Analysis of heart rate response to obstructive apnea/hypopnea events in patients with Parkinson's disease with relatively severe sleep apnea syndrome

• Main Authors: Kohzoh Yoshino, Ayano Kawaguchi, Shogo Yata, Akinori Iyama, Saburo Sakoda
• Format: Article
• Language: English
• Published: Elsevier 2021-01-01
• Series: Informatics in Medicine Unlocked
• Subjects: Sleep apnea; Parkinson's disease; Autonomic nervous system; Sympathetic; Hypopnea; Heart rate
• Online Access: http://www.sciencedirect.com/science/article/pii/S2352914821000447

Detection of non-motor symptoms specific to patients with Parkinson's disease (PD) is an important area for investigation because it may lead to early PD diagnosis. The aim of this study is to (i) verify whether there were differences between patients with PD and concurrent relatively severe sleep apnea syndrome (SAS) and non-PD patients with relatively severe SAS in terms of heart rate response to obstructive apnea/hypopnea events during sleep and (ii) to clarify the correlation between the extent of the heart rate response and the level of cardiac sympathetic denervation measured by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. We analyzed the heart rate response to obstructive apnea/hypopnea events during sleep in 23 patients with PD and concomitant relatively severe SAS as well as in 36 non-PD patients with relatively severe SAS. The amplitude of increase in the heart rate in response to apnea/hypopnea events was significantly lower for patients in the PD group with SAS than for those in the non-PD group with SAS. A relatively strong positive correlation was found between the amplitude of heart rate increase in response to apnea/hypopnea events and the H/M ratio on 123I-MIBG scintigraphy in the PD group with SAS. Our results suggest that the amplitude of heart rate increase in response to obstructive apnea/hypopnea events reflects cardiac sympathetic nerve activity, and that in patients with relatively severe SAS concomitant with PD, the reactive increase in heart rate is suppressed due to degeneration of the cardiac sympathetic nervous system.