Modeling hypersomnolence in sleep-disordered breathing - A novel approach using survival analysis

Citation
Nm. Punjabi et al., Modeling hypersomnolence in sleep-disordered breathing - A novel approach using survival analysis, AM J R CRIT, 159(6), 1999, pp. 1703-1709
Citations number
16
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
159
Issue
6
Year of publication
1999
Pages
1703 - 1709
Database
ISI
SICI code
1073-449X(199906)159:6<1703:MHISB->2.0.ZU;2-7
Abstract
The etiology of excessive daytime sleepiness in patients with sleep-disorde red breathing (SDB) is not well defined. In this study, we examined the rel ationships between several clinical and polysomnographic parameters and the degree of hypersomnolence in 741 patients with SDB (apnea-hypopnea index [ AHI] greater than or equal to 10 events/h). The study sample was obese (bod y mass index [BMI]: 35.3 +/- 8.5 kg/m(2)) and had evidence of moderate SDB (AHI: 47.6 +/- 29.3 events/h). Hypersomnolence was quantified with the mult iple sleep latency test (MSLT) and survival analysis was used to assess the risk factors for hypersomnolence. In a multivariate proportional hazards m odel, AHI and nocturnal hypoxemia were independent predictors of hypersomno lence (MSLT < 10 min). The adjusted relative risks (RR) of hypersomnolence were 1.00, 1.30, and 1.65 for patients with an AHI of 10 to 29.9, 30 to 59. 9, and greater than or equal to 60 events/h, respectively. A positive assoc iation between hypersomnolence and oxyhemoglobin desaturation (Delta Sa(O2) ) was observed with RR of 1.00, 1.18, 1.43, and 1.94 for a Delta Sa(O2) of less than or equal to 5%, 5.1 to 10%, 10.1 to 15%, and >15%, respectively. Sleep fragmentation, as assessed by the distribution of sleep stages, was a lso an independent predictor of hypersomnolence. Using stage 1 sleep as a r eference, an increase in stage 2 and slow wave sleep (SWS) were protective from hypersomnolence. For a 10% increase in stage 2 or SWS the adjusted RR for hypersomnolence were 0.93 and 0.79, respectively. REM sleep showed no s ignificant association with the degree of hypersomnolence. These results su ggest that AHI, nocturnal hypoxemia, and sleep fragmentation are independen t determinants of hypersomnolence in SDB.