Slow Adaptation of Ventricular Repolarization as a Cause of Arrhythmia?

A. Bueno-Orovio; B. M. Hanson; J. S. Gill; P. Taggart; B. Rodriguez

doi:10.3414/ME13-02-0039

Methods of Information in Medicine, Table of Contents

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?

Authors

A. Bueno-Orovio

¹Department of Computer Science, University of Oxford, Oxford, UK
B. M. Hanson

²Department of Mechanical Engineering, University College of London, London, UK
J. S. Gill

³Guy’s and St. Thomas’ Hospital, London, UK
P. Taggart

⁴The Neurocardiology Research Unit, University College Hospital, London, UK
B. Rodriguez

¹Department of Computer Science, University of Oxford, Oxford, UK

Abstract

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 (ΔT_s) was greater in LV than RV (ΔT_s ^LV = 31.8 ± 13.2, ΔT_s ^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

Full Text

References

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