVD-VTs and determining an ablation strategy. Linear ablation across a critical isthmus or between the early activation and the exit point can effectively cure these arrhythmias.
BACKGROUND: Ablation of ventricular tachycardias in arrhythmogenic right ventricular dysplasia (ARVD-VTs) still remains a clinical challenge. We reported the value of abnormal electrophysiological substrate mapping for guiding ablation of ARVD-VTs using a non-contact mapping system. METHODS AND RESULTS: Dynamic substrate mapping was performed in three male ARVDpatients during sinus rhythm. The sites of earliest activation, exit point and activation sequence were mapped for each induced VT. Three different patterns of substrates were determined in 3 patients and located in right ventricular outflow tract, anterior right ventricular wall, and anterolateral right ventricular wall, respectively. Five different clinical VTs (mean CL, 348 +/- 65 ms) were induced. Of 5 VTs, three originated from or near the boundary of substrate, and two had a remote origin. One VT conducted through the substrate. Linear ablations were created between the sites of the earliest ventricular activation and the VT exit point, or across the critical isthmus. The five clinical VTs were successfully ablated with a median of 17 radiofrequency applications. One patient was treated with amiodarone for a VT not clinically observed. There were no VT recurrences during 8.6 months of follow-up. CONCLUSIONS: Defining the abnormal anatomical VT substrates is useful for understanding the mechanisms of ARVD-VTs and determining an ablation strategy. Linear ablation across a critical isthmus or between the early activation and the exit point can effectively cure these arrhythmias.