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.
5The 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 colleagues 6 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 owing to haemodynamic intolerance of VT. These observations not only refined the mechanistic understanding of VT reentrant pathways in TOF, but also provided a rationale for an empiric ablation lesion set based solely on substrate mapping that could be used in the operating room or electrophysiology laboratory for TOF patients with unstable VT.In the current issue of this journal, Kapel et al. 7 provide an elegant follow-up to Zeppenfeld's 2007 report by examining the anatomy and electrophysiological properties of these anatomical isthmuses in more detail. The authors performed careful substrate analysis during electrophysiological testing in 74 TOF patients, including 13 subjects who had both clinical and inducible VT, another 15 who had inducible (but no clinical) VT, and 46 with neither clinical nor inducible VT. Patients were chosen for study on the basis of one or more non-invasive risk factors. Isthmus zones were identified and characterized in all patients according to their voltage, conduction velocity, and dimensions. The data are extremely compelling, and suggest that an anatomical isthmus in the RV outflow region of TOF will only support sustained VT when the corridor is long, narrow, slowly conducting, and low voltage. A low conduction velocity index appears to be the most critical variable, and the conal septum (isthmus #3) seems to be the zone most likely to support a VT circuit in this series. These observations are in complete accord with the classical model of cardiac muscle reentry that stresses the role of a protected zone of slow conduction. Moreover, the data are in perfect agreement with the known natural history of ventricular arrhythmias...