High density mapping of ventricular scar- a comparison of ventricular tachycardia supporting channels with channels that do not support VT

Abstract

Introduction: Surviving myocytes within scar may form channels that become critical component of a ventricular tachycardia (VT) reentrant circuit. There is little data on the physiognomies of channels that comprise VT circuits and those which are non-VT channels. Methods: Twenty-two patients with ischemic cardiomyopathy (LVEF 32±8%) and multiple inducible VT (n=73) were evaluated. Left ventricular endocardial mapping was done with high-density PentaRay™ catheter connected to the Ensite Velocity™ system. Pacing was done from bipoles showing low voltage (≤1.5V) with late potentials and/ or fractionation. A channel was defined as series of matching pace-maps with stimulus (S) to QRS time ≥40ms. Sites were determined to be part of VT channel if there were matching pace-maps to the induced VT morphology. This was confirmed with entrainment mapping when possible. The anatomical and electrophysiologic properties of these channels were evaluated. Results: A mean of 760±205 voltage points were taken, with 431±137 within dense scar (≤0.5mV). Overall 2507 pace maps (114±62 per patient) were performed. Of the 238 channels identified, 57 channels corresponded to an inducible VT. Channels that were part of a VT circuit were of greater length (mean 52±31 vs 36±26mm), had longer S-QRS (73±60 vs 62±25ms), longer conduction time (108±90 vs 35±25ms) and slower conduction velocity (CV) (0.7±0.5 vs 1.3±1.1m/s) than non-VT channels (p 80ms was 5.3 times higher in a VT channel relative to an unshared non-VT channel (95% CI 2.6 to 10.6, p<0.01). VT channels were more commonly located within dense scar (95% vs 81% non-VT channels, p=0.04). Of all the fractionated (mean 130±105) late (mean 10±5) and very late (mean 4±3) potentials located in scar, only 22%, 30% and 35% respectively were recorded within VT channels. Compared to elsewhere within the scar, in the region of VT channels fractionated potentials were longer in duration (104±26ms vs 95±26ms, p<0.001), and very late potentials were poorly coupled (309±159ms vs 240±119ms, p=0.04) to the intrinsic QRS. Following ablation targeting channels, the clinical VT was abolished in 95% of patients, and no VT could be induced in 64%. Conclusion: High density mapping shows substantial differences among channels in ventricular scar. Channels supporting VT are more commonly located in dense scar, longer than non-VT channels, and have slower CV. Only a minority of scar related potentials participate in the VT supporting channels. These findings have pertinent implications for substrate based ablation strategies.