The transmural activation interval: a new mapping tool to identify ventricular tachycardia substrates in right ventricular cardiomyopathy

AIMS: In right ventricular cardiomyopathy (RVCM), intramural scar may prevent rapid transmural activation, which may facilitate subepicardial ventricular tachycardia (VT) circuits. A critical transmural activation delay determined during sinus rhythm (SR) may identify VT substrates in RVCM. METHODS AND RESULTS: Consecutive patients with RVCM who underwent detailed endocardial-epicardial mapping and ablation for scar-related VT were enrolled. The transmural activation interval (TAI, first endocardial to first epicardial activation) and maximal activation interval (MAI, first endocardial to last epicardial activation) were determined in endocardial-epicardial point pairs located <10 mm apart. VT-related sites were determined by conventional substrate mapping and limited activation mapping when possible. Nineteen patients (46 ± 16 years, 84% male, 63% arrhythmogenic right ventricular cardiomyopathy, 37% exercise-induced arrhythmogenic remodelling) were inducible for 44 VT [CL 283 (interquartile range, IQR 240–325)ms]. A total of 2569 endocardial-epicardial coupled point pairs were analysed, including 98 (4%) epicardial VT-related sites. The TAI and MAI were significantly longer at VT-related sites compared with other electroanatomical scar sites [TAI median 31 (IQR 11–50) vs. 2 (−7–11)ms, P < 0.001; MAI median 65 (IQR 45–87) vs. 23 (13–39)ms, P < 0.001]. TAI and MAI allowed highly accurate identification of epicardial VT-related sites (optimal cut-off TAI 17 ms and MAI 45 ms, both AUC 0.81). Both TAI and MAI had a better predictive accuracy for VT-related sites than endocardial and epicardial voltage and electrogram (EGM) duration (AUC 0.51–0.73). CONCLUSION: The transmural activation delay in SR can be used to identify VT substrates in patients with RVCM and predominantly hemodynamically non-tolerated VT, and may be an important new mapping tool for substrate-based ablation.