Effect of Aging on Cardiac and Electroencephalographic Arousal in Sleep Apnea/Hypopnea Syndrome

To the Editor: Prevalence of sleep disordered breathing increases with age.1,2 However, effects of aging on the pathology of apnea/hypopnea in clinical settings have not been clearly investigated. We designed the present study to determine whether cardiac arousal, an abrupt increase in heart rate at a termination of apnea/hypopnea, and electroencephalographic (EEG) arousal are influenced by aging in patients with sleep apnea syndrome (SAS). Subjects were 14 middle-aged patients more than 40 years of age (mean age 48.4 years) with SAS and 11 older patients more than 60 years of age (mean age 70.5 years). We polygraphically evaluated numbers of apnea per hour (apnea index: AI), number of hypopneas per hour (hypopnea index: HI), and apnea/hypopnea index (AHI) as a summation of AI and HI. We calculated %AI (AI/AHI × 100) and %HI (HI/AHI × 100). Duration in which nocturnal oxygen saturation (SaO2) decreased below 90% (duration of SaO2 < 90%) was measured with pulse oximetry. SAS was diagnosed when AHI was greater than 10.3 We measured heart rate during the 10-second-epoch soon before and after apnea/hypopnea termination on polysomnography recording. Cardiac arousal was defined when heart rate increased at a termination of apnea/hypopnea by 10% or more. We calculated number of apnea/hypopneas per hour associated with cardiac arousal (XI).% Cardiac arousal was assessed with the ratio of XI to AHI (XI/AHI × 100). EEG arousal was defined according to the report of 1992 American Sleep Disorders Association.4 We calculated number of apnea/hypopneas per hour with EEG arousal (YI). %EEG arousal was assessed with the ratio of YI to AHI (YI/AHI × 100). Between middle-aged and older patients, we did not find any significant differences in height, weight, body mass index, AHI, or the ratio of occurrence of central apneas to total episodes of apnea/hypopnea. %Cardiac and %EEG arousal, %AI and duration of SaO2 < 90% were greater in middle-aged than in older patients. In contrast, %HI was significantly greater in older than middle-aged patients (Table 1). %Cardiac and %EEG arousal significantly correlated with AI, AHI, and the duration of SaO2 < 90% in middle-aged patients, and with AI and AHI in older patients. We summarized the characteristics of sleep disordered breathing in older, compared with middle-aged, patients with SAS as follows: (1) arousal response at a termination of apnea/hypopnea was more suppressed in older patients; (2) contribution of hypopneas to sleep disordered breathing was greater; (3) severity of nocturnal oxygen desaturation was milder. In middle-aged patients, arousal response correlated with severity of oxygen desaturation, but not in older patients, suggesting that milder hypoxia might lead to a suppressed arousal response in older patients.5 Abnormalities in respiratory rhythm during sleep, characterized mostly by periodic breathing, are found frequently in geriatric populations.6,7 A report on the theoretical model of a respiratory control system8 showed that periodic breathing depends on the circulation time and the sensitivity of the upper airway and chest wall to chemical stimuli; hence, an obstructive apnea is possibly produced by control system instability.6,8 Other investigators showed that periodic breathing and an obstructive sleep apnea in older people may occur as a result of an increase in upper airway resistance leading to a decrease in tidal volume.8,9 The increased contribution of hypopneas in older people may reflect the two mechanisms described above. Moreover, a recent study in canines10 showed that aging was accompanied by diminished alveolar ventilation and by blunted ventilatory and arousal responses to hypoxia. The authors pointed out possible contributing factors to the blunted arousal in older people, such as aging of carotid bodies and reduced afferent stimuli from the ventilatory organs, both of which might have played pathogenic roles in our findings. We conclude that a detailed observation of cardiac and EEG arousal at the termination of apnea/hypopnea provides significant information about the effects of aging on the pathophysiology of SAS.