The effect of simulated obstructive apnea and hypopnea on aortic diameter and BP.

BACKGROUND: Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation. The mechanisms through which OSA may promote thoracic aortic dilatation are incompletely understood. Therefore, we studied the acute effects of simulated apnea and hypopnea on aortic diameter and BP in humans. METHODS: The diameter of the aortic root was measured in 20 healthy volunteers by echocardiography, and peripheral BP was continuously recorded prior, during, and immediately after simulated obstructive hypopnea (inspiration through threshold load), simulated obstructive apnea (Müller maneuver), end-expiratory central apnea, and normal breathing in randomized order. RESULTS: Proximal aortic diameter increased significantly during inspiration through a threshold load (+6.48%; SE, 3.03; P = .007), but not during Müller maneuver (+3.86%; SE, 2.71; P = .336) or end-expiratory central apnea (+0.62%; SE, 2.94; P = .445). Maneuver-induced changes in mean BP were observed during inspiration through a threshold load (-10.5 mm Hg; SE, 2.2; P < .001), the Müller maneuver (-8.8 mm Hg; SE, 2.4; P < .001), and end-expiratory central apnea (-4.2 mm Hg; SE, 1.4; P = .052). There was a significant increase in mean BP on release of threshold load inspiration (+8.1 mm Hg; SE, 2.9 mm Hg; P = .002), Müller maneuver (+10.7 mm Hg; SE, 2.9; P < .001), and end-expiratory central apnea (+10.6 mm Hg; SE, 2.5; P < .001). CONCLUSIONS: Simulated obstructive hypopnea/apnea and central apnea induced considerable changes in BP, and obstructive hypopnea was associated with an increase in proximal aortic diameter. Further studies are needed to investigate effects of apnea and hypopnea on transmural aortic pressure and aortic diameter to define the role of OSA in the pathogenesis of aortic dilatation

The effects of simulated obstructive apnea and hypopnea on arrhythmic potential in healthy subjects

Preliminary evidence supports an association between OSA and cardiac dysrhythmias. Negative intrathoracic pressure, as occurring during OSA, may provoke cardiac dysrhythmias. Thus, we aimed to study the acute effects of simulated apnea and hypopnea on arrhythmic potential and measures of cardiac repolarization [QT(C) and T (peak) to T (end) intervals ([Formula: see text])] in humans. In 41 healthy volunteers, ECG was continuously recorded prior, during and after simulated obstructive hypopnea (inspiration through a threshold load), simulated apnea (Mueller maneuver), end-expiratory central apnea and normal breathing in randomized order. The number of subjects with premature beats was significantly higher during inspiration through a threshold load (n = 7), and the Mueller maneuver (n = 7) compared to normal breathing (n = 0) (p = 0.008 for all comparisons), but not during end-expiratory central apnea (n = 3, p = 0.125). Inspiration through a threshold load was associated with a non-significant mean (SD) increase of the QT(C) interval [+5.4 (22.4) ms, 95 %CI -1.7 to +12.4 ms, p = 0.168] and a significant increase of the [Formula: see text] interval [+3.7 (8.9) ms, 95 %CI +0.9 to +6.6 ms, p = 0.010]. The Mueller maneuver induced a significant increase of the QT(C) interval [+8.3 (23.4) ms, 95 %CI 0.9 to +15.6 ms, p = 0.035] and the [Formula: see text] interval (+4.2 (8.2) ms, 95 %CI +1.6 to +6.8 ms, p = 0.002). There were no significant changes of the QT(C) and [Formula: see text] intervals during central end-expiratory apnea. These data indicate that simulated obstructive apnea and hypopnea are associated with an increase of premature beats and prolongation of QT(C) and [Formula: see text] intervals. Therefore, negative intrathoracic pressure changes may be a contributory mechanism for the association between OSA and cardiac dysrhythmias

Quantitative changes in the sleep EEG at moderate altitude (1630 m and 2590 m)

BACKGROUND: Previous studies have observed an altitude-dependent increase in central apneas and a shift towards lighter sleep at altitudes >4000 m. Whether altitude-dependent changes in the sleep EEG are also prevalent at moderate altitudes of 1600 m and 2600 m remains largely unknown. Furthermore, the relationship between sleep EEG variables and central apneas and oxygen saturation are of great interest to understand the impact of hypoxia at moderate altitude on sleep. METHODS: Fourty-four healthy men (mean age 25.0±5.5 years) underwent polysomnographic recordings during a baseline night at 490 m and four consecutive nights at 1630 m and 2590 m (two nights each) in a randomized cross-over design. RESULTS: Comparison of sleep EEG power density spectra of frontal (F3A2) and central (C3A2) derivations at altitudes compared to baseline revealed that slow-wave activity (SWA, 0.8-4.6 Hz) in non-REM sleep was reduced in an altitude-dependent manner (∼4% at 1630 m and 15% at 2590 m), while theta activity (4.6-8 Hz) was reduced only at the highest altitude (10% at 2590 m). In addition, spindle peak height and frequency showed a modest increase in the second night at 2590 m. SWA and theta activity were also reduced in REM sleep. Correlations between spectral power and central apnea/hypopnea index (AHI), oxygen desaturation index (ODI), and oxygen saturation revealed that distinct frequency bands were correlated with oxygen saturation (6.4-8 Hz and 13-14.4 Hz) and breathing variables (AHI, ODI; 0.8-4.6 Hz). CONCLUSIONS: The correlation between SWA and AHI/ODI suggests that respiratory disturbances contribute to the reduction in SWA at altitude. Since SWA is a marker of sleep homeostasis, this might be indicative of an inability to efficiently dissipate sleep pressure