Mechanism underlying impaired cardiac pacemaking rhythm during ischemiaCitation formats

  • External authors:
  • Xiangyun Bai
  • Kuanquan Wang
  • Yongfeng Yuan
  • Qince Li
  • Jules C. Hancox
  • Henggui Zhang

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Mechanism underlying impaired cardiac pacemaking rhythm during ischemia : A simulation study. / Bai, Xiangyun; Wang, Kuanquan; Yuan, Yongfeng; Li, Qince; Dobrzynski, Halina; Boyett, Mark R.; Hancox, Jules C.; Zhang, Henggui.

In: Chaos, Vol. 27, No. 9, 093934, 2017.

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Bai, Xiangyun ; Wang, Kuanquan ; Yuan, Yongfeng ; Li, Qince ; Dobrzynski, Halina ; Boyett, Mark R. ; Hancox, Jules C. ; Zhang, Henggui. / Mechanism underlying impaired cardiac pacemaking rhythm during ischemia : A simulation study. In: Chaos. 2017 ; Vol. 27, No. 9.

Bibtex

@article{5b3b22d734484f4ab0b70c8c2b29d1da,
title = "Mechanism underlying impaired cardiac pacemaking rhythm during ischemia: A simulation study",
abstract = "Ischemia in the heart impairs function of the cardiac pacemaker, the sinoatrial node (SAN). However, the ionic mechanisms underlying the ischemia-induced dysfunction of the SAN remain elusive. In order to investigate the ionic mechanisms by which ischemia causes SAN dysfunction, action potential models of rabbit SAN and atrial cells were modified to incorporate extant experimental data of ischemia-induced changes to membrane ion channels and intracellular ion homeostasis. The cell models were incorporated into an anatomically detailed 2D model of the intact SAN-atrium. Using the multi-scale models, the functional impact of ischemia-induced electrical alterations on cardiac pacemaking action potentials (APs) and their conduction was investigated. The effects of vagal tone activity on the regulation of cardiac pacemaker activity in control and ischemic conditions were also investigated. The simulation results showed that at the cellular level ischemia slowed the SAN pacemaking rate, which was mainly attributable to the altered Na+-Ca2+ exchange current and the ATP-sensitive potassium current. In the 2D SAN-atrium tissue model, ischemia slowed down both the pacemaking rate and the conduction velocity of APs into the surrounding atrial tissue. Simulated vagal nerve activity, including the actions of acetylcholine in the model, amplified the effects of ischemia, leading to possible SAN arrest and/or conduction exit block, which are major features of the sick sinus syndrome. In conclusion, this study provides novel insights into understanding the mechanisms by which ischemia alters SAN function, identifying specific conductances as contributors to bradycardia and conduction block.",
author = "Xiangyun Bai and Kuanquan Wang and Yongfeng Yuan and Qince Li and Halina Dobrzynski and Boyett, {Mark R.} and Hancox, {Jules C.} and Henggui Zhang",
year = "2017",
doi = "10.1063/1.5002664",
language = "English",
volume = "27",
journal = "Chaos",
issn = "1054-1500",
publisher = "A I P Publishing LLC",
number = "9",

}

RIS

TY - JOUR

T1 - Mechanism underlying impaired cardiac pacemaking rhythm during ischemia

T2 - A simulation study

AU - Bai, Xiangyun

AU - Wang, Kuanquan

AU - Yuan, Yongfeng

AU - Li, Qince

AU - Dobrzynski, Halina

AU - Boyett, Mark R.

AU - Hancox, Jules C.

AU - Zhang, Henggui

PY - 2017

Y1 - 2017

N2 - Ischemia in the heart impairs function of the cardiac pacemaker, the sinoatrial node (SAN). However, the ionic mechanisms underlying the ischemia-induced dysfunction of the SAN remain elusive. In order to investigate the ionic mechanisms by which ischemia causes SAN dysfunction, action potential models of rabbit SAN and atrial cells were modified to incorporate extant experimental data of ischemia-induced changes to membrane ion channels and intracellular ion homeostasis. The cell models were incorporated into an anatomically detailed 2D model of the intact SAN-atrium. Using the multi-scale models, the functional impact of ischemia-induced electrical alterations on cardiac pacemaking action potentials (APs) and their conduction was investigated. The effects of vagal tone activity on the regulation of cardiac pacemaker activity in control and ischemic conditions were also investigated. The simulation results showed that at the cellular level ischemia slowed the SAN pacemaking rate, which was mainly attributable to the altered Na+-Ca2+ exchange current and the ATP-sensitive potassium current. In the 2D SAN-atrium tissue model, ischemia slowed down both the pacemaking rate and the conduction velocity of APs into the surrounding atrial tissue. Simulated vagal nerve activity, including the actions of acetylcholine in the model, amplified the effects of ischemia, leading to possible SAN arrest and/or conduction exit block, which are major features of the sick sinus syndrome. In conclusion, this study provides novel insights into understanding the mechanisms by which ischemia alters SAN function, identifying specific conductances as contributors to bradycardia and conduction block.

AB - Ischemia in the heart impairs function of the cardiac pacemaker, the sinoatrial node (SAN). However, the ionic mechanisms underlying the ischemia-induced dysfunction of the SAN remain elusive. In order to investigate the ionic mechanisms by which ischemia causes SAN dysfunction, action potential models of rabbit SAN and atrial cells were modified to incorporate extant experimental data of ischemia-induced changes to membrane ion channels and intracellular ion homeostasis. The cell models were incorporated into an anatomically detailed 2D model of the intact SAN-atrium. Using the multi-scale models, the functional impact of ischemia-induced electrical alterations on cardiac pacemaking action potentials (APs) and their conduction was investigated. The effects of vagal tone activity on the regulation of cardiac pacemaker activity in control and ischemic conditions were also investigated. The simulation results showed that at the cellular level ischemia slowed the SAN pacemaking rate, which was mainly attributable to the altered Na+-Ca2+ exchange current and the ATP-sensitive potassium current. In the 2D SAN-atrium tissue model, ischemia slowed down both the pacemaking rate and the conduction velocity of APs into the surrounding atrial tissue. Simulated vagal nerve activity, including the actions of acetylcholine in the model, amplified the effects of ischemia, leading to possible SAN arrest and/or conduction exit block, which are major features of the sick sinus syndrome. In conclusion, this study provides novel insights into understanding the mechanisms by which ischemia alters SAN function, identifying specific conductances as contributors to bradycardia and conduction block.

UR - http://www.scopus.com/inward/record.url?scp=85029783114&partnerID=8YFLogxK

U2 - 10.1063/1.5002664

DO - 10.1063/1.5002664

M3 - Article

VL - 27

JO - Chaos

JF - Chaos

SN - 1054-1500

IS - 9

M1 - 093934

ER -