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170/Ripple mapping guided ablation of conduction channel entrances with loss of latest potentials as an endpoint for substrate modification for ischaemic ventricular tachycardia

European Journal of Arrhythmia & Electrophysiology. 2019;5(Suppl. 1):abstr170

Introduction: Surviving myocardium within ischaemic ventricular scar can form a substrate for electrical re-entry. Several approaches have been described for ”substrate modification” of this surviving myocardium; targeting late abnormal ventricular activities (LAVAs) or late potentials (LP), scar homogenisation and scar encirclement amongst others. We have previously used ripple mapping (RM) to demonstrate distinct channels of surviving myocardium critical for the VT circuit. We tested whether ablation at the entrance of these channels would abolish later potentials, without direct ablation.

Methods: Patients with recurrent implantable defibrillator therapy referred for catheter ablation of ischaemic VT were prospective enrolled. All procedures were performed on the CARTO3v6 system with the CONFIDENSE module.

Ripple Mapping Protocol:
A dense 3D scar map was collected using a PentaRay catheter. The ripple map was then reviewed backwards frame-by-frame from the end of T wave to QRS onset. When > three ripple bars appeared together, the area was marked on the surface geometry with a circle to designate a patch of LPs. The QRS-T time window was divided into four equal time-segments and patches were colour-coded from the earliest LPs to the latest LPs.

Ablation Protocol and End-point:
Ablation was commenced at the patch of earliest LPs. After ablation of each patch, the PentaRay was returned to the patch of latest LPs to determine if LPs were still present. If channel entrances had been transected then electrical activity would not be able to reach the dense scar with the latest potential. The procedure end-point was abolition of LPs in the latest patches.


Four patients have been studied. All were male with a mean age of 69.3 years. Mean LVEF 32.5% and all patients had undergone previous percutaneous coronary intervention (PCI) but had a recent angiogram excluding new targets. One patient had undergone two CABG procedures in addition to PCI. The referring reason for ablation was multiple shocks in two and a single shock in two.

The mean number of points collected was 2,248. Scar was present basally in three (two inferior and one superior near the mitral annulus) and apically in one. A mean of 24 ripple patches were identified per scar, of which on a mean of eight per scar was identified as being in the earliest timing interval.

In 3/4 cases the latest ripple patch potentials were eliminated by ablation in the earliest patches only. In one case ablation had to be performed in ripple patches whose LPs arose after the QRS complex. No patient required ablation in the latest patch. VT induction was opted for by the operators for all four cases, no sustained monomorphic VT was induced following ablation.

Conclusion: Ripple mapping provides a feasible alternative to guide substrate modification of ischaemic VT by catheter ablation. RM allows identification and elimination of entrance sites for channels of viable tissue within the ischaemic scar.

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