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Obstructive sleep apnea (OSA) is a respiratory condition characterized by interrupted sleep due to repeated, temporary collapse of the soft tissue of the upper airway that can lead to a cascade of physiological and psychological adverse health outcomes. The most common therapeutic interventions for OSA patients include the application of continuous positive airway pressure (CPAP) which acts to keep the airway open and, as such, provides less interrupted and more restorative sleep. Improved sleep has been linked to more efficacious treatments for psychiatric conditions most notably those that include cognitive-behavioral elements, new learning, and memory consolidation. In the current study, we investigated the acquisition, inhibition, and extinction of conditioned fear in OSA patients, before and after CPAP therapy, using an established fear-potentiated startle paradigm. Patients with OSA displayed an intact ability to acquire, inhibit, and extinguish fear prior to CPAP treatment and this ability was significantly enhanced following CPAP usage. In addition, those patients with more severe OSA, as measured by apnea-hypopnea index (AHI), were more likely to show improved fear inhibition and extinction. Lastly, we observed impairments in discrimination between reinforced and nonreinforced conditioned stimuli, in the inhibition of fear, and in fear extinction in a subset of patients with OSA and co-morbid posttraumatic stress disorder (PTSD). These data suggest that evolving treatment algorithms for PTSD should address disrupted sleep problems prior to initiation of inhibition/extinction-based exposure therapies., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Obstructive sleep apnea (OSA) severity might be correlated to the flow characteristics of the upper airways. We aimed to investigate the severity of OSA based on 3D models constructed from CT scans coupled with computational fluid dynamics (CFD) simulations. The CT scans of seven adult patients diagnosed with OSA were used to reconstruct the 3D models of the upper airways and CFD modeling and analyses were performed. Results from the fluid simulations were compared with the apnea-hypopnea index. Here we show a correlation between a CFD-based parameter, the adjusted pressure coefficient (Cp*), and the respective apnea-hypopnea index (Pearson's r = 0.91, p = 0.004), which suggests that the anatomical-based model coupled with CFD could provide functional and localized information for different regions of the upper airways., Competing Interests: Competing interestsThe authors declare no competing interests, (© The Author(s) 2019.)

Study Objectives: The primary objective of this study was to determine if nonadherence to continuous positive airway pressure (CPAP) is associated with increased 30-day all-cause, cardiovascular-cause, and pulmonary-cause hospital readmissions., Methods: Retrospective cohort study at a Veterans Affairs hospital of patients with obstructive sleep apnea (OSA) who were hospitalized from January 1, 2007 to December 31, 2015. Odds ratio of 30-day readmission was calculated for all-cause, cardiovascular-cause, and pulmonary-cause readmissions. Logistic regression model was used to evaluate odds of nonadherent versus adherent group while adjusting for age, sex, body mass index, living situation, race, comorbidities, and medication adherence., Results: Out of 2,077 records reviewed, 345 patients (183 adherent and 162 nonadherent) met our inclusion criteria. The adherent group had a total of 215 initial admissions, and the nonadherent group had a total of 268 index admissions. Thirty-day all-cause readmission rate was significantly higher in the nonadherent group, with an adjusted odds ratio (OR) of 3.52 (95% confidence interval [CI], 2.04-6.08, P < .001). Thirty-day cardiovascular-cause readmission rate was significantly higher in the nonadherent group, with an adjusted OR of 2.31 (95% CI, 1.11-4.78, P = .024). Difference in 30-day pulmonary-cause readmissions was not statistically significant, with an adjusted OR of 3.66 (95% CI, 0.41-32.76, P = .25)., Conclusions: Nonadherence to CPAP is associated with increased 30-day all-cause and cardiovascular-cause readmission in patients with OSA. Ensuring CPAP adherence is crucial in addressing general and cardiovascular-related healthcare utilization and morbidity in patients with OSA., Commentary: A commentary on this article appears in this issue on page 161., (© 2018 American Academy of Sleep Medicine)

Obstructive sleep apnea (OSA) is present in more than 50% of patients referred to cardiac rehabilitation units. However, it has been under-recognized in patients after stroke and heart failure. Those with concurrent OSA have a worse clinical course. Early treatment of coexisting OSA with continuous positive airway pressure (CPAP) results in improved rehabilitation outcomes and quality of life. Possible mechanisms by which CPAP may improve recovery include decreased blood pressure fluctuations associated with apneas, and improved left ventricular function, cerebral blood flow, and oxygenation. Early screening and treatment of OSA should be integral components of patients entering cardiac rehabilitation units., (Published by Elsevier Inc.)

