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Electrophysiologic features of protected channels in late postinfarction patients with and without spontaneous ventricular tachycardia

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Abstract

Purpose

Protected channels of surviving myocytes in late postinfarction ventricular scar predispose to ventricular tachycardia (VT). However, only a few patients develop VT spontaneously. We studied differences in electric remodeling and protected channels in late postinfarction patients with and without spontaneous VT.

Methods

Patients with ischemic cardiomyopathy (ICM) with recurrent sustained monomorphic VT (n = 22) were compared with stable ICM patients without spontaneous VT (control group; n = 5). Left ventricular mapping was performed with a 20-pole catheter. Detailed pace mapping was used to identify channels of protected conduction, and confirmed, when feasible, by entrainment. Anatomical and electrophysiological properties of VT channels and non-VT channels in VT patients and channels in controls were evaluated.

Results

Seventy-three (median 3) VTs were inducible in VT patients compared to two (median 0) in controls. The VT channels in VT patients (n = 57, 3 ± 1 per patient) were lengthier (mean ± SEM 53 ± 5 vs. 33 ± 4 vs. 24 ± 8 mm), had longer S-QRS (73 ± 4 vs. 63 ± 3 vs. 44 ± 8 ms), longer conduction time (103 ± 13 vs. 33 ± 4 vs. 24 ± 8 ms), and slower conduction velocity (CV) (0.85 ± 0.21 vs. 1.39 ± 0.20 vs. 1.31 ± 0.41 m/s) than non-VT channels in VT patients (n = 183, 8 ± 6 per patient) (p ≤ 0.01) and channels in controls (n = 46, 9 ± 8 per patient) (p ≤ 0.01). Additionally, non-VT channels in VT patients had longer S-QRS (p = 0.02); however, they were similar in length, conduction time, and CV compared to channels in controls.

Conclusions

Channels supporting VT are lengthier, with longer conduction times and slower CV compared to channels in patients without spontaneous VT. These observations may explain why some ICM patients have spontaneous VT and others do not.

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Funding

This work was supported by the Robert J. Craig Electrophysiology Scholarship from the University of Adelaide (S.N), the National Heart Foundation of Australia (A.G., P.K., K.R-T., P.S.), Early Career Health Practitioner Fellowship from the National Health and Medical Research Council of Australia (A.G.), the Practitioner Fellowship from the National Health and Medical Research Council of Australia (P.S.), and the Sylvia & Charles Viertel Foundation Australia (K.R-T.).

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Authors and Affiliations

  1. Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Level 5, McEwin Building, North Terrace, Adelaide, SA, 5000, Australia

    Sachin Nayyar, Lauren Wilson, Anand Ganesan, Pawel Kuklik, Glenn Young, Prashanthan Sanders & Kurt C. Roberts-Thomson

  2. School of Public Health, University of Adelaide, Adelaide, Australia

    Thomas Sullivan

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  1. Sachin Nayyar
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  2. Lauren Wilson
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  3. Anand Ganesan
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  4. Thomas Sullivan
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  5. Pawel Kuklik
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Correspondence to Kurt C. Roberts-Thomson.

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Conflict of interest

Dr. Roberts-Thomson reports having served on the advisory board of St Jude Medical. Dr. Sanders reports having served on the advisory board of Biosense-Webster, Medtronic, CathRx, and St Jude Medical; received lecture and/or consulting fees from Biosense-Webster, Medtronic, St Jude Medical, and Boston Scientific; and received research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik, and Sorin.

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Nayyar, S., Wilson, L., Ganesan, A. et al. Electrophysiologic features of protected channels in late postinfarction patients with and without spontaneous ventricular tachycardia. J Interv Card Electrophysiol 51, 13–24 (2018). https://doi.org/10.1007/s10840-017-0299-6

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  • DOI: https://doi.org/10.1007/s10840-017-0299-6

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