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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 6h for consecutive 3days 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.

Background Heart failure (HF) causes atrial remodeling and increases the incidence of atrial fibrillation (AF). Renal denervation (RDN) has been shown to decrease the development of AF. This study aimed to identify the effects of RDN on the atrial arrhythmogenic substrates in HF. Methods Rabbits were classified into four groups: control (n=9), RDN (n=10), HF (n=6) and HF-RDN (n=9). Surgical and chemical RDN was approached through bilateral retroperitoneal flank incisions in RDN and HF-RDN. Rapid ventricular pacing of 400bpm for 4weeks was applied in HF and HF-RDN. After 4weeks, the rabbits were sacrificed and atrial myocardium were harvested for Western blot and Trichrome stain. Results The bi-atrial effective refractory period (ERP) of HF was significantly longer compared with that of control and RDN. In right atrium, the ERP of HF was also significantly longer compared with that of HF-RDN, but there was no significant difference in left atrial ERP. In bi-atrium, ion channel protein expressions of CaV1.2, NaV1.5, Kir2.1 SERCA2 and NCX were similar among 4 groups. However, the degree of atrial fibrosis was extensive in bi-atrium of HF, when compared to that of control, RDN and HF-RDN. Conclusion The ERP of HF-RDN is partially shortened by RDN compared with that of HF. There are no differences ionic channel protein expressions in bi-atrium among all groups. The degree of atrial fibrosis is severe in HF, but not in HF-RDN, suggesting that RDN may regulate the atrial arrhythmogenic substrates in HF mostly through reverse structural remodeling.