A Retrospective Study to Compare the Use of the Mean Apnea-Hypopnea Duration and the Apnea-Hypopnea Index with Blood Oxygenation and Sleep Patterns in Patients with Obstructive Sleep Apnea Diagnosed by Polysomnography

Abstract

BackgroundThe apnea-hypopnea index (AHI) and the mean apnea-hypopnea duration (MAD) are used to measure the severity of the symptoms of obstructive sleep apnea (OSA). The aim of this study was to compare the use of the MAD with the AHI as indicators of clinical and demographic parameters, blood oxygenation, and sleep parameters in patients diagnosed with OSA by polysomnography (PSG).Material/MethodsA retrospective study included 511 patients with OSA diagnosed by PSG and who had the AHI and the MAD measured according to the guidelines from the American Academy of Sleep Medicine (AASM). The patients were divided into two groups: patients with a short MAD and with a long MAD, according to median duration, and using the inter-quartile range (IQR), as the data were not normally distributed. Clinical and demographic parameters were recorded. Pulse oximetry was used to measure blood oxygen saturation during sleep, sleep structure was recorded, and the Epworth Sleepiness Scale (ESS) questionnaire was used to measure daytime sleepiness.ResultsIn all 511 patients with OSA, the MAD was significantly, but weakly, correlated with the AHI (r=0.17, P<0.01), but showed no significant associations with patient age (r=0.08, P=0.06), body weight (r=0.014, P=0.75), and height (r=0.06, P=0.16). Patients with a long MAD or severe OSA (n=260) had significantly worse blood oxygen levels and sleep parameters.ConclusionsFor patients with severe OSA, this study showed that the MAD was a useful indicator of blood oxygenation and sleep parameters.

Association ofPrevotellaenterotype with polysomnographic data in obstructive sleep apnea/hypopnea syndrome patients

“…BP was not significantly different among the three enterotype AHI≥15 patient groups, but mean diastolic pressure during sleep was >80 mmHg, which was similar to that observed in a previous study [10]. MDA can act as an indicator of the levels of sleep parameters and blood oxygenation for the evaluation of severe OSAHS patients [33]. When MAD is elevated, sleep apnea appears to be more likely to cause respiratory arousal and might impair sleep stability, resulting in SF.…”

“…When MAD is elevated, sleep apnea appears to be more likely to cause respiratory arousal and might impair sleep stability, resulting in SF. This outcome might then be that the transition of the N2 sleep stage (the longest stage of sleep) to the N3 sleep stage is a vulnerable period, which is interrupted in OSAHS patients, and the overall sleep pattern becomes light sleep [33]. Additionally, chronic SF induction elevates fat mass, alters fecal microbiota, promotes increased gut permeability, leads to systemic and adipose tissue inflammatory changes, and accompanies metabolic dysfunction [3].…”

Disruption of sleep architecture in Prevotella enterotype of patients with obstructive sleep apnea‐hypopnea syndrome

“…BP was not significantly different among the three enterotype AHI ≥ 15 patient groups, but mean diastolic pressure during sleep was > 80 mmHg, which was similar to that observed in a previous study (Shao et al, ). MAD can act as an indicator of the levels of sleep parameters and blood oxygenation for the evaluation of severe OSAHS patients (Zhan, Fang, Wu, Pinto, & Wei, ). When MAD is elevated, sleep apnea appears to be more likely to cause respiratory arousal and might impair sleep stability, resulting in SF.…”

“…When MAD is elevated, sleep apnea appears to be more likely to cause respiratory arousal and might impair sleep stability, resulting in SF. This outcome might then be that the transition of the N2 sleep stage (the longest stage of sleep) to the N3 sleep stage is a vulnerable period, which is interrupted in OSAHS patients, and the overall sleep pattern becomes light sleep (Zhan et al, ). Additionally, chronic SF induction elevates fat mass, alters fecal microbiota, promotes increased gut permeability, leads to systemic and adipose tissue inflammatory changes, and accompanies metabolic dysfunction (Poroyko et al, ).…”

“…Contrastingly, evidence has shown that N1, N3, and REM sleep stages decrease and the N2 sleep stage increases in OSAHS patients (Rosenzweig et al, ). However, a higher N1 percentage, a longer MAD, and a shortened REM sleep stage were revealed in AHI ≥ 15 patients with OSAHS‐induced hypertension (Shao et al, ; Zhan et al, ). Our findings reveal that BP plays a vital role, particularly for SAS, where BP is comprehensively regulated by the peripheral and central systems.…”