Search Results (1,266)

Obstructive sleep apnea (OSA)-induced hypoxia modulates inflammatory mediators associated with atherosclerosis and cardiovascular diseases. ICAM-1, VCAM-1, TNF-α and IL-6 are involved in atherogenesis, but their expression in the aortic walls of OSA patients remains unknown. This study aimed to determine the relationship between OSA severity and inflammatory markers expression in aortic tissue from patients undergoing coronary artery bypass grafting (CABG). This study included 46 patients who underwent CABG. OSA severity was assessed using the WatchPAT™ home sleep apnea test, classifying patients into control and mild (0 < AHI < 15) and moderate-to-severe (AHI ≥ 15) OSA groups. Aortic wall samples were collected intraoperatively, and ICAM-1, VCAM-1, TNF-α and IL-6 expression was evaluated using immunohistochemistry. Statistical analysis compared protein expression across OSA severity groups. Compared with control and mild OSA, in aorta of the moderate-to-severe OSA group, significant differences for ICAM-1 (p = 0.001) and VCAM-1 (p = 0.006) expression were demonstrated. This study provides novel evidence of significantly increased ICAM-1 and VCAM-1 expression in the aortic walls of patients with moderate-to-severe OSA. No statistically significant differences were observed for TNF-α and IL-6. Our findings offer a rationale for integrating vascular inflammation markers into cardiovascular risk stratification in OSA. They also support the concept of OSA as a systemic inflammatory disorder, with tangible effects on large-vessel morphology. Full article

Background/Objectives: Mood disorders, such as major depressive disorder (MDD) and bipolar disorder (BD), along with obstructive sleep apnea (OSA), are prevalent conditions that have serious effects on affected individuals and public health. These issues have received more attention recently, as research shows there are similar risk factors and they can influence each other by worsening symptoms and treatment response. However, there is still no clear understanding of the extent of this co-occurrence and the factors that influence it. Methods: A systematic review of comorbid OSA and mood disorders was conducted from EMBASE, Ovid MEDLINE, Global Health, and APA PsycINFO (1 January 2013–25 July 2025), with meta-analyses applying random-effects models in R (metafor). Heterogeneity, publication bias, subgroup effects, and meta-regression analyses were performed by assessing demographic, clinical, and study quality variables. Results: Out of 6221 screened studies, 23 articles met eligibility criteria, yielding 2,380,986 OSA patients, with 446,495 comorbid mood disorders (MDD = 446,290; BD = 205), and 5724 mood disorder patients (MDD = 1987; BD = 3737) with 450 comorbid OSA. All meta-analyses demonstrated a significant prevalence of comorbidity, accompanied by substantial heterogeneity. Meta-regression analyses identified mean age (β = 0.18, 95% CI 0.03–0.33, p = 0.02) and mean body mass index (β = −0.18, 95% CI −0.32 to −0.04, p = 0.01) as significant moderators of OSA prevalence. Conclusions: This meta-analysis indicates a high prevalence of comorbidity between OSA and mood disorders, including MDD and BD, with significant heterogeneity. Age and body mass index emerged as significant moderators of OSA prevalence, emphasizing the need for systematic screening and tailored approaches in both clinical practice and research. Full article

Sleep-disordered breathing (SDB)—including obstructive sleep apnea (OSA) and central sleep apnea (CSA)—is highly prevalent among individuals with heart failure (HF), yet frequently underdiagnosed. Increasing evidence shows that SDB and HF interact in a vicious cycle: recurrent hypoxic episodes, fluctuations in intrathoracic pressure, and autonomic dysregulation further strain cardiac function, while HF itself predisposes to the development of apnea. This interplay worsens arrhythmia burden, symptom severity, and long-term prognosis. This review will explore how OSA and CSA influence HF progression and outcomes, elucidate the underlying mechanisms linking these conditions, and discuss diagnostic challenges—from simple screening questionnaires to advanced telemonitoring approaches. We will critically evaluate current therapeutic options, including continuous positive airway pressure (CPAP), adaptive servo-ventilation (ASV), and emerging technologies, in light of major clinical trials and guideline recommendations. Finally, we will highlight the importance of a multidisciplinary, patient-centered approach to improve outcomes in this complex patient population. Full article

