Sleep-related changes in cardiovascular autonomic regulation in left coronary artery ligation rats: Neural mechanism facilitating arrhythmia after myocardial infarction

Wei Lun Lin, Li Wei Lo, Hau Ruey Chen, Chun Ting Lai, Shinya Yamada, Shin Huei Liu, Yu Hui Chou, Shih Ann Chen, Yun Ching Fu, Terry B.J. Kuo

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background Autonomic imbalance with increased sympathetic and decreased parasympathetic activities is observed in patients after myocardial infarction (MI). We aimed to investigate sleep-related changed in autonomic regulation in left coronary artery (LCA) ligation rats. Methods Wireless transmission of polysomnographic recording was performed in sham and LCA ligation male rats during normal daytime sleep with and without atenolol treatment. Spectral analyses of the electroencephalogram (EEG) and electromyogram (EMG) were evaluated to define active waking (AW), quiet and paradoxical sleeps (QS, PS). Cardiac autonomic activities were measured by analyzing the power spectrum of heart rate variability (HRV). EEG, EMG and HRV were recorded over 6 h for consecutive 3 days in all groups. Results In LCA ligation group, there were higher LF and LF/HF ratio on QS phase, but not AW and PS phases, compared to atenolol treated sham and LCA ligation groups, respectively. The HF component was not significantly changed on all groups in both sleep and awake phases. Sleep interruption was more frequent in LCA ligation rats compared to sham, and it was not found in LCA ligation with atenolol treatment group. Increased AW, PS and decreased QS time were noted in LCA ligation group, compared to sham and it was restored to baseline in LCA ligation with atenolol treatment group. Conclusions Our results demonstrate significant sleep fragmentations with sympathetic hyperactivity during QS stages after MI, and atenolol could restore the autonomic dysfunction and sleep disturbance. The finding explains the cause of sleep-related fetal arrhythmia and sudden cardiac death after MI.

Original languageEnglish
Pages (from-to)65-72
Number of pages8
JournalInternational Journal of Cardiology
Volume225
DOIs
Publication statusPublished - Dec 15 2016
Externally publishedYes

Fingerprint

Ligation
Cardiac Arrhythmias
Coronary Vessels
Sleep
Atenolol
Myocardial Infarction
Electromyography
Electroencephalography
Heart Rate
Sleep Deprivation
Sudden Cardiac Death
REM Sleep
Therapeutics

Keywords

  • Autonomic
  • Heart rate variability
  • Myocardial infarction
  • Sleep

ASJC Scopus subject areas

  • Medicine(all)
  • Cardiology and Cardiovascular Medicine

Cite this

Sleep-related changes in cardiovascular autonomic regulation in left coronary artery ligation rats : Neural mechanism facilitating arrhythmia after myocardial infarction. / Lin, Wei Lun; Lo, Li Wei; Chen, Hau Ruey; Lai, Chun Ting; Yamada, Shinya; Liu, Shin Huei; Chou, Yu Hui; Chen, Shih Ann; Fu, Yun Ching; Kuo, Terry B.J.

In: International Journal of Cardiology, Vol. 225, 15.12.2016, p. 65-72.

Research output: Contribution to journalArticle

Lin, Wei Lun ; Lo, Li Wei ; Chen, Hau Ruey ; Lai, Chun Ting ; Yamada, Shinya ; Liu, Shin Huei ; Chou, Yu Hui ; Chen, Shih Ann ; Fu, Yun Ching ; Kuo, Terry B.J. / Sleep-related changes in cardiovascular autonomic regulation in left coronary artery ligation rats : Neural mechanism facilitating arrhythmia after myocardial infarction. In: International Journal of Cardiology. 2016 ; Vol. 225. pp. 65-72.
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abstract = "Background Autonomic imbalance with increased sympathetic and decreased parasympathetic activities is observed in patients after myocardial infarction (MI). We aimed to investigate sleep-related changed in autonomic regulation in left coronary artery (LCA) ligation rats. Methods Wireless transmission of polysomnographic recording was performed in sham and LCA ligation male rats during normal daytime sleep with and without atenolol treatment. Spectral analyses of the electroencephalogram (EEG) and electromyogram (EMG) were evaluated to define active waking (AW), quiet and paradoxical sleeps (QS, PS). Cardiac autonomic activities were measured by analyzing the power spectrum of heart rate variability (HRV). EEG, EMG and HRV were recorded over 6 h for consecutive 3 days in all groups. Results In LCA ligation group, there were higher LF and LF/HF ratio on QS phase, but not AW and PS phases, compared to atenolol treated sham and LCA ligation groups, respectively. The HF component was not significantly changed on all groups in both sleep and awake phases. Sleep interruption was more frequent in LCA ligation rats compared to sham, and it was not found in LCA ligation with atenolol treatment group. Increased AW, PS and decreased QS time were noted in LCA ligation group, compared to sham and it was restored to baseline in LCA ligation with atenolol treatment group. Conclusions Our results demonstrate significant sleep fragmentations with sympathetic hyperactivity during QS stages after MI, and atenolol could restore the autonomic dysfunction and sleep disturbance. The finding explains the cause of sleep-related fetal arrhythmia and sudden cardiac death after MI.",
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T1 - Sleep-related changes in cardiovascular autonomic regulation in left coronary artery ligation rats