Background: Obstructive sleep apnea (OSA) is a highly prevalent disorder affecting 15-24% of adults and triples the risk for hypertension independent of other risk factors. The exact mechanisms of endothelial dysfunction and variable susceptibility to hypertension in OSA are not entirely clear. No biomarker to date has been found to be associated with hypertension in OSA. Chitinase-3-like protein-1(YKL-40) is a circulating moiety with roles in injury, repair and angiogenesis that is dysregulated in atherosclerosis and correlates with increased cardiovascular morbidity and mortality. We sought to determine the role of YKL-40, as a biomarker, for endothelial dysfunction and hypertension in OSA., Methods: All subjects underwent polysomnography for suspected sleep-disordered breathing. Endothelial-dependent vasodilatory capacity was assessed using flow-mediated vasodilation (FMD). YKL-40 was measured in plasma using ELISA methodology., Results: We studied 95 subjects in four groups according to OSA and hypertension status. FMD was markedly impaired in hypertensive OSA (8.0% ± 0.5 vasodilation) compared to normotensive OSA (13.5% ± 0.5, P <0.0001) and non-OSA with hypertension (10.5% ± 0.8, P <0.01) and without hypertension (16.1% ± 1.0, P <0.0001). YKL-40 was significantly elevated only in hypertensive OSA compared to other three groups and had a negative correlation with FMD (r=-0.37, P = 0.0008). Receiver operating characteristic (ROC) curve analysis for YKL-40 in predicting endothelial dysfunction had a sensitivity of 71% and a specificity of 64% with AUC = 0.68, 0.57 to 0.80, P = 0.004., Conclusions: Elevated circulating levels of YKL-40 are observed in only hypertensive OSA and have a significant negative correlation with endothelial function. This specificity suggests YKL-40 could be a potential biomarker for endothelial dysfunction in OSA., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Purpose: Obstructive sleep apnea (OSA) is a common disorder affecting 15-24% of the adults and is associated with increased risk of hypertension and atherosclerosis. The exact mechanisms underlying hypertension in OSA are not entirely clear. YKL-40/Chitinase-3-like protein-1 is a circulating moiety with roles in injury, repair and angiogenesis that is dysregulated in atherosclerosis and a number of other diseases. We sought to determine the role of YKL-40 in endothelial dysfunction and hypertension in OSA., Methods: We studies 23 normotensive OSA (N-OSA) and 14 hypertensive OSA (H-OSA) without diabetes and apparent cardiovascular disease. Endothelial-dependent nitric oxide-mediated vasodilatory capacity was assessed by flow-mediated vasodilation (FMD). YKL-40, vascular endothelial growth factor (VEGF) and the soluble form of VEGF receptor-1 or sFlt-1 were measured in plasma using ELISA methodology., Results: N-OSA subjects aged 49.1 ± 2.3 years and H-OSA aged 51.3 ± 1.9 years with BMI 36.1 ± 1.6 and 37.6 ± 1.9 kg/m(2), respectively. The apnea-hypopnea index (AHI) was 41 ± 5 events/hr in N-OSA and 46 ± 6 in H-OSA with comparable degree of oxygen desaturations during sleep. FMD was markedly impaired in H-OSA (8.3% ± 0.8) compared to N-OSA (13.2% ± 0.6, P<0.0001). Plasma YKL-40 was significantly elevated in H-OSA (55.2 ± 7.9 ng/ml vs. 35.6 ± 4.2 ng/ml in N-OSA, P = 0.02) and had an inverse relationship with FMD (r = -0.52, P = 0.013). There was a significant positive correlation between sFlt-1/VEGF, a measure of decreased VEGF availability, and YKL-40 (r = 0.42, P = 0.04)., Conclusion: The levels of plasma YKL-40 were elevated in H-OSA group and inversely correlated with the endothelial-dependent vasodilatory capacity whereas there was a positive correlation between sFlt-1/VEGF and YKL-40. These findings suggest that YKL-40 is dysregulated, in part, due to perturbation of VEGF signaling, and may contribute to endothelial dysfunction and hypertension in OSA.

