Sleep
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The consequences of obstructive sleep apnea (OSA) are largely mediated by chronic intermittent hypoxia and sleep fragmentation. The primary molecular domains affected are sympathetic activity, oxidative stress and inflammation. Other affected domains include adipokines, adhesion molecules and molecules that respond to endoplasmic reticulum stress. ⋯ Thus, a challenge to establishing a molecular signature for OSA is to separate the effects of OSA from obesity. We propose that the optimal strategy is to evaluate the temporal changes in relevant molecular pathways during sleep and, in particular, the alterations from before to after sleep when assessed in blood and/or urine. Such changes will be at least partly a consequence of chronic intermittent hypoxia and sleep fragmentation that occurs during sleep.
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Many patients with obstructive sleep apnea (OSA) have spontaneous periods of stable flow limited breathing during sleep without respiratory events or arousals. In addition, OSA is often more severe during REM than NREM and more severe during stage 2 than slow wave sleep (SWS). The physiological mechanisms for these observations are unknown. Thus we aimed to determine whether the activity of two upper airway dilator muscles (genioglossus and tensor palatini) or end-expiratory lung volume (EELV) differ between (1) spontaneously occurring stable and cyclical breathing and (2) different sleep stages in OSA. ⋯ Increased genioglossus muscle tone is associated with spontaneous periods of stable flow limited breathing in the OSA subjects studied. Reductions in genioglossus activity during REM may explain the higher severity of OSA in that stage. Increased lung volume and tensor palatini activity do not appear to be major mechanisms enabling spontaneous stable flow limited breathing periods.
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Randomized Controlled Trial Multicenter Study
Effect of continuous positive airway pressure on sleep structure in heart failure patients with central sleep apnea.
At termination of obstructive apneas, arousal is a protective mechanism that facilitates restoration of upper airway patency and airflow. Treating obstructive sleep apnea (OSA) by continuous positive airway pressure (CPAP) reduces arousal frequency indicating that such arousals are caused by OSA. In heart failure (HF) patients with central sleep apnea (CSA), however, arousals frequently occur several breaths after apnea termination, and there is uncertainty as to whether arousals from sleep are a consequence of CSA. If so, they should diminish in frequency when CSA is attenuated. We therefore sought to determine whether attenuation of CSA by CPAP reduces arousal frequency. ⋯ These data suggest that attenuation of CSA by CPAP does not reduce arousal frequency in HF patients. We conclude that arousals were not mainly a consequence of CSA, and may not have been acting as a defense mechanism to terminate apneas in the same way they do in OSA.
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Comparative Study
Insomnia did not predict incident hypertension in older adults in the cardiovascular health study.
We hypothesized that the sleep complaints of insomnia predict incident hypertension, particularly in African Americans. The purpose of this study was to analyze insomnia complaints as predictors of incident hypertension in the Cardiovascular Health Study (CHS), stratifying by gender and allowing for race and sleep variable interaction. ⋯ Insomnia did not predict hypertension in this older cohort which was free of hypertension at baseline. Difficulty falling asleep was associated with reduced risk of hypertension in non-African American men.
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To develop models based on craniofacial photographic analysis for the prediction of obstructive sleep apnea (OSA). ⋯ Craniofacial photographic analysis provides detailed anatomical data useful in the prediction of OSA. This method allows OSA risk stratification by craniofacial morphological phenotypes.