T2 - Neural mechanism facilitating arrhythmia after myocardial infarction

AU - Lin, Wei Lun

AU - Lo, Li Wei

AU - Chen, Hau Ruey

AU - Lai, Chun Ting

AU - Yamada, Shinya

AU - Liu, Shin Huei

AU - Chou, Yu Hui

AU - Chen, Shih Ann

AU - Fu, Yun Ching

AU - Kuo, Terry B.J.

PY - 2016/12/15

Y1 - 2016/12/15

N2 - Background Autonomic imbalance with increased sympathetic and decreased parasympathetic activities is observed in patients after myocardial infarction (MI). We aimed to investigate sleep-related changed in autonomic regulation in left coronary artery (LCA) ligation rats. Methods Wireless transmission of polysomnographic recording was performed in sham and LCA ligation male rats during normal daytime sleep with and without atenolol treatment. Spectral analyses of the electroencephalogram (EEG) and electromyogram (EMG) were evaluated to define active waking (AW), quiet and paradoxical sleeps (QS, PS). Cardiac autonomic activities were measured by analyzing the power spectrum of heart rate variability (HRV). EEG, EMG and HRV were recorded over 6 h for consecutive 3 days in all groups. Results In LCA ligation group, there were higher LF and LF/HF ratio on QS phase, but not AW and PS phases, compared to atenolol treated sham and LCA ligation groups, respectively. The HF component was not significantly changed on all groups in both sleep and awake phases. Sleep interruption was more frequent in LCA ligation rats compared to sham, and it was not found in LCA ligation with atenolol treatment group. Increased AW, PS and decreased QS time were noted in LCA ligation group, compared to sham and it was restored to baseline in LCA ligation with atenolol treatment group. Conclusions Our results demonstrate significant sleep fragmentations with sympathetic hyperactivity during QS stages after MI, and atenolol could restore the autonomic dysfunction and sleep disturbance. The finding explains the cause of sleep-related fetal arrhythmia and sudden cardiac death after MI.

AB - Background Autonomic imbalance with increased sympathetic and decreased parasympathetic activities is observed in patients after myocardial infarction (MI). We aimed to investigate sleep-related changed in autonomic regulation in left coronary artery (LCA) ligation rats. Methods Wireless transmission of polysomnographic recording was performed in sham and LCA ligation male rats during normal daytime sleep with and without atenolol treatment. Spectral analyses of the electroencephalogram (EEG) and electromyogram (EMG) were evaluated to define active waking (AW), quiet and paradoxical sleeps (QS, PS). Cardiac autonomic activities were measured by analyzing the power spectrum of heart rate variability (HRV). EEG, EMG and HRV were recorded over 6 h for consecutive 3 days in all groups. Results In LCA ligation group, there were higher LF and LF/HF ratio on QS phase, but not AW and PS phases, compared to atenolol treated sham and LCA ligation groups, respectively. The HF component was not significantly changed on all groups in both sleep and awake phases. Sleep interruption was more frequent in LCA ligation rats compared to sham, and it was not found in LCA ligation with atenolol treatment group. Increased AW, PS and decreased QS time were noted in LCA ligation group, compared to sham and it was restored to baseline in LCA ligation with atenolol treatment group. Conclusions Our results demonstrate significant sleep fragmentations with sympathetic hyperactivity during QS stages after MI, and atenolol could restore the autonomic dysfunction and sleep disturbance. The finding explains the cause of sleep-related fetal arrhythmia and sudden cardiac death after MI.

KW - Autonomic

KW - Heart rate variability

KW - Myocardial infarction

KW - Sleep

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