Tingting Wang1, Juan Yang1, Yingjie Song1, Feng Pang2, Xinwen Guo3, Yuxi Luo4,5. 1. School of Biomedical Engineering, Sun Yat-Sen University, Guangzhou, China. 2. Sleep-Disordered Breathing Center, the Sixth Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China. 3. Psychology Department, Guangdong 999 Brain Hospital, Guangzhou, China. 4. School of Biomedical Engineering, Sun Yat-Sen University, Guangzhou, China. luoyuc@163.com. 5. Key Laboratory of Sensing Technology and Biomedical Instrument of Guangdong Province, Sun Yat-Sen University, Guangzhou, China. luoyuc@163.com.
Abstract
PURPOSE: Sleep apnea-hypopnea syndrome (SAHS) is an independent risk factor for various cardiovascular and cerebrovascular diseases, but the underlying relationship of its physiological subsystems remains unclear. Thus, we aimed to investigate the effect of SAHS on central and autonomic nervous system (CNS-ANS) interactions during sleep. METHODS: Thirty-five patients with SAHS and 19 healthy age-matched controls underwent overnight polysomnography. The absolute spectral powers of five frequency bands from six EEG channels and ECG morphological features (HR, PR interval, QT interval) were calculated. Multivariable transfer entropy was applied to analyze the differences of the CNS-ANS network interactions between patients with SAHS of different severities and healthy controls during deep, light, and rapid eye movement sleep. RESULTS: The CNS-ANS network interacted bidirectionally in all researched groups, with the cardiac information modulating the brain activity. The information strength from QT to most EEG components and PR to some EEG components was significantly affected by SAHS severity during light sleep, which indicates the coupling features of QT-brain nodes are important indicators. The driver effects from the β-band significantly increased in patients with SAHS. CONCLUSIONS: Respiratory events may be the main reason for the CNS-ANS interaction changes in SAHS. These findings help explain the physiological regulation process of SAHS and provide valuable information for analysis of the development of SAHS-related cardiovascular and chronic diseases.
PURPOSE: Sleep apnea-hypopnea syndrome (SAHS) is an independent risk factor for various cardiovascular and cerebrovascular diseases, but the underlying relationship of its physiological subsystems remains unclear. Thus, we aimed to investigate the effect of SAHS on central and autonomic nervous system (CNS-ANS) interactions during sleep. METHODS: Thirty-five patients with SAHS and 19 healthy age-matched controls underwent overnight polysomnography. The absolute spectral powers of five frequency bands from six EEG channels and ECG morphological features (HR, PR interval, QT interval) were calculated. Multivariable transfer entropy was applied to analyze the differences of the CNS-ANS network interactions between patients with SAHS of different severities and healthy controls during deep, light, and rapid eye movement sleep. RESULTS: The CNS-ANS network interacted bidirectionally in all researched groups, with the cardiac information modulating the brain activity. The information strength from QT to most EEG components and PR to some EEG components was significantly affected by SAHS severity during light sleep, which indicates the coupling features of QT-brain nodes are important indicators. The driver effects from the β-band significantly increased in patients with SAHS. CONCLUSIONS: Respiratory events may be the main reason for the CNS-ANS interaction changes in SAHS. These findings help explain the physiological regulation process of SAHS and provide valuable information for analysis of the development of SAHS-related cardiovascular and chronic diseases.
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