Non-invasive epicardial and endocardial electrocardiographic imaging for scar-related ventricular tachycardia

Linwei Wang, Omar A. Gharbia, Saman Nazarian, B. Milan Horáček, John L. Sapp

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

23 Citas (Scopus)

Resumen

Aims Contact mapping is currently used to guide catheter ablation of scar-related ventricular tachycardia (VT) but usually provides incomplete assessment of 3D re-entry circuits and their arrhythmogenic substrates. This study investigates the feasibility of non-invasive electrocardiographic imaging (ECGi) in mapping scar substrates and reentry circuits throughout the epicardium and endocardium. Methods Four patients undergoing endocardial and epicardial mapping and ablation of scar-related VT had computed tomog- and results raphy scans and a 120-lead electrocardiograms, which were used to compute patient-specific ventricular epicardial and endocardial unipolar electrograms (CEGMs). Native-rhythm CEGMs were used to identify sites of myocardial scar and signal fractionation. Computed electrograms of induced VT were used to localize re-entrant circuits and exit sites. Results were compared to in vivo contact mapping data and epicardium-based ECGi solutions. During native rhythm, an average of 493 ± 18 CEGMs were analysed on each patient. Identified regions of scar and fractionation comprised, respectively, 25 ± 4% and 2 ± 1% of the ventricular surface area. Using a linear mixed-effects model grouped at the level of an individual patient, CEGM voltage and duration were significantly associated with contact bipolar voltage. During induced VT, the inclusion of endocardial layer in ECGi made it possible to identify two epicardial vs. three endocardial VT exit sites among five reconstructed re-entry circuits. Conclusion Electrocardiographic imaging may be used to reveal sites of signal fractionation and to map short-lived VT circuits. Its capacity to map throughout epicardial and endocardial layers may improve the delineation of 3D re-entry circuits and their arrhythmogenic substrates.

Idioma originalEnglish
Páginas (desde-hasta)F263-F272
PublicaciónEuropace
Volumen20
N.ºFI2
DOI
EstadoPublished - sep. 1 2018

Nota bibliográfica

Funding Information:
This work was supported by the US National Institutes of Health [R21HL125998 and R01HL116280], the US National Science Foundation [ACI-1350374], the Canadian Institutes of Health Research, and the Heart & Stroke Foundation of Nova Scotia. J.L.S is also a Canadian Arrhythmia Network Investigator.

Funding Information:
We would like to thank Jaume Coll-Font and Dana H. Brooks at the Northeastern University for participating in the discussion regarding the relationship between electrogram- and phase-derived activation sequence, and for sharing their software to extract time of activation from unipolar electrograms. This work was supported by the US National Institutes of Health [R21HL125998 and R01HL116280], the US National Science Foundation [ACI-1350374], the Canadian Institutes of Health Research, and the Heart & Stroke Foundation of Nova Scotia. J.L.S is also a Canadian Arrhythmia Network Investigator.

Funding Information:
Conflict of interest: S.N. is a scientific advisor to CardioSolv, St. Jude medical, Biosense Webster, and Simens and receive funding from Biosense Webster, Siemens, and Imricor. J.L.S. has served as a consultant to Biosense Webster, has received research funding from Biosense, St. Jude and Philips and has received speaker honoraria from Medtronic and St. Jude. This work has no relationship with industry.

Publisher Copyright:
© 2018 Oxford University Press. All rights reserved.

ASJC Scopus Subject Areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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