Obstructive sleep apnea in adults with Down syndrome.

OBJECTIVES: A high proportion of children with Down syndrome (DS) have the obstructive sleep apnea syndrome (OSAS). Although adults with DS have many predisposing factors for OSAS, this population has not been well studied. We hypothesized that OSAS is common in adults with DS, and that the severity of OSAS is worse in DS adults who are more obese. DESIGN: Cohort study. SETTING: Sleep laboratory. PARTICIPANTS: 16 adults with DS underwent evaluation for sleep disordered breathing. INTERVENTIONS: Polysomnographic results were compared to a retrospective sample of adult patients referred for clinically suspected OSAS. MEASUREMENTS AND RESULTS: Polysomnograms were abnormal in 94% of DS subjects. The median apnea hypopnea index (AHI) was 37/h (range 0-118). The median arterial oxygen saturation nadir was 75% (23% to 95%), and the median peak end-tidal CO2 was 58 (47-66) mm Hg. There was a significant correlation between body mass index and AHI (r = 0.53, p < 0.05). Sixty-three percent had an Epworth score > 10. The AHI and saturation nadir were significantly worse in DS than non-DS patients. CONCLUSIONS: Adults with DS frequently have OSAS, with obstructive apnea, hypoxemia, hypoventilation, and sleep fragmentation. The severity of OSAS correlated with obesity. We speculate that the complications of untreated OSAS (cardiovascular disease, increased mortality, and neurobehavioral morbidities including daytime sleepiness and impaired cognitive function) commonly overlap with the manifestations of DS and therefore may not elicit a prompt investigation in these patients. We speculate that OSAS is an important, but potentially treatable, cause of morbidity in adults with DS.

Hypoxia, not the frequency of sleep apnea, induces acute hemodynamic stress in patients with chronic heart failure.

OBJECTIVES: This study was conducted to evaluate whether brain (B-type) natriuretic peptide (BNP) changes during sleep are associated with the frequency and severity of apneic/hypopneic episodes, intermittent arousals, and hypoxia. BACKGROUND: Sleep apnea is strongly associated with heart failure (HF) and could conceivably worsen HF through increased sympathetic activity, hemodynamic stress, hypoxemia, and oxidative stress. If apneic activity does cause acute stress in HF, it should increase BNP. METHODS: Sixty-four HF patients with New York Heart Association functional class II and III HF and ejection fraction <40% underwent a baseline sleep study. Five patients with no sleep apnea and 12 with severe sleep apnea underwent repeat sleep studies, during which blood was collected every 20 min for the measurement of BNP. Patients with severe sleep apnea also underwent a third sleep study with frequent BNP measurements while they were administered oxygen. This provided 643 observations with which to relate apnea to BNP. The association of log BNP with each of 6 markers of apnea severity was evaluated with repeated measures regression models. RESULTS: There was no relationship between BNP and the number of apneic/hypopneic episodes or the number of arousals. However, the burden of hypoxemia (the time spent with oxygen saturation <90%) significantly predicted BNP concentrations; each 10% increase in duration of hypoxemia increased BNP by 9.6% (95% confidence interval: 1.5% to 17.7%, p = 0.02). CONCLUSIONS: Hypoxemia appears to be an important factor that underlies the impact of sleep abnormalities on hemodynamic stress in patients with HF. Prevention of hypoxia might be especially important for these patients.