Therapeutic hypothermia (30° C) enhances arrhythmogenic substrates, including spatially discordant alternans, and facilitates pacing-induced ventricular fibrillation in isolated rabbit hearts

Yu Cheng Hsieh, Shien-Fong Lin, Tung Chao Lin, Chih Tai Ting, Tsu Juey Wu

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: Therapeutic hypothermia (TH, 30°C) protects the brain from hypoxic injury. However, TH may potentiate the occurrence of lethal ventricular fibrillation (VF), although the mechanism remains unclear. The present study explored the hypothesis that TH enhances wavebreaks during VF and S1 pacing, facilitates pacing-induced spatially discordant alternans (SDA), and increases the vulnerability of pacing-induced VF. Methods and Results: Using an optical mapping system, epicardial activations of VF were studied in 7 Langendorff-perfused isolated rabbit hearts at baseline (37°C), TH (30°C), and rewarming (37°C). Action potential duration (APD)/conduction velocity (CV) restitution and APD alternans (n=6 hearts) were determined by S1 pacing at these 3 stages. During TH, there was a higher percentage of VF duration containing epicardial repetitive activities (spatiotemporal periodicity) (P<0.001). However, TH increased phase singularity number (wave-breaks) during VF (P<0.05) and S1 pacing (P<0.05). TH resulted in earlier onset of APD alternans (P<0.001), which was predominantly SDA (P<0.05), and increased pacing-induced VF episodes (P<0.05). TH also decreased CV, shortened wavelength, and enhanced APD dispersion and the spatial heterogeneity of CV restitution. Conclusions: TH (30°C) increased the vulnerability of pacing-induced VF by (1) facilitating wavebreaks during VF and S1 pacing, and (2) enhancing proarrhythmic electrophysiological parameters, including promoting earlier onset of APD alternans (predominantly SDA) during S1 pacing.

Original languageEnglish
Pages (from-to)2214-2222
Number of pages9
JournalCirculation Journal
Volume73
Issue number12
DOIs
StatePublished - 2009

Fingerprint

Induced Hypothermia
Ventricular Fibrillation
Rabbits
Action Potentials
Epicardial Mapping
Rewarming
Optical Devices
Periodicity
Brain Injuries

Keywords

  • Cardiac alternans
  • Hypothermia
  • Optical mapping
  • Restitution
  • Ventricular fibrillation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Therapeutic hypothermia (30° C) enhances arrhythmogenic substrates, including spatially discordant alternans, and facilitates pacing-induced ventricular fibrillation in isolated rabbit hearts. / Hsieh, Yu Cheng; Lin, Shien-Fong; Lin, Tung Chao; Ting, Chih Tai; Wu, Tsu Juey.

In: Circulation Journal, Vol. 73, No. 12, 2009, p. 2214-2222.

Research output: Contribution to journalArticle

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abstract = "Background: Therapeutic hypothermia (TH, 30°C) protects the brain from hypoxic injury. However, TH may potentiate the occurrence of lethal ventricular fibrillation (VF), although the mechanism remains unclear. The present study explored the hypothesis that TH enhances wavebreaks during VF and S1 pacing, facilitates pacing-induced spatially discordant alternans (SDA), and increases the vulnerability of pacing-induced VF. Methods and Results: Using an optical mapping system, epicardial activations of VF were studied in 7 Langendorff-perfused isolated rabbit hearts at baseline (37°C), TH (30°C), and rewarming (37°C). Action potential duration (APD)/conduction velocity (CV) restitution and APD alternans (n=6 hearts) were determined by S1 pacing at these 3 stages. During TH, there was a higher percentage of VF duration containing epicardial repetitive activities (spatiotemporal periodicity) (P<0.001). However, TH increased phase singularity number (wave-breaks) during VF (P<0.05) and S1 pacing (P<0.05). TH resulted in earlier onset of APD alternans (P<0.001), which was predominantly SDA (P<0.05), and increased pacing-induced VF episodes (P<0.05). TH also decreased CV, shortened wavelength, and enhanced APD dispersion and the spatial heterogeneity of CV restitution. Conclusions: TH (30°C) increased the vulnerability of pacing-induced VF by (1) facilitating wavebreaks during VF and S1 pacing, and (2) enhancing proarrhythmic electrophysiological parameters, including promoting earlier onset of APD alternans (predominantly SDA) during S1 pacing.",
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T1 - Therapeutic hypothermia (30° C) enhances arrhythmogenic substrates, including spatially discordant alternans, and facilitates pacing-induced ventricular fibrillation in isolated rabbit hearts

