Sleep-Related Changes in Cardiovascular Autonomic Regulation and Arrhythmogenesis After Myocardial Infarction

• Main Authors: Wei-Lun Lin, 林瑋倫
• Other Authors: Shih-Ann Chen
• Format: Others
• Language: en_US
• Published: 2018
• Online Access: http://ndltd.ncl.edu.tw/handle/frqm5r

博士 === 國立陽明大學 === 臨床醫學研究所 === 106 === Background Cardiovascular disease is the most common cause of death in the world, contributing to an estimated 17.3 million (31.5%) of 54 million total deaths. Autonomic imbalance with increased sympathetic and decreased parasympathetic activities is observed in patients after myocardial infarction (MI). Sleep is not an entirely protected period, as 20% of MI and 15% of sudden cardiac deaths occur at night. Sleep cycle also affects a series of changes in autonomic function, and previous study has confirmed that quiet sleep (QS) is associated with an increase in vagal function and a decrease in sympathetic function. In a previous report, 50 to 66% of patients with MI also experienced sleep apnea. Methods Wireless transmission of polysomnographic recording was performed in sham and LCA ligation male rats during normal daytime sleep with and without atenolol or captopril treatment. We used the mini-pump that was implanted subcutaneously to deliver drugs or vehicle solution in rats, respectively. Spectral analyses of the electroencephalogram (EEG) and electromyogram (EMG) were evaluated to define active waking (AW), QS and paradoxical sleep (PS). Cardiac autonomic activities were measured by analyzing the power spectrum of heart rate variability (HRV). Central sleep apnea (CSA) events were measured by analyzing the electromyogram of the diaphragm (DEMG). EEG, EMG, HRV and DEMG were recorded 24 hours for consecutive 3 days in all rats weekly. The end of recording, rats were euthanized under anesthesia and heart tissues were harvested to evaluate fibrosis degree. Results In LCA ligation group, there were higher LF (low frequency) and LF/HF (high frequency) ratio on QS phase, but not AW and PS phases, compared to sham group. The HF components were not significantly changed in all groups in both sleep and awake phases, respectively. Sleep interruption was more frequent in LCA ligation rats compared to sham rats. Increased AW, PS and decreased QS times were noted in LCA ligation group compared to sham group. CSA events were significantly increased in the MI group, and were restored to the normal level after captopril treatment. These changes were restored to baseline after atenolol or captopril treatment in the MI group. Conclusions Our results demonstrate significant sleep fragmentation with sympathetic hyperactivity after MI, and that atenolol or captopril restores the autonomic dysfunction and sleep disorder. The findings suggest that beta-block or angiotensin-converting-enzyme inhibitor (ACEI) improved sleep-related respiration disorder after MI by restoring autonomic homeostasis, and this finding provides a hypothesis generating for future studies in humans.