Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure

Masahiro Ogawa, Norishige Morita, Liang Tang, Hrayr S. Karagueuzian, James N. Weiss, Shien-Fong Lin, Peng-Sheng Chen

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Background: Successful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear. Objective: The purpose of this study was to determine the mechanisms of spontaneous VF after initial successful defibrillation in a rabbit model of heart failure (HF). Methods: Simultaneous optical mapping of intracellular calcium (Cai) and membrane potential (Vm) was performed in 12 rabbit hearts with chronic pacing-induced heart failure, in 4 sham-operated hearts, and in 5 normal hearts during fibrillation-defibrillation episodes. Results: Twenty-eight spontaneous VF episodes were recorded after initial successful defibrillation in 4 failing hearts (SVF group) but not in the remaining 8 failing hearts (no-SVF group) or in the normal or sham-operated hearts. The action potential duration (APD80) before pacing-induced VF was 209 ± 9 ms in the SVF group and 212 ± 14 ms in the no-SVF group (P = NS). After successful defibrillation, APD80 shortened to 147 ± 26 ms in the SVF group and to 176 ± 14 ms in the no-SVF group (P = .04). However, the duration of Cai after defibrillation was not different between the two groups (246 ± 21 ms vs 241 ± 17 ms, P = NS), resulting in elevated Cai during late phase 3 or phase 4 of the action potential. Standard glass microelectrode recording in an additional 5 failing hearts confirmed postshock APD shortening and afterdepolarizations. APD80 of normal and sham-operated hearts was not shortened after defibrillation. Conclusion: HF promotes acute shortening of APD immediately after termination of VF in failing hearts. Persistent Cai elevation during late phase 3 and phase 4 of the shortened action potential result in afterdepolarizations, triggered activity, and spontaneous VF.

Original languageEnglish
Pages (from-to)784-792
Number of pages9
JournalHeart Rhythm
Volume6
Issue number6
DOIs
StatePublished - Jun 2009

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Ventricular Fibrillation
Heart Failure
Rabbits
pamidronate
Action Potentials
Calcium
Intracellular Membranes
Microelectrodes
Membrane Potentials
Glass

Keywords

  • Action potential duration
  • Electrophysiology
  • Heart failure
  • Intracellular calcium
  • Spontaneous ventricular fibrillation
  • Sudden cardiac death

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure. / Ogawa, Masahiro; Morita, Norishige; Tang, Liang; Karagueuzian, Hrayr S.; Weiss, James N.; Lin, Shien-Fong; Chen, Peng-Sheng.

In: Heart Rhythm, Vol. 6, No. 6, 06.2009, p. 784-792.

Research output: Contribution to journalArticle

Ogawa, Masahiro ; Morita, Norishige ; Tang, Liang ; Karagueuzian, Hrayr S. ; Weiss, James N. ; Lin, Shien-Fong ; Chen, Peng-Sheng. / Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure. In: Heart Rhythm. 2009 ; Vol. 6, No. 6. pp. 784-792.
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abstract = "Background: Successful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear. Objective: The purpose of this study was to determine the mechanisms of spontaneous VF after initial successful defibrillation in a rabbit model of heart failure (HF). Methods: Simultaneous optical mapping of intracellular calcium (Cai) and membrane potential (Vm) was performed in 12 rabbit hearts with chronic pacing-induced heart failure, in 4 sham-operated hearts, and in 5 normal hearts during fibrillation-defibrillation episodes. Results: Twenty-eight spontaneous VF episodes were recorded after initial successful defibrillation in 4 failing hearts (SVF group) but not in the remaining 8 failing hearts (no-SVF group) or in the normal or sham-operated hearts. The action potential duration (APD80) before pacing-induced VF was 209 ± 9 ms in the SVF group and 212 ± 14 ms in the no-SVF group (P = NS). After successful defibrillation, APD80 shortened to 147 ± 26 ms in the SVF group and to 176 ± 14 ms in the no-SVF group (P = .04). However, the duration of Cai after defibrillation was not different between the two groups (246 ± 21 ms vs 241 ± 17 ms, P = NS), resulting in elevated Cai during late phase 3 or phase 4 of the action potential. Standard glass microelectrode recording in an additional 5 failing hearts confirmed postshock APD shortening and afterdepolarizations. APD80 of normal and sham-operated hearts was not shortened after defibrillation. Conclusion: HF promotes acute shortening of APD immediately after termination of VF in failing hearts. Persistent Cai elevation during late phase 3 and phase 4 of the shortened action potential result in afterdepolarizations, triggered activity, and spontaneous VF.",
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AU - Weiss, James N.

AU - Lin, Shien-Fong

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AB - Background: Successful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear. Objective: The purpose of this study was to determine the mechanisms of spontaneous VF after initial successful defibrillation in a rabbit model of heart failure (HF). Methods: Simultaneous optical mapping of intracellular calcium (Cai) and membrane potential (Vm) was performed in 12 rabbit hearts with chronic pacing-induced heart failure, in 4 sham-operated hearts, and in 5 normal hearts during fibrillation-defibrillation episodes. Results: Twenty-eight spontaneous VF episodes were recorded after initial successful defibrillation in 4 failing hearts (SVF group) but not in the remaining 8 failing hearts (no-SVF group) or in the normal or sham-operated hearts. The action potential duration (APD80) before pacing-induced VF was 209 ± 9 ms in the SVF group and 212 ± 14 ms in the no-SVF group (P = NS). After successful defibrillation, APD80 shortened to 147 ± 26 ms in the SVF group and to 176 ± 14 ms in the no-SVF group (P = .04). However, the duration of Cai after defibrillation was not different between the two groups (246 ± 21 ms vs 241 ± 17 ms, P = NS), resulting in elevated Cai during late phase 3 or phase 4 of the action potential. Standard glass microelectrode recording in an additional 5 failing hearts confirmed postshock APD shortening and afterdepolarizations. APD80 of normal and sham-operated hearts was not shortened after defibrillation. Conclusion: HF promotes acute shortening of APD immediately after termination of VF in failing hearts. Persistent Cai elevation during late phase 3 and phase 4 of the shortened action potential result in afterdepolarizations, triggered activity, and spontaneous VF.

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KW - Sudden cardiac death

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