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Methods Inf Med 2014; 53(04): 320-323
DOI: 10.3414/ME13-02-0039
Focus Theme – Original Articles
Schattauer GmbH

Slow Adaptation of Ventricular Repolarization as a Cause of Arrhythmia?

A. Bueno-Orovio
1   Department of Computer Science, University of Oxford, Oxford, UK
,
B. M. Hanson
2   Department of Mechanical Engineering, University College of London, London, UK
,
J. S. Gill
3   Guy’s and St. Thomas’ Hospital, London, UK
,
P. Taggart
4   The Neurocardiology Research Unit, University College Hospital, London, UK
,
B. Rodriguez
1   Department of Computer Science, University of Oxford, Oxford, UK
› Author Affiliations
Further Information

Publication History

received:14 October 2013

accepted:12 February 2014

Publication Date:
20 January 2018 (online)

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Summary

Introduction: This article is part of the Focus Theme of Methods of Information in Medicine on “Biosignal Interpretation: Advanced Methods for Studying Cardiovascular and Respiratory Systems”.

Background: Adaptation of the QT-interval to changes in heart rate reflects on the body-surface electrocardiogram the adaptation of action potential duration (APD) at the cellular level. The initial fast phase of APD adaptation has been shown to modulate the arrhythmia substrate. Whether the slow phase is potentially proarrhythmic remains unclear.

Objectives: To analyze in-vivo human data and use computer simulations to examine effects of the slow APD adaptation phase on dispersion of repolarization and reentry in the human ventricle.

Methods: Electrograms were acquired from 10 left and 10 right ventricle (LV/RV) endocardial sites in 15 patients with normal ventricles during RV pacing. Activation-recovery intervals, as a surrogate for APD, were measured during a sustained increase in heart rate. Observed dynamics were studied using computer simulations of human tissue electrophysiology.

Results: Spatial heterogeneity of rate adaptation was observed in all patients. Inhomogeneity in slow APD adaptation time constants (ΔTs) was greater in LV than RV (ΔTs LV = 31.8 ± 13.2, ΔTs RV = 19.0 ± 12.8 s, P < 0.01). Simulations showed that altering local slow time constants of adaptation was sufficient to convert partial wavefront block to block with successful reentry.

Conclusions: Using electrophysiological data acquired in-vivo in human and computer simulations, we identify heterogeneity in the slow phase of APD adaptation as an important component of arrhythmogenesis.

Keywords

Cardiac arrhythmias - repolarization and QT interval - reentry
 

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