Early Results on the Utilisation of ECG-Imaging During Catheter Ablation Procedures for Prediction of Sites of Earliest Activation During Re-entrant Ventricular Tachycardia

Michele Orini1, Adam Graham2, Mehul Dhinoja2, Ross Hunter2, Richard Schilling2, Anthony Chow2, Peter Taggart3, Pier Lambiase2
1University College London, Department of Mechanical Engineering, 2St Bartholomew's Hospital Barts Heart Centre, 3University College London


Abstract

Introduction: Success rate of ventricular tachycardia (VT) ablation remains sub-optimal. Current technology does not allow accurate localization of VT initiation sites in life-threatening hemodynamically non-tolerated VT. Non-invasive panoramic ECG-imaging (ECGi) offers the possibility of studying the interaction between arrhythmogenic substrate and earliest sites of activation during VT to improve ablation strategies.

Methods: Five patients were studied during catheter ablation using CardioInsight (Medtronic). Ventricular pacing was delivered from the RV and reconstructed unipolar electrograms from a single short-coupled beat (cycle length 360 ms) were analysed to measure activation time (AT), repolarization time (RT) and activation recovery interval (ARI). Three indices mechanistically related to arrhythmia susceptibility were measured at each ventricular site: Re-entry vulnerability index (RVI), local dispersion of AT (LDAT) and local dispersion of ARI (LDARI). Regions of high susceptibility were defined as those corresponding to the bottom 5% of RVI and the upper 5% of LDAT and LDARI. Morphologically distinct VTs were analysed to measure the AT sequence and localise the region of earliest epicardial activation (AT<5 ms).

Results: In total, 20 VTs were analysed (4.0±1.2 per patient, range 3-6). Distance between the region of high vulnerability and the region of earliest AT during VT was 5.6±8.6 mm for RVI, 6.1±10.8 mm for LDAT and 12.8±22.4 mm for LDARI (P>0.13 for all pair-wise comparison). The vulnerability region overlapped with the region of earliest AT during VT (indicating perfect prediction of epicardial breakthrough) in 50%, 55% and 50% of all VTs for RVI, LDAT and LDARI, respectively. At least 2 VTs per patients were localised correctly by RVI and LDAT.

Conclusion: Early data confirm the mechanistic link between markers of arrhythmogenic risk and VT initiation and suggest that ECGi could be potentially used for targeting ablation in non-inducible or hemodynamically non-tolerated VTs.