Suppressed cardiac and electroencephalographic arousal on apnea/hypopnea termination in elderly patients with cerebral infarction.

Abstract

The goal of the present investigation is to show the clinical significance of arousal response at termination of apnea/hypopnea in patients with sleep apnea syndrome (SAS) after cerebral infarction. We polygraphically assessed "cardiac arousal," which is defined as an abrupt increase in heart rate at a termination of sleep apnea/hypopnea, and electroencephalographic (EEG) arousal. There were six elderly subjects, bedridden after cerebral infarction, with SAS aged 71-87 years (mean 72.3 years) and 11 age-matched patients with SAS aged 61-78 years (mean 62.3 years) as controls. The following sleep parameters were measured: number of apneas per hour (apnea index [AI]), number of hypopneas per hour (hypopnea index [HI]), summation of the two (apnea/hypopnea index [AHI]), and duration in which nocturnal oxygen saturation was decreased below 90% (duration of SaO2 < 90%). We calculated the ratio of apnea/hypopnea per hour with cardiac arousal to total apnea/hypopneas (XI) (% cardiac arousal [XI/AHI x 100]) and the ratio of that with EEG arousal (YI) (% EEG arousal [YI/AHI x 100]). Between the two groups, we found no significant difference in body mass index, the ratio of central apnea to total apnea/hypopnea, AHI, duration of apnea/hypopnea, lowest SaO2, and duration of SaO2 < 90%. Compared with controls, % cardiac and % EEG arousals were significantly lower in patients with cerebral infarction. In contrast, the ratio of HI to AHI was significantly higher in patients with cerebral infarction than in control subjects. Our findings indicate that cardiac and EEG arousals at termination of apnea/hypopnea are significantly suppressed in elderly patients with SAS after cerebral infarction, which may provide useful information on the pathophysiology of SAS in patients with cerebrovascular disease.