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Evidence of reverse electrical remodelling by non-invasive electrocardiographic imaging to assess acute and chronic changes in bulk ventricular activation following cardiac resynchronisation therapy

Research output: Contribution to journalArticlepeer-review

Original languageEnglish
Pages (from-to)96-102
Number of pages7
JournalJournal of Electrocardiology
Published1 Jan 2020

Bibliographical note

Copyright © 2019. Published by Elsevier Inc.

King's Authors


Introduction: Cardiac resynchronisation therapy (CRT) corrects electrical dyssynchrony. However, the temporal changes in the electrical timing according to substrate are unclear. We used electrocardiographic imaging (ECGi) for serial non-invasive assessment of the underlying electrical substrate and its response to resynchronisation. Material and methods: ECGi activation maps were constructed 1 day and 6 months post CRT implant. ECGi maps were analysed offline to determine the total ventricular activation time (TVaT) and the time for the bulk of ventricular activation (10th to 90th percentile activation; VaT10 90 Index). Statistical analysis was performed using repeated measures ANOVA with post-hoc pairwise comparisons using paired t-tests. The % relative change within each time point was also calculated and compared between the two time points. Results: Eleven CRT patients were studied. Both total and bulk ventricular activation significantly decreased with CRT turned ON at day 1. Intrinsic (CRT OFF) TVaT and VaT10 90 Index at day 1 were 143 ± 23 and 84 ± 20 ms, respectively, and they significantly decreased post CRT to 115 ± 26 ms (P < 0.001) and 49 ± 17 ms (P < 0.05), respectively. The relative change at day 1 was also statistically significant for TVaT (19 ± 12%, P < 0.001) and VaT10 90 Index (39 ± 25%, P < 0.001). After 6 months, the relative decrease in TVaT with CRT ON remained stable (19% vs. 18% at day 1 and 6 months, respectively) whereas reduction the in VaT10 90 Index was decreased 39% vs. 26% at day 1 and 6 months, respectively. In non-ischaemic patients both total and bulk activation times reduced following CRT. Volumetric responders exhibited an electrical remodelling for bulk activation not apparent in Non-responders, after 6 months of CRT ON. Conclusions: Intrinsic bulk myocardium activation becomes more rapid and synchronous with CRT. The bulk activation time is more susceptible to improvement by CRT in ischaemic patients and volumetric responders. These observations are consistent with CRT causing reverse electrophysiological remodelling in the bulk myocardium, but not in late-activating ischaemic or fibrotic regions.

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