Search

Background: Sympathetic hyperactivity and poor sleep quality have been reported in patients with myocardial infarction (MI). Sleep is an important modulator of cardiovascular function. We aimed to evaluate the effects of renal denervation (RDN) on cardiac autonomic activity and disordered sleep patterns in rats with MI.Methods: Wireless transmission of polysomnographic recordings was performed in sham and left coronary artery (LCA) ligation male rats during normal daytime sleep before and after RDN. Spectral analyses of electroencephalogram and electromyogram (EMG) recordings were performed to define active waking, quiet sleep, and paradoxical sleep. Cardiac autonomic activity was measured by analyzing the power spectrum of heart rate variability. Central sleep apnea events were measured by analyzing the EMG recordings of the diaphragm.Results: In the LCA ligation group, there was a higher low-frequency (LF)/high-frequency (HF) power ratio during sleep; the LF/HF ratio decreased significantly in the rats that underwent RDN in all sleep stages when compared with that in the rats that did not. The frequency of sleep interruptions increased without RDN in the LCA ligation group when compared with that in the sham group. This change was ameliorated and prevented with RDN in the LCA ligation group.Conclusions: Our results demonstrate significant sleep fragmentation with sympathetic hyperactivity after MI and that RDN prevents autonomic dysfunction and disordered sleep. RDN may then reduce sleep apnea and sleep-related sudden cardiac death after MI by restoring autonomic homeostasis. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]