Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice. / Speerschneider, T; Grubb, Søren Jahn; Olesen, S P; Calloe, K; Thomsen, M B.

In: Acta Physiologica, Vol. 219, No. 3, 09.02.2017, p. 662-670.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Speerschneider, T, Grubb, SJ, Olesen, SP, Calloe, K & Thomsen, MB 2017, 'Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice', Acta Physiologica, vol. 219, no. 3, pp. 662-670. https://doi.org/10.1111/apha.12761

APA

Speerschneider, T., Grubb, S. J., Olesen, S. P., Calloe, K., & Thomsen, M. B. (2017). Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice. Acta Physiologica, 219(3), 662-670. https://doi.org/10.1111/apha.12761

Vancouver

Speerschneider T, Grubb SJ, Olesen SP, Calloe K, Thomsen MB. Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice. Acta Physiologica. 2017 Feb 9;219(3):662-670. https://doi.org/10.1111/apha.12761

Author

Speerschneider, T ; Grubb, Søren Jahn ; Olesen, S P ; Calloe, K ; Thomsen, M B. / Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice. In: Acta Physiologica. 2017 ; Vol. 219, No. 3. pp. 662-670.

Bibtex

@article{00317a11f25945279776e7cb1f787103,
title = "Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice",
abstract = "AIM: In this study, we investigate the impact of altered action potential durations (APD) on ventricular repolarization time and proarrhythmia in mice with and without genetic deletion of the K(+) -channel-interacting protein 2 (KChIP2(-/-) and WT respectively). Moreover, we examine the interrelationship between the dispersion of repolarization time and current pulse amplitude in provoking ventricular arrhythmia.METHODS: Intracardiac pacing in anesthetized mice determined refractory periods and proarrhythmia susceptibility. Regional activation time (AT), APD and repolarization time (=AT + APD) were measured in isolated hearts using floating microelectrodes.RESULTS: Proarrhythmia in WT and KChIP2(-/-) was not sensitive to changes in refractory periods. Action potentials were longer in KChIP2(-/-) hearts compared to WT hearts. Isolated WT hearts had large apico-basal dispersion of repolarization time, whereas hearts from KChIP2(-/-) mice had large left-to-right ventricular dispersion of repolarization time. Pacing from the right ventricle in KChIP2(-/-) mice in vivo revealed significant lower current pulse amplitudes needed to induce arrhythmias in these mice.CONCLUSION: Large heterogeneity of repolarization time is proarrhythmic when pacing is delivered from the location of earlier repolarization time. Ventricular repolarization time, location of the pacing stimulus and the amplitude of the stimulating current pulse are critical parameters underlying arrhythmia vulnerability.",
author = "T Speerschneider and Grubb, {S{\o}ren Jahn} and Olesen, {S P} and K Calloe and Thomsen, {M B}",
note = "{\circledC} 2016 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.",
year = "2017",
month = "2",
day = "9",
doi = "10.1111/apha.12761",
language = "English",
volume = "219",
pages = "662--670",
journal = "Acta Physiologica (Print)",
issn = "1748-1708",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - Ventricular repolarization time, location of pacing stimulus and current pulse amplitude conspire to determine arrhythmogenicity in mice

AU - Speerschneider, T

AU - Grubb, Søren Jahn

AU - Olesen, S P

AU - Calloe, K

AU - Thomsen, M B

N1 - © 2016 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

PY - 2017/2/9

Y1 - 2017/2/9

N2 - AIM: In this study, we investigate the impact of altered action potential durations (APD) on ventricular repolarization time and proarrhythmia in mice with and without genetic deletion of the K(+) -channel-interacting protein 2 (KChIP2(-/-) and WT respectively). Moreover, we examine the interrelationship between the dispersion of repolarization time and current pulse amplitude in provoking ventricular arrhythmia.METHODS: Intracardiac pacing in anesthetized mice determined refractory periods and proarrhythmia susceptibility. Regional activation time (AT), APD and repolarization time (=AT + APD) were measured in isolated hearts using floating microelectrodes.RESULTS: Proarrhythmia in WT and KChIP2(-/-) was not sensitive to changes in refractory periods. Action potentials were longer in KChIP2(-/-) hearts compared to WT hearts. Isolated WT hearts had large apico-basal dispersion of repolarization time, whereas hearts from KChIP2(-/-) mice had large left-to-right ventricular dispersion of repolarization time. Pacing from the right ventricle in KChIP2(-/-) mice in vivo revealed significant lower current pulse amplitudes needed to induce arrhythmias in these mice.CONCLUSION: Large heterogeneity of repolarization time is proarrhythmic when pacing is delivered from the location of earlier repolarization time. Ventricular repolarization time, location of the pacing stimulus and the amplitude of the stimulating current pulse are critical parameters underlying arrhythmia vulnerability.

AB - AIM: In this study, we investigate the impact of altered action potential durations (APD) on ventricular repolarization time and proarrhythmia in mice with and without genetic deletion of the K(+) -channel-interacting protein 2 (KChIP2(-/-) and WT respectively). Moreover, we examine the interrelationship between the dispersion of repolarization time and current pulse amplitude in provoking ventricular arrhythmia.METHODS: Intracardiac pacing in anesthetized mice determined refractory periods and proarrhythmia susceptibility. Regional activation time (AT), APD and repolarization time (=AT + APD) were measured in isolated hearts using floating microelectrodes.RESULTS: Proarrhythmia in WT and KChIP2(-/-) was not sensitive to changes in refractory periods. Action potentials were longer in KChIP2(-/-) hearts compared to WT hearts. Isolated WT hearts had large apico-basal dispersion of repolarization time, whereas hearts from KChIP2(-/-) mice had large left-to-right ventricular dispersion of repolarization time. Pacing from the right ventricle in KChIP2(-/-) mice in vivo revealed significant lower current pulse amplitudes needed to induce arrhythmias in these mice.CONCLUSION: Large heterogeneity of repolarization time is proarrhythmic when pacing is delivered from the location of earlier repolarization time. Ventricular repolarization time, location of the pacing stimulus and the amplitude of the stimulating current pulse are critical parameters underlying arrhythmia vulnerability.

U2 - 10.1111/apha.12761

DO - 10.1111/apha.12761

M3 - Journal article

C2 - 27459728

VL - 219

SP - 662

EP - 670

JO - Acta Physiologica (Print)

JF - Acta Physiologica (Print)

SN - 1748-1708

IS - 3

ER -

ID: 167474234