Abstract
Case presentation A 63-year-old man with ischemic cardiomyopathy, severely impaired left ventricular systolic function, and an implantable defibrillator presented with multiple episodes of protracted slow ventricular tachycardia (VT). He was brought to the electrophysiology laboratory for catheter ablation. Initial programmed stimulation induced VT at 154 bpm that was associated with hemodynamic instability necessitating cardioversion. Subsequently, a substrate-based mapping approach was undertaken with pacing from the right ventricle (RV) at 50 bpm. An electroanatomic voltage map (using CARTO-3 mapping system, Biosense Webster, Diamond Bar, CA) was created with tagging of late potentials/late abnormal ventricular activity along with pace-mapping where appropriate. Figure 1A shows the intracardiac electrogram (IEGM) seen during mapping within the scar in the mid-anterior wall of the left ventricle and with RV pacing. Figure 1B shows the IEGMs and surface QRS morphology during pace-mapping from the ablation catheter at 600 ms at this site. Figure 2A shows the last 3 beats of pacing from the ablation catheter and onset of VT immediately after pacing. Radiofrequency ablation was then performed at 50 W (NaviStar catheter, Biosense Webster) at this site. Figure 2B shows the response after 15 seconds of ablation. Based on these observations, what is the mechanism of initiation of VT? Crucially, where is this site in relation to the VT circuit, and is this an optimal site for ablation? Finally, was VT initiated during or after pacing?
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