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Orini M, Taggart P, Bhuva A, et al. Direct in vivo assessment of global and regional mechanoelectric feedback in the intact human heart. Heart Rhythm. 2021;18(8):1406-1413doi: 10.1016/j.hrthm.2021.04.026.
Orini, M., Taggart, P., Bhuva, A., Roberts, N., Di Salvo, C., Yates, M., Badiani, S., Van Duijvenboden, S., Lloyd, G., Smith, A., & Lambiase, P. D. (2021). Direct in vivo assessment of global and regional mechanoelectric feedback in the intact human heart. Heart rhythm, 18(8), 1406-1413. https://doi.org/10.1016/j.hrthm.2021.04.026
Orini, Michele, et al. "Direct in vivo assessment of global and regional mechanoelectric feedback in the intact human heart." Heart rhythm vol. 18,8 (2021): 1406-1413. doi: https://doi.org/10.1016/j.hrthm.2021.04.026
Orini M, Taggart P, Bhuva A, Roberts N, Di Salvo C, Yates M, Badiani S, Van Duijvenboden S, Lloyd G, Smith A, Lambiase PD. Direct in vivo assessment of global and regional mechanoelectric feedback in the intact human heart. Heart Rhythm. 2021 Aug;18(8):1406-1413. doi: 10.1016/j.hrthm.2021.04.026. Epub 2021 Apr 29. PMID: 33932588; PMCID: PMC8353585.
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Heart Rhythm. 2021 Aug;18(8):1406-1413. doi: 10.1016/j.hrthm.2021.04.026. Epub 2021 Apr 29.

Direct in vivo assessment of global and regional mechanoelectric feedback in the intact human heart.

Heart rhythm

Michele Orini, Peter Taggart, Anish Bhuva, Neil Roberts, Carmelo Di Salvo, Martin Yates, Sveeta Badiani, Stefan Van Duijvenboden, Guy Lloyd, Andrew Smith, Pier D Lambiase

Affiliations

  1. Electrophysiology Department, Barts Heart Centre at St. Bartholomew's Hospital, London, United Kingdom; Institute of Cardiovascular Science, University College London, London, United Kingdom.
  2. Institute of Cardiovascular Science, University College London, London, United Kingdom. Electronic address: [email protected].
  3. Electrophysiology Department, Barts Heart Centre at St. Bartholomew's Hospital, London, United Kingdom.
  4. Institute of Cardiovascular Science, University College London, London, United Kingdom.

PMID: 33932588 PMCID: PMC8353585 DOI: 10.1016/j.hrthm.2021.04.026

Abstract

BACKGROUND: Inhomogeneity of ventricular contraction is associated with sudden cardiac death, but the underlying mechanisms are unclear. Alterations in cardiac contraction impact electrophysiological parameters through mechanoelectric feedback. This has been shown to promote arrhythmias in experimental studies, but its effect in the in vivo human heart is unclear.

OBJECTIVE: The purpose of this study was to quantify the impact of regional myocardial deformation provoked by a sudden increase in ventricular loading (aortic occlusion) on human cardiac electrophysiology.

METHODS: In 10 patients undergoing open heart cardiac surgery, left ventricular (LV) afterload was modified by transient aortic occlusion. Simultaneous assessment of whole-heart electrophysiology and LV deformation was performed using an epicardial sock (240 electrodes) and speckle-tracking transesophageal echocardiography. Parameters were matched to 6 American Heart Association LV model segments. The association between changes in regional myocardial segment length and activation-recovery interval (ARI; a conventional surrogate for action potential duration) was studied using mixed-effect models.

RESULTS: Increased ventricular loading reduced longitudinal shortening (P = .01) and shortened ARI (P = .02), but changes were heterogeneous between cardiac segments. Increased regional longitudinal shortening was associated with ARI shortening (effect size 0.20 [0.01-0.38] ms/%; P = .04) and increased local ARI dispersion (effect size -0.13 [-0.23 to -0.03] ms/%; P = .04). At the whole organ level, increased mechanical dispersion translated into increased dispersion of repolarization (correlation coefficient r = 0.81; P = .01).

CONCLUSION: Mechanoelectric feedback can establish a potentially proarrhythmic substrate in the human heart and should be considered to advance our understanding and prevention of cardiac arrhythmias.

Copyright © 2021 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.

Keywords: Arrhythmia; Cardiac strain; Electromechanical coupling; Mechanoelectric feedback; Repolarization

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