Background and Objectives: Obstructive sleep apnea (OSA) is characterized by recurrent upper airway collapse, leading to intermittent hypoxia, oxidative stress, and systemic inflammation. Hypoxia-inducible factor-1α (HIF-1α) plays a central role in cellular adaptation to hypoxia, whereas Netrin family members have emerged as regulators of inflammatory and endothelial responses. However, the roles of Netrin-1 and Netrin-4 in OSA-related intermittent hypoxia remain unclear. This study aimed to investigate circulating HIF-1α, Netrin-1, and Netrin-4 levels in patients with OSA and to evaluate their associations with disease severity and hypoxic burden. Materials and Methods: This study included 52 patients with newly diagnosed OSA and 26 healthy controls. Participants were classified as severe OSA, mild-moderate OSA, or control according to apnea–hypopnea index (AHI) values. All participants underwent overnight polysomnography. Serum HIF-1α, Netrin-1, and Netrin-4 levels were measured using ELISA. ROC curve analyses were performed to assess the ability of the investigated biomarkers to distinguish patients with OSA from controls. Correlation analyses evaluated associations between biomarkers and polysomnographic parameters, while multiple linear regression analyses adjusted for BMI, age, gender, CRP, and LDL levels were used to identify independent associations. Results: Serum HIF-1α, Netrin-1, and Netrin-4 levels differed significantly among the groups (p < 0.0001) and progressively increased from controls to mild-moderate and severe OSA groups. ROC curve analyses demonstrated excellent discriminative performance for HIF-1α (AUC = 0.9072) and Netrin-1 (AUC = 0.8928), while Netrin-4 also showed good discriminative ability (AUC = 0.8284). HIF-1α levels were positively correlated with both AHI, reflecting disease severity, and T90, reflecting nocturnal hypoxic burden (p < 0.0001). Similar positive correlations were observed between Netrin-1, Netrin-4, and both AHI and T90 (p < 0.0001). In multiple linear regression analyses, AHI remained independently associated with HIF-1α, Netrin-1, and Netrin-4 after adjustment for BMI, age, gender, CRP, and LDL levels (p < 0.0001). In contrast, BMI, age, gender, CRP, and LDL were not significantly associated with any of these biomarker levels in the adjusted models. Conclusions: Circulating HIF-1α, Netrin-1, and Netrin-4 levels are significantly elevated in patients with OSA and are positively associated with disease severity and hypoxic burden. The independent relationship between AHI and these biomarkers suggests that intermittent hypoxia may contribute to activation of HIF-1α–related and Netrin-associated pathways in OSA. These findings indicate that Netrin family members may have potential relevance as biomarkers of hypoxia-associated inflammatory and endothelial alterations in OSA. Full article

Circadian rhythm disruptions are increasingly recognized in disorders such as obstructive sleep apnea (OSA), yet analysis of 24 h gene expression patterns remains challenging due to the lack of reliable reference genes for normalization. Even commonly used housekeeping genes may exhibit circadian oscillations, which can confound rhythmic gene expression analyses and hinder biomarker identification. To address this limitation, we evaluated the gene expression stability of 11 commonly used housekeeping genes in blood collected every 6 h over 24 h period from 40 adults with varying OSA severity and controls. Stability ranking by analytical tools RefFinder and EndoGeneAnalyzer identified ACTB (β-actin) and RPL13A (ribosomal protein L13a) as the most consistent reference genes, with minimal intra- and inter-individual variability across sampling times and disease groups. Their suitability was assessed by personalized cosinor analysis of core clock genes (BMAL1, PER2, CRY1), demonstrating that appropriate normalization enables detection of circadian oscillations in clinical samples. Using the optimal normalization, CosinorPy analysis of the core clock genes revealed significant circadian oscillations of at least one clock gene in the studied participants. These findings establish ACTB and RPL13A as robust reference genes for blood-based circadian studies of OSA and provide an important methodological framework for future circadian biomarker research. Full article

Goldenhar syndrome is a developmental defect of the 1st and 2nd brachial arches. Facial asymmetry and ear–eye abnormalities are observed. Frequent presence of concomitant issues, including severe OSA (obstructive sleep apnea) and sialorrhea, have also been recorded. The presentation of Goldenhar syndrome is highly variable, and treatment procedures also differ, with surgical treatment often being mandatory. Common symptoms of OSA include loud snoring, gasping, and morning headaches. If untreated, it may lead to high blood pressure, hyperinsulinemia, heart problems, stroke, and daytime sleepiness. Its etiology in Goldenhar syndrome is primarily anatomical and multifactorial. The most common treatment options are based on surgical procedures. Continuous positive airway pressure (CPAP) could be considered for use in individuals with Goldenhar syndrome. Mandibular advancement is a standard procedure for relieving the symptoms of OSA. In general, mandibular advancement would reduce apnea and hypopnea. Another method of managing OSA is hypoglossal nerve stimulation (HNS). Adenotonsillectomy is often the first-line surgical treatment for OSA but it is rarely curative in Goldenhar patients due to underlying skeletal issues. In contrast to American Academy of Sleep Science recommendations of managing OSA, in patients with congenital syndromes, surgical intervention seems to be the most optimal method of treatment. Full article

