Introduction Ventricular Tachycardia (VT) is a common cause of mortality post myocardial infarction. Any mortality benefit of an implantable cardiac defibrillator (ICD) may be offset by the significant morbidity caused by VT shocks from the device. The VT circuit is dependent upon channels of surviving myocardium within the infarct substrate. As VT is often poorly tolerated, ablation of characteristic electrograms (fractionated and late potentials) associated with these channels in sinus rhythm is preferred to reduce ICD therapies, though recurrence rates remain high. Ripple Mapping (RM) displays all electrogram components from each anatomical point as a dynamic bar that protrudes from its 3D location. We have described how RM might visualize “conducting channels” (RM-CCs) of these characteristic electrograms within the infarcted substrate in a retrospective series. In this study, we used RM prospectively (CARTO3v4™) to characterize the VT substrate to guide ablation.

Methods Consecutive pts referred for VT ablation following episodes of sustained VT or ICD therapies post distant MI were included. High point density bipolar LV endocardial electrograms were collected in sinus rhythm or ventricular pacing within the infarct “scar” (<1.5mV) and reviewed for RMCC identification. Ablation targeted all RMCCs and isolated clusters of late activation considered an endocardial portion of an intramural/epicardial RMCC. Programmed ventricular stimulation assessed VT inducibility post procedure as a marker of immediate efficacy and device interrogations were conducted at 1, 3, 6, and 12 months to determine time to VT recurrence.

Results 15 consecutive pts (median age 68yrs, LVEF 30%) were studied (6 month pre-procedural ICD therapies: median 19 ATP events (IQR=4–93) and 1 shock (IQR=0–3)). Scar (<1.5mV) occupied a median 29% of the total surface area (median 523 scar points). A median of 2 RMCCs were seen within each scar (length 60mm; far field peak amplitude 0.43mV; local 0.19mV; conduction 53cm/s). The Figure illustrates two RMCCs enhanced with design lines within a large anterior scar containing distinct late potentials ascending up the scar. This is readily apparent without manual annotation or point tagging. Ablation was performed along all RMCCs (median 19 lesions (IQR=10–23)) and any non-connected sites (median 6 lesions (IQR=2–12). The diastolic isthmus in VT was mapped in 3 pts and co-located within the RMCCs identified. VT was non-inducible in 85% of patients post ablation. There were no complications during the procedures. In this cohort, 71% remain free of VT recurrence at 6 month median follow up. Interestingly, during redo ablation in a patient with recurrence, an RMCC identified during the index procedure had not been completely eliminated.

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Abstract 68 Figure 1

The path of RMCC activation at 4 time points (i-iv) within scar, with associated electrograms and ablation lesions (v)

Conclusions RM identifies conducting channels within the post-infarct scar that might support re-entrant VT and can be used to guide substrate based ablation to reduce future ICD therapies.