AU - Hsieh, Yu Cheng

AU - Lin, Shien-Fong

AU - Lin, Tung Chao

AU - Ting, Chih Tai

AU - Wu, Tsu Juey

PY - 2009

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N2 - Background: Therapeutic hypothermia (TH, 30°C) protects the brain from hypoxic injury. However, TH may potentiate the occurrence of lethal ventricular fibrillation (VF), although the mechanism remains unclear. The present study explored the hypothesis that TH enhances wavebreaks during VF and S1 pacing, facilitates pacing-induced spatially discordant alternans (SDA), and increases the vulnerability of pacing-induced VF. Methods and Results: Using an optical mapping system, epicardial activations of VF were studied in 7 Langendorff-perfused isolated rabbit hearts at baseline (37°C), TH (30°C), and rewarming (37°C). Action potential duration (APD)/conduction velocity (CV) restitution and APD alternans (n=6 hearts) were determined by S1 pacing at these 3 stages. During TH, there was a higher percentage of VF duration containing epicardial repetitive activities (spatiotemporal periodicity) (P<0.001). However, TH increased phase singularity number (wave-breaks) during VF (P<0.05) and S1 pacing (P<0.05). TH resulted in earlier onset of APD alternans (P<0.001), which was predominantly SDA (P<0.05), and increased pacing-induced VF episodes (P<0.05). TH also decreased CV, shortened wavelength, and enhanced APD dispersion and the spatial heterogeneity of CV restitution. Conclusions: TH (30°C) increased the vulnerability of pacing-induced VF by (1) facilitating wavebreaks during VF and S1 pacing, and (2) enhancing proarrhythmic electrophysiological parameters, including promoting earlier onset of APD alternans (predominantly SDA) during S1 pacing.

AB - Background: Therapeutic hypothermia (TH, 30°C) protects the brain from hypoxic injury. However, TH may potentiate the occurrence of lethal ventricular fibrillation (VF), although the mechanism remains unclear. The present study explored the hypothesis that TH enhances wavebreaks during VF and S1 pacing, facilitates pacing-induced spatially discordant alternans (SDA), and increases the vulnerability of pacing-induced VF. Methods and Results: Using an optical mapping system, epicardial activations of VF were studied in 7 Langendorff-perfused isolated rabbit hearts at baseline (37°C), TH (30°C), and rewarming (37°C). Action potential duration (APD)/conduction velocity (CV) restitution and APD alternans (n=6 hearts) were determined by S1 pacing at these 3 stages. During TH, there was a higher percentage of VF duration containing epicardial repetitive activities (spatiotemporal periodicity) (P<0.001). However, TH increased phase singularity number (wave-breaks) during VF (P<0.05) and S1 pacing (P<0.05). TH resulted in earlier onset of APD alternans (P<0.001), which was predominantly SDA (P<0.05), and increased pacing-induced VF episodes (P<0.05). TH also decreased CV, shortened wavelength, and enhanced APD dispersion and the spatial heterogeneity of CV restitution. Conclusions: TH (30°C) increased the vulnerability of pacing-induced VF by (1) facilitating wavebreaks during VF and S1 pacing, and (2) enhancing proarrhythmic electrophysiological parameters, including promoting earlier onset of APD alternans (predominantly SDA) during S1 pacing.

KW - Cardiac alternans

KW - Hypothermia

KW - Optical mapping

KW - Restitution

KW - Ventricular fibrillation

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