The carotid body (CB) is an interoceptive organ that transmits afferent information to the brain via the carotid sinus nerve (CSN) to maintain homeostasis, i.e., the regulation of internal equilibrium despite external changes. It functions as a complex polymodal receptor capable of sensing multiple stimuli, including blood flow, osmolarity, pO₂, pH, pCO₂, CO₂/H⁺, and temperature. In addition, the CB responds to a wide range of circulating molecules such as angiotensin II, endothelin-1, aldosterone, insulin, histamine, and leptin, and expresses receptors for interleukins (ILs) and tumor necrosis factor-α (TNF-α) (1). CB dysfunction has been associated with conditions such as obstructive sleep apnea (OSA), in which intermittent hypoxemia induces an inflammatory response mediated, among other mechanisms, by reactive oxygen species (ROS). This process contributes to alterations in respiratory drive and enhanced sympathetic nervous system activity. Following streptococcal toxic shock syndrome due to Streptococcus Pyogenes, severe abdominal septic shock, and multiple infectious complications, our patient developed an altered respiratory pattern and a hypercatabolic state that precluded weaning from mechanical ventilation (MV) despite respiratory physiotherapy. Given treatment failure, we hypothesized underlying carotid body (CB) hyperexcitability, likely pre-existing due to obstructive sleep apnea (OSA) and exacerbated by cytokine storm and severe systemic inflammation related to Strept. Pyogenes toxins and subsequent abdominal sepsis from colonic perforation. This may have contributed to sustained sympathetic overactivation and immune dysregulation. Clinically, the patient exhibited increased respiratory drive (30–35 breaths/min), excessive inspiratory effort, and marked patient–ventilator asynchrony in the absence of hypoxemia. Non-targeted physiotherapy may have acted as a second inflammatory hit, perpetuating the inflammatory cycle. Full article

Mitochondria regulate cellular energetics, redox balance, apoptosis, and inflammatory signaling in oral, airway, and systemic tissues. Hypoxia is a powerful modulator of mitochondrial function, with effects ranging from adaptive hormesis to overt injury. Cyclic altitude training, most often delivered as intermittent hypoxic exposure or intermittent hypoxia training (IHT), has been proposed as a strategy to improve mitochondrial efficiency and exercise performance. By contrast, obstructive sleep apnea (OSA) exposes patients to uncontrolled chronic intermittent hypoxia (CIH), a pattern increasingly linked to endothelial dysfunction, ceramide-mediated mitochondrial dysfunction, insulin resistance, systemic inflammation, oral dysbiosis, and periodontitis. This narrative review covers intermittent hypoxia, mitochondrial biogenesis, hypoxia-inducible factor signaling, OSA, periodontitis, oral microbiome shifts, nitric oxide biology, and smoke-related mitochondrial injury. Appropriately dosed IHT can increase mitochondrial biogenesis, improve mitochondrial morphology, and augment oxidative capacity through pathways involving PGC-1alpha, hypoxia-inducible signaling, mitochondrial dynamics, and reactive oxygen species-dependent hormesis. In contrast, CIH in OSA promotes oxidative stress, sympathetic activation, endothelial injury, and inflammatory signaling and is associated with worse periodontal status and altered salivary microbiome profiles. Controlled IHT and OSA-related CIH, therefore, represent opposite ends of a hypoxia continuum, and mitochondrial health connects sleep-disordered breathing, periodontal inflammation, environmental exposures, and systemic cardiometabolic risk within a single conceptual frame. Sphingolipid signaling—particularly hypoxia- and toxicant-driven ceramide accumulation—connects CIH, inhaled environmental exposures, mitochondrial fragmentation, and the development of insulin resistance. Full article