Unlabelled: Obstructive sleep apnea (OSA) commonly coexists with epilepsy, and treatment of OSA may decrease seizure frequency. However, it is unclear whether patients with medically refractory epilepsy have a higher incidence of OSA compared with well-controlled epilepsy patients and whether the two groups carry different risk factors., Purpose: This study aimed to investigate the presence of OSA in patients with refractory vs. well-controlled epilepsy and their associated risk factors. We also assessed the benefits of treatment of OSA with continuous positive airway pressure (CPAP) in refractory epilepsy patients., Methods: We retrospectively reviewed data from patients who presented to the Jacobs Neurological Institute Comprehensive Epilepsy Center of University at Buffalo from 2007 to 2010., Results: There is a tendency for much higher incidence of OSA in our epilepsy population compared with the general population (15.2% vs. 4.41%). For patients with well-controlled epilepsy, older age, male gender, and higher seizure frequency were predictors of a diagnosis of OSA. However, in medically refractory epilepsy patients, diabetes and snoring predicted a diagnosis of OSA. Treatment of OSA with CPAP in refractory epilepsy patients improved their seizure control (p<0.02)., Conclusion: This study confirms that OSA is common in epilepsy patients and treatment of OSA can improve seizure control in medically refractory cases. Patients with refractory epilepsy who have diabetes are more likely to have OSA., (Copyright © 2012 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.)

Background: Obstructive sleep apnea (OSA) is a highly prevalent disorder that increases the risk of systemic hypertension and cardiovascular diseases. Heme oxygenase (HO) has been shown to be upregulated in patients with OSA and its overexpression in mice causes hypertension. End products of HO are carbon monoxide (CO) and bilirubin. CO exerts a pleiotropic action on vasoregulation. Despite high prevalence and incident of hypertension in OSA, its pathophysiology is not well-understood, particularly in regard to varying susceptibility of patients to hypertension. We investigated the role of HO in endothelial dysfunction and hypertension in OSA., Methods: We determined flow-mediated vasodilatation (FMD) as a measure of endothelial-dependent vasodilatory capacity, exhaled CO, bilirubin, and guanosine 3',5'-cyclic monophosphate (cGMP) in 63 subjects with OSA (normotensive 27, hypertensive 36) and in 32 subjects without OSA (normotensive 19, hypertensive 13)., Results: Hypertensive OSA demonstrated marked impairment in FMD (8.0 ± 0.5% vasodilatation) compared to 10.5 ± 0.8% in hypertensives non-OSA (P < 0.01) and 13.5 ± 0.5% in normotensive OSA (P < 0.001) and 16.1 ± 1.1% in normotensive non-OSA (P < 0.0001). HO was upregulated and plasma nitric oxide (NO) was significantly increased in hypertensive OSA compared to normotensive OSA and hypertensive non-OSA. Conversely, serum cGMP was markedly decreased in hypertensive OSA (12.9 ± 1.8 pmol/ml vs. 20.6 ± 3.7 in normotensive OSA, P = 0.032). There was an inverse relationship between FMD and CO and bilirubin concentrations (r = 0.43, P = 0.0001 and r = 0.28, P = 0.01, respectively)., Conclusions: These data show that increased CO in the setting of elevated NO concentrations is associated with decreased cGMP, impaired FMD, and hypertension in patient with OSA.

Background: Obstructive sleep apnea (OSA) is a common disorder with multifactorial pathogenesis. It has been proposed that rostral fluid displacement contributes to the pathogenesis of OSA. We hypothesized that if fluid shift is an important factor in OSA, then it would be more severe during the second one-half of the night when there is maximally displaced fluid rostrally., Methods: We prospectively enrolled 135 patients who underwent polysomnography. Neck and leg circumferences were measured to determine rostral fluid shift in recumbent position before and after sleep study. Breathing disturbance index (BDI) was derived for non-rapid eye movement sleep during the first and second one-half of the night in the same position., Results: Sixty-five patients with demonstrable rostral fluid shift overnight were included in the analyses. Thirty-two (age, 52.5 ± 2.2 years) had OSA with a mean BDI of 27 ± 3/h (range, 5-80/h), whereas the other 33 with mainly upper airway resistance syndrome (age, 48.7 ± 2.4 years) had a BDI of 13 ± 2/h. Patients in both groups were obese. There was a statistically significant increase in neck circumference in patients with OSA (41.5 ± 0.8 to 42.6 ± 0.7 cm, P < .0001) and without OSA (38.6 ± 0.6 to 40.2 ± 0.6 cm, P < .0001) overnight, with concomitant decreases in leg circumferences. In spite of the fluid shift, BDI did not change (18 ± 3/h and 20 ± 3/h) between the first and second one-half of the night., Conclusions: There is a significant fluid shift rostrally to the neck overnight in patients with and without OSA. However, this fluid shift is not associated with worsening of OSA, thus making it unlikely that fluid displacement is a contributing factor in the pathogenesis or severity of OSA.