Isochronal late activation mapping during extra-stimulus pacing unmasks hidden zones of conduction slowing and functional conduction block

Abstract Background Isochronal late activation mapping (ILAM) is an electrogram annotation and display strategy in which conduction slowing is visually represented by isochronal crowding (IC). Areas of IC have been shown to effectively identify substrate for reentrant VT, which have been called deceleration zones (DZ). Extra-stimulus (ES) mapping is a strategy to unmask arrhythmic substrate by introducing premature complexes. The impact of ES pacing on the location of DZ identified using ILAM is unknown. Purpose To compare ILAM maps created during ES pacing, created using the S1 and S2 stimuli, to consider the impact of S2 on activation patterns and the location of DZ. Methods A cohort of seven patients, four with ischaemic and three with non-ischaemic cardiomyopathy, were analysed using the electro-anatomical mapping data collected during a clinical ablation procedure. Electrograms were processed using a custom filtering algorithm based on automated pacing artefact annotation to exclude bipolar electrograms (bip-EGMs) that do not match the specified S2 coupling interval, defined by the operator during the ablation procedure. The last deflection (LD) of the selected bip-EGMs, marking the end of local ventricular activity, was automatically annotated. Bip-EGM selection and annotation was manually verified. LD maps were visualised using eight equally spaced isochrones, reflecting the ILAM strategy. A delta-S1S2 map was generated, displaying the difference between S1 and S2 LD time at corresponding locations during ES mapping, computed as S2-S1. Areas of isochronal crowding, defined as >3 isochrones within a 1cm radius, were classified as primary DZ or other DZ and compared between the S1 and S2 ILAM maps. Results 23.79±8.37% of the chamber mapped demonstrated earlier activation during S2 mapping, indicating conduction block proximal to the site, 56.99±9.32% of the chamber demonstrated no significant change (<±20ms), and 19.21±6.48% of the chamber mapped demonstrated later activation during S2 mapping, indicating conduction delay. An average of 1.71 DZ were identified on S1 maps, and 2.14 DZ identified on S2 maps. Primary DZ were localised to a different area in 6/7 patients when comparing S1 and S2 ILAM maps. The delta-S1S2 map visualises areas with differences in LD time between the S1 and S2 stimulus, with areas activated later following S2 displayed as blue, and areas activated earlier following S2 displayed in red. A representative example is shown demonstrating isochronal crowding only evident during S2 pacing that localises to the interface between low and normal range bipolar voltage. Conclusion ILAM identifies different DZ when applied to ES pacing. ES pacing effectively induces decrement in some regions, however functional conduction block may obscure or reveal substrate. A novel method is presented for aggregation of data collected during ES pacing to help visualise global LV activation differences during S1 and S2 mapping.