Non-invasive epicardial and endocardial electrocardiographic imaging for scar-related ventricular tachycardia. Issue Volume 20:Issue FI 2(2018) (18th April 2018)

• Record Type: Journal Article
• Authors: Wang, Linwei; Gharbia, Omar A; Nazarian, Saman; Horáček, B Milan; Sapp, John L
• Is Part Of: Europace. Volume 20:Issue FI 2(2018)
• Page Start: f263
• Page End: f272
• Publication Date: 2018-04-18
• Subjects: Electrocardiographic imaging -- Scar-related ventricular tachycardia -- Substrate mapping -- Re-entry circuits; Arrhythmia -- Treatment -- Periodicals; Cardiac pacing -- Periodicals; Catheter ablation -- Periodicals; Heart -- Physiology -- Periodicals; Electrophysiology -- Periodicals; 617.4120645
• DOI: 10.1093/europace/euy082
• Languages: English
• ISSNs: 1099-5129

Abstract

Abstract: 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 re-entry circuits throughout the epicardium and endocardium. Methods and results: Four patients undergoing endocardial and epicardial mapping and ablation of scar-related VT had computed tomography 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.