Background Catheter ablation of ventricular tachycardia (VT) in structural heart disease is challenging because of noninducibility or hemodynamic compromise. Ablation often depends on elimination of local abnormal ventricular activities (LAVAs) but which may be hidden in far-field signal. We investigated whether altering activation wavefront affects activation timing and LAVA characterization and allows a better understanding of isthmus anatomy. Methods Patients with ischemic cardiomyopathy underwent mapping using the ultra-high density Rhythmia system (Boston Scientific). Maps were generated for all stable VTs and with pacing from the atrium, right ventricular apex, and an left ventricular branch of the coronary sinus. Results Fifty-six paced maps and 23 VT circuits were mapped in 22 patients. In 79% of activation maps, there was ≥1 line of block in the paced conduction wavefront, with 93% having fixed block and 32% showing functional partial block. Bipolar scar was larger with atrial than right ventricular (31.7±18.5 versus 27.6±16.3 cm2, P=0.003) or left ventricular pacing (31.7±18.5 versus 27.0±19.2 cm2, P=0.009); LAVA areas were smaller with atrial than right ventricular (12.3±10.5 versus 18.4±11.0 cm2, P<0.001) or left ventricular pacing (12.3±10.5 versus 17.1±10.7 cm2, P<0.001). LAVA areas were larger with wavefront propagation perpendicular versus parallel to the line of block along isthmus boundaries (19.3±7.1 versus 13.6±7.4 cm2, P=0.01). All patients had successful VT isthmus ablation. In 11±8 months follow-up, 2 patients had a recurrence. Conclusions Wavefronts of conduction slowing/block may aid identification of critical isthmuses in unmappable VTs. Altering the activation wavefront leads to significant differences in conduction properties of myocardial tissue, along with scar and LAVA characterization. In patients where few LAVAs are identified during substrate mapping, using an alternate activation wavefront running perpendicular to the VT isthmus may increase sensitivity to detect arrhythmogenic substrate and critical sites for reentry.
Keywords: cardiomyopathies; tachycardia, ventricular; ventricular dysfunction.