CPAP withdrawal usually leads to a rapid recurrence of OSA, a return of subjective sleepiness, and is associated with impaired endothelial function, increased urinary catecholamines, blood pressure, and heart rate. Thus the proposed study model appears to be suitable to evaluate physiological and therapeutic effects in OSA. Clinical trial registered with www.controlled-trials.com (ISRCTN93153804).

Continuous positive airway pressure withdrawal is associated with the prolongation of the QT(c) and TpTe(c) intervals and TpTe/QT ratio, which may provide a possible mechanistic link between OSA, cardiac dysrhythmias, and thus sudden cardiac death.

Arterial tonometry is a method to assess arterial stiffness and has become a valuable tool in the stratification of cardiovascular risk. The arterial tonometry-derived augmentation index (AIx) is a marker of arterial stiffness and an independent predictor of mortality. As the AIx is relatively cumbersome to obtain, simpler methods such as analysis of pulse waves obtained by digital photoplethysmography have been proposed to estimate arterial stiffness. The objective of this study is to compare the usefulness of the stiffness index (SI) derived from digital photoplethysmography and the AIx derived from radial tonometry for stratification of cardiovascular risk. We studied 83 subjects with a heterogeneous cardiovascular risk profile and determined the ability of the two devices to differentiate subjects with low from subjects with high cardiovascular risk estimated by the Europe (EU)-heart score. Failure rate in both devices was similar (3.6%). AIx and SI were modestly correlated (r¼0.48, Po0.001) and both indexes correlated with the EU-score (r¼0.54, Po0.001) and (r¼0.56, Po0.001), respectively. Both devices discriminated accurately between subjects with high cardiovascular risk (upper tertile of the EU-score) and low cardiovascular risk (lower tertile). However, only the SI differentiated significantly between subjects with intermediate risk (middle tertile) and high risk (upper tertile). Compared with the AIx, assessment of the SI derived by digital photoplethysmography is simple and possibly yields an advantage in risk stratification of subjects with intermediate and high cardiovascular risk. Therefore, digital pulse wave analysis may be a valuable tool to estimate arterial stiffness in large clinical studies.

Background: Obstructive sleep apnea has been associated with impaired endothelial function; however, the mechanisms underlying this association are not completely understood. Cell-derived microparticles may provide a link between obstructive sleep apnea and endothelial dysfunction. Objectives: This randomized controlled trial aimed to examine the effect of a 2-week withdrawal of continuous positive airway pressure (CPAP) therapy on levels of circulating microparticles. Methods: Forty-one obstructive sleep apnea patients established on CPAP treatment were randomized to either CPAP withdrawal (subtherapeutic CPAP) or continuing therapeutic CPAP, for 2 weeks. Polysomnography was performed and circulating levels of microparticles were analyzed by flow cytometry at baseline and 2 weeks. Results: CPAP withdrawal led to a recurrence of obstructive sleep apnea. Levels of CD62E+ endothelium-derived microparticles increased significantly in the CPAP withdrawal group compared to the continuing therapeutic CPAP group (median difference in change +32.4 per µl; 95% CI +7.3 to +64.1 per µl, p = 0.010). CPAP withdrawal was not associated with a statistically significant increase in granulocyte, leukocyte, and platelet-derived microparticles when compared with therapeutic CPAP. Conclusions: Short-term withdrawal of CPAP therapy leads to a significant increase in endothelium-derived microparticles, suggesting that microparticle formation may be causally linked to obstructive sleep apnea and may promote endothelial activation.

BackgroundPrevious 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.MethodsFourty-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.ResultsComparison 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).ConclusionsThe 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.