Recent studies have demonstrated that obstructive sleep apnea (OSA) is associated with the development and evolution of nonalcoholic fatty liver disease (NAFLD), independent of obesity or other shared risk factors. Like OSA, NAFLD is a prevalent disorder associated with major adverse health outcomes: Patients with NAFLD may develop cirrhosis, liver failure, and hepatocellular carcinoma. One major finding that has emerged from these studies is that the OSA/NAFLD association is related to the degree of nocturnal hypoxemia in OSA. Animal models have therefore largely focused on intermittent hypoxia, a key manifestation of OSA, in order to shed light on the mechanisms by which OSA may give rise to the complex metabolic disturbances that are seen in NAFLD. Intermittent hypoxia leads to tissue hypoxia, and can result in oxidative stress, mitochondrial dysfunction, inflammation, and over-activation of the sympathetic nervous system, among many other maladaptive effects. In such models, intermittent hypoxia has been shown to cause insulin resistance, dysfunction of key steps in hepatic lipid metabolism, atherosclerosis, and hepatic steatosis and fibrosis, each of which is pertinent to the development and/or progression of NAFLD. However, many intriguing questions remain unanswered: Principally, how aggressively should the clinician screen for NAFLD in OSA patients, and vice-versa? In this review we attempt to apply the best evidence from animal and human studies to highlight the relationship between these two disorders and to advocate for further trials aimed at defining these relationships more precisely.

Patients with both heart failure and obstructive sleep apnea often have poor, repeatedly disrupted sleep, and yet they frequently do not complain of excessive daytime sleepiness. Understanding this lack of perceived sleepiness is crucial for the case identification and treatment of obstructive sleep apnea in the heart failure population at high risk of this disease, especially given the association between untreated obstructive sleep apnea and mortality among patients with heart failure. In this review, we present epidemiologic evidence concerning the lack of sleepiness symptoms in heart failure and obstructive sleep apnea, explore possible mechanistic explanations for this relationship, assess the benefits of treatment in this population, discuss implications for clinical practice and explore directions for future research.

The primary aim of the current study was to assess the effects of oropharingeal muscle exercises in obstruction severity on stroke patients with OSAS. The secondary aims were to evaluate the effects of the exercises on rehabilitation of neurological function, sleeping, and morphology change of upper airway. An open-label, single-blind, parallel-group, randomized, controlled trial was designed. Fifty post-stroke patients with moderate OSAS were randomly assigned into 2 groups (25 in each group). For the therapy group, oropharyngeal muscle exercise was performed during the daytime for 20 min, twice a day, for 6 weeks. The control group was subjected to sham therapy of deep breathing. Primary outcomes were the obstruction severity by polysomnography. Secondary outcomes included recovery of motor and neurocognitive function, personal activities of daily living assessment (ADL), sleep quality and sleepiness scale. It also included upper airway magnetic resonance imaging (MRI) measurements. Assessments were made at baseline and after 6-week exercise. Finally, 49 patients completed the study. The apnea-hypopnea index, snore index, arousal index, and minimum oxygen saturation improved after exercise (P < 0.05). Oropharyngeal muscle exercises improved subjective measurements of sleep quality (P = 0.017), daily sleepiness (P = 0.005), and performance (both P < 0.05) except for neurocognition (P = 0.741). The changes in obstruction improvement, sleep characteristics and performance scale were also associated with training time, as detected by Pearson's correlation analysis. The anatomic structural remodeling of the pharyngeal airway was measured using MRI, including the lager retropalatal distance (P = 0.018) and shorter length of soft palate (P = 0.044) compared with the baseline. Hence, oropharyngeal muscle exercise is a promising alternative treatment strategy for stroke patients with moderate OSAS. Clinical Trial Registration: http://www.chictr.org.cn. Unique identifier: ChiCTR-IPR-16009970.

Insomnia and obstructive sleep apnea (OSA) are often both present in patients with sleep-disordered-breathing (SDB). The coexistence of the two disorders shows an increase in cumulative morbidity and an overall greater illness severity. There is still considerable controversy regarding management decisions in this group of patients. This systematic review focused on more recent evidence regarding treatment of patients presenting with both clinical entities of comorbid insomnia and OSA (COMISA) in terms of their management, especially using combinations of positive airway pressure [PAP, namely aPAP, cPAP, adaptive servo-ventilation (ASV)] and CBTi as well as each one of these two modalities alone. As a conclusion it is necessary to specifically target distinct combinations of both insomnia (initial, middle, late) and OSA (mild, moderate, severe) phenotypes. The present review gives reason to assume that both CBTi and PAP-therapy are necessary. However, it appears that distinct treatment patterns may suit different COMISA phenotypes.

The increasing prevalence of overweight or obese children and adolescents is a significant global health concern. Although the effect of obesity on cardiovascular function has been investigated, little is known on the impact of associated obstructive sleep apnea (OSA) in obese youth. The aim of the present study was to investigate the influence of OSA on cardiovascular functional parameters in obese youth. This is a prospective single-center observational cross-sectional study. Forty-four obese patients and 44 age- and gender-matched control subjects were included. All patients underwent polysomnography and cardiovascular assessment including functional echocardiography and carotid-femoral pulse wave velocity (PWV). Obese patients had higher left ventricular (LV) mass/height2.7, preserved LV systolic parameters, differences in LV diastolic parameters, and increased PWV and systolic blood pressure at rest compared with control group. In obese youth, 14 of 44 (32%) had OSA. There was no correlation between obesity and the apnea-hypopnea index (AHI). LV mass/height2.7 significantly correlated with body mass index z-score (r = 0.648, p <0.001) whereas PWV correlated with AHI (r = 0.352, p = 0.038). In obese patients, body mass index z-score was an independent predictor for LV mass/height2.7 (r = 0.61, p <0.001) and AHI was an independent predictor for higher PWV (r = 0.352, p = 0.038). In conclusion, both obesity and OSA influence cardiovascular performance in obese youth. Although obesity is associated with increased LV mass and reduced LV diastolic function, OSA is associated with changes in arterial stiffness.