LAUSR

This editorial refers to ‘Arrhythmogenic anatomical isthmuses identified by electroanatomical mapping are the substrate for ventricular tachycardia in repaired tetralogy of Fallot’, by G.F.L. Kapel et al ., doi:10.1093/eurheartj/ehw202 In 1980, Horowitz et al .1 performed the first detailed electrophysiological studies of monomorphic ventricular tachycardia (VT) in patients with tetralogy of Fallot (TOF). Despite the limitations in mapping technology of that era, they were able to prove conclusively that the mechanism involved macroreentry related to tissue in the right ventricular (RV) outflow tract. Successful surgical ablation soon followed,2 and reports of successful transcatheter ablation for this condition began to appear by 1993.3 Since then, extensive clinical research has concentrated on improved identification of TOF patients at highest risk for VT,4 as well as refinements in ablative technology for this unusual anatomy.5 The RV outflow tract in repaired TOF is a complex region involving incisional scars, surgical patches, and several protected corridors of thick and fibrotic ventricular myocardium that constitute an ideal environment for monomorphic macroreentrant circuits. In a landmark 2007 paper, Zeppenfeld and colleagues6 described several discrete anatomical isthmuses as the potential routes for macroreentry, and proved these sites were clinically relevant by eliminating VT with catheter ablation at strategic points that interrupted conduction through each isthmus. Importantly, ablation was accomplished effectively even when formal propagation mapping was not possible …