Arrhythmogenesis in heart failure

M. J. Janse; J. T. Vermeulen; T. Opthof; R. Coronel; F. J. Wilms-Schopman; H. M. Rademaker; A. Baartscheer; L. R. Dekker

doi:https://doi.org/10.1046/j.1540-8167.2001.00496.x

Arrhythmogenesis in heart failure

M. J. Janse, J. T. Vermeulen, T. Opthof, R. Coronel, F. J. Wilms-Schopman, H. M. Rademaker, A. Baartscheer, L. R. Dekker

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Research output: Contribution to journal › Article › Academic › peer-review

27 Citations (Scopus)

Abstract

In a rabbit model of heart failure produced by combined pressure and volume overload, nonsustained ventricular tachycardias developed in 15 of 23 failing rabbits. Sinus rate was increased in rabbits dying suddenly, but was decreased in survivors. This also was true in isolated preparations. Microelectrode recordings from ventricular trabeculae both from patients with end-stage failure and from failing rabbits showed that in half of the preparations, delayed afterdepolarizations and triggered activity occurred, but only in the presence of norepinephrine and a lowered extracellular K+ concentration of 3 mM. This was due to spontaneous release of Ca2+ from the sarcoplasmic reticulum

Original language	English
Pages (from-to)	496-499
Journal	Journal of cardiovascular electrophysiology
Volume	12
Issue number	4
DOIs	https://doi.org/10.1046/j.1540-8167.2001.00496.x
Publication status	Published - 2001

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https://doi.org/10.1046/j.1540-8167.2001.00496.x

Cite this

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title = "Arrhythmogenesis in heart failure",

abstract = "In a rabbit model of heart failure produced by combined pressure and volume overload, nonsustained ventricular tachycardias developed in 15 of 23 failing rabbits. Sinus rate was increased in rabbits dying suddenly, but was decreased in survivors. This also was true in isolated preparations. Microelectrode recordings from ventricular trabeculae both from patients with end-stage failure and from failing rabbits showed that in half of the preparations, delayed afterdepolarizations and triggered activity occurred, but only in the presence of norepinephrine and a lowered extracellular K+ concentration of 3 mM. This was due to spontaneous release of Ca2+ from the sarcoplasmic reticulum",

author = "Janse, {M. J.} and Vermeulen, {J. T.} and T. Opthof and R. Coronel and Wilms-Schopman, {F. J.} and Rademaker, {H. M.} and A. Baartscheer and Dekker, {L. R.}",

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doi = "https://doi.org/10.1046/j.1540-8167.2001.00496.x",

language = "English",

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journal = "Journal of cardiovascular electrophysiology",

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T1 - Arrhythmogenesis in heart failure

AU - Janse, M. J.

AU - Vermeulen, J. T.

AU - Opthof, T.

AU - Coronel, R.

AU - Wilms-Schopman, F. J.

AU - Rademaker, H. M.

AU - Baartscheer, A.

AU - Dekker, L. R.

PY - 2001

Y1 - 2001

N2 - In a rabbit model of heart failure produced by combined pressure and volume overload, nonsustained ventricular tachycardias developed in 15 of 23 failing rabbits. Sinus rate was increased in rabbits dying suddenly, but was decreased in survivors. This also was true in isolated preparations. Microelectrode recordings from ventricular trabeculae both from patients with end-stage failure and from failing rabbits showed that in half of the preparations, delayed afterdepolarizations and triggered activity occurred, but only in the presence of norepinephrine and a lowered extracellular K+ concentration of 3 mM. This was due to spontaneous release of Ca2+ from the sarcoplasmic reticulum

AB - In a rabbit model of heart failure produced by combined pressure and volume overload, nonsustained ventricular tachycardias developed in 15 of 23 failing rabbits. Sinus rate was increased in rabbits dying suddenly, but was decreased in survivors. This also was true in isolated preparations. Microelectrode recordings from ventricular trabeculae both from patients with end-stage failure and from failing rabbits showed that in half of the preparations, delayed afterdepolarizations and triggered activity occurred, but only in the presence of norepinephrine and a lowered extracellular K+ concentration of 3 mM. This was due to spontaneous release of Ca2+ from the sarcoplasmic reticulum

U2 - https://doi.org/10.1046/j.1540-8167.2001.00496.x

DO - https://doi.org/10.1046/j.1540-8167.2001.00496.x

M3 - Article

C2 - 11332576

SN - 1045-3873

VL - 12

SP - 496

EP - 499

JO - Journal of cardiovascular electrophysiology

JF - Journal of cardiovascular electrophysiology

IS - 4

ER -