Background: Systematic among patients with bilateral vocal fold paralysis (BVFP), the most clinically significant symptom is dyspnea, which often requires surgical intervention. One of the most common causes of BVFP is iatrogenic injury during thyroidectomy. Some patients report not only day time breathing difficulties but also a deterioration in sleep quality since the onset of BVFP. Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder caused by recurrent upper airway obstruction during sleep. Although it is usually associated with pharyngeal collapse, fixed laryngeal obstruction has also been suggested as a potential contributor to sleep-disordered breathing. Therefore, we aimed to assess the impact of surgical treatment of OSA in patients with BVFP. Methods: Between 2022 and 2025, 18 patients with BVFP were screened. Patients who met diagnostic criteria for OSA based on preoperative polysomnography (PSG) and the Epworth Sleepiness Scale (ESS) AHI ≥ 15 events/h or AHI ≥ 5 events/h with associated symptoms were included in the study. Five female patients met the criteria and underwent arytenoidectomy combined with posterior cordectomy. A follow-up PSG and re-evaluation of ESS were performed 6–12 months after surgery, and patients were asked about their subjective perception of sleep quality improvement. Results: An improvement in sleep quality, decrease in the median ESS score and respiratory parameters showed an improvement, although this was not statistically significant due to the small sample size (n = 5). Conclusions: These results indicate a positive postoperative trend in sleep quality among patients with BVFP however, given the limited sample size, further studies are required to confirm these observations. Full article

Background/Objectives: Obstructive sleep apnea (OSA) is highly prevalent in children with unilateral cleft lip and palate (UCLP) due to maxillary retrusion and upper airway compromise. While palatal morphology may influence pediatric OSA, three-dimensional (3D) evaluations in this population remain limited. This study evaluated palatal dimensions and maxillary widths in UCLP children with and without OSA using cone-beam computed tomography (CBCT) and examined their associations with OSA severity (apnea–hypopnea index, AHI). Methods: Forty CBCT scans of Thai children with non-syndromic UCLP (mean age 8.98 ± 1.99 years) were analyzed. Participants were categorized into OSA (n = 20; AHI ≥ 1) and non-OSA (n = 20; AHI < 1) groups. Reconstructed palatal structures were measured for surface area, volume, height, and transverse maxillary widths. Group differences were assessed using independent t-tests, and associations with AHI were examined via Pearson’s correlation and linear regression (p < 0.05). Results: Children with OSA exhibited significantly reduced palatal surface area, volume, height, and buccal alveolar crest width compared with those without OSA (p < 0.05). Other transverse widths showed no significant intergroup differences. Linear regression identified palatal volume as the only variable independently associated with AHI (β = −0.631, p < 0.001). Conclusions: Children with UCLP and OSA exhibit significantly constricted palatal morphology. Among the measured parameters, reduced three-dimensional palatal volume was the only variable independently associated with increased OSA severity in this sample. Thus, CBCT-based palatal volume assessment may serve as a preliminary screening parameter to help identify OSA risk within multidisciplinary cleft care, though further validation is needed. Full article

Objective: The objective of this study is to investigate the clinical value of the triglyceride-glucose (TyG) index combined with alanine aminotransferase (ALT) in identifying prevalent metabolic-associated fatty liver disease (MAFLD) in patients with obstructive sleep apnea (OSA), and to construct and validate a diagnostic risk-stratification model. Methods: Clinical data of OSA patients were retrospectively collected from two centers: the Department of Geriatrics, Peking University People’s Hospital (August 2021 to December 2025) and the Department of Geriatrics, Shijiazhuang People’s Hospital (June 2023 to December 2025). MAFLD was diagnosed by abdominal ultrasonography performed by experienced radiologists blinded to laboratory results. Candidate predictors were selected using univariate logistic regression, LASSO regression, and bootstrap stability testing. Model performance was assessed by discrimination (area under the receiver operating characteristic curve, AUC), calibration (Hosmer–Lemeshow test, calibration curves), and clinical utility (decision curve analysis). Internal validation was performed using 10-fold cross-validation and bootstrap resampling with optimism correction. External validation was conducted in an independent cohort. Sensitivity analyses included subgroup analyses stratified by sex, age, BMI, and OSA severity. Results: A total of 962 patients were included in the development set and 116 in the external validation set. Multivariate analysis identified TyG index (OR = 1.95, 95% CI: 1.51–2.53), LDL-C (OR = 1.24, 95% CI: 1.02–1.49), BMI (OR = 1.21, 95% CI: 1.16–1.26), and ALT (OR = 1.04, 95% CI: 1.02–1.05) as variables independently associated with prevalent MAFLD, while platelet-to-lymphocyte ratio (PLR) was protective (OR = 0.996, 95% CI: 0.993–0.999). The simplified TyG-ALT model achieved an AUC of 0.714 (95% CI: 0.685–0.744) in the development set, with an optimism-corrected AUC of 0.712, and an AUC of 0.783 (95% CI: 0.701–0.866) in external validation. The model demonstrated good calibration and favorable clinical net benefit within the threshold range of 0.30–0.70. The optimal cutoff was 0.564, with sensitivity of 68.7% and specificity of 79.6%. Conclusions: The TyG-ALT model demonstrates good discriminative ability, calibration, and clinical utility for case-finding and risk stratification of prevalent MAFLD in OSA patients, particularly for identifying high-risk individuals requiring confirmatory imaging. Full article

Objective: The association of smoking with sleep apnea is often based on subjective data. This study quantified the effects of smoking on sleep architecture using exhaled carbon monoxide (eCO) and polysomnography (PSG). Methods: A total of 183 patients with suspected obstructive sleep apnea (OSA) were included in this prospective study. Following full-night PSG, eCO was measured within 10 min. Data were analyzed using the Generalized Linear Model (GLM). Results: Although initial unadjusted analyses showed an inverse correlation between eCO levels and central apnea count, GLM revealed that male gender was the only independent predictor for central apnea, negating the effect of eCO. GLM analyses, adjusted for age, gender, BMI, and alcohol and drug use, revealed that cumulative smoking load (pack-years) was independently associated after multivariable adjustment with reduced REM sleep duration (B = −0.345, 95% CI [−0.571; −0.119], p = 0.003) and REM sleep percentage (B = −0.099, 95% CI [−0.158; −0.040], p = 0.001). Similarly, smoking duration (years) significantly predicted decreased REM sleep duration (B = −0.426, 95% CI [−0.724; −0.128], p = 0.005) and REM percentage (B = −0.119, 95% CI [−0.197; −0.041], p = 0.003). Formal interaction analyses did not detect a statistically significant interaction with body mass index (BMI) (p > 0.05 for all interaction terms). Conclusions: In OSA, smoking is independently associated with alterations in REM sleep architecture rather than respiratory events. Cumulative smoking load and smoking duration are independently associated with alterations in REM sleep after adjusting for any other major clinical comorbidities. Full article

Background: The financial burden of diagnostic testing for obstructive sleep apnea (OSA) represents a substantial barrier to treatment initiation, with cost-related access disparities disproportionately affecting the low-income and underinsured population. Home sleep testing (HST) offers a cost-effective diagnostic alternative, yet economic patterns across provider types remain unclear. This study assessed whether board-certified sleep medicine provider (BCSMP) status is associated with differences in provider-billed HST charges and evaluated how organizational and payment contexts influence these charges. Methods: A retrospective cross-sectional analysis was conducted using 2019 data from Optum’s de-identified Clinformatics^® Data Mart Database (N = 61,531 adult HST claims). The main exposure was provider status (BCSMP vs. non-BCSMP). The outcome was total provider-requested charge per HST procedure. Generalized Linear Models with a gamma distribution estimated adjusted charge differences, controlling for organizational context, place of service, and payer type. Results: BCSMP encounters had significantly lower adjusted mean HST charges than non-BCSMPs (mean difference: −$78.04; 95% CI: −$89.06 to −$67.02; p < 0.001). Individual practitioners charged $168.48 less than hospital-affiliated providers, while group practices and other facilities charged more (all p < 0.001). Fee-for-service arrangements were associated with lower charges than commercial and Medicare Advantage plans (p < 0.001). Conclusions: Board-certified sleep medicine providers and individual practice settings were associated with lower billed charges for home sleep testing; however, these findings do not necessarily reflect actual cost reduction. To translate these baseline charge differences into equitable clinical protocols and healthcare policies, future research must analyze negotiated reimbursement rates, billing structures, and practice environments to determine how these cost parameters impact the overall cost of an OSA diagnosis. Full article

Glaucoma is a chronic, progressive optic neuropathy and the second leading cause of irreversible blindness worldwide. Although elevated intraocular pressure (IOP) remains the principal modifiable risk factor, it is neither necessary nor sufficient for disease development. The literature indicates that systemic conditions such as obstructive sleep apnea (OSA) may contribute to its pathogenesis. The pathophysiology of glaucoma is supported by several theories, primarily the mechanical and vascular theories. This review describes the pathophysiological links between OSA and glaucoma considering current theories. The principal connecting mechanism appears to be chronic intermittent hypoxia and reduced ocular perfusion pressure, which trigger optic nerve head hypoxia, oxidative stress, and biomechanical remodeling of the lamina cribrosa. These processes interact within a vicious cycle that progressively compromises the metabolic support of optic nerve axons. The mechanisms described are particularly relevant to normal-tension glaucoma, which may be associated with OSA. Retinal nerve fiber layer thinning appears among the earliest markers of optic nerve vulnerability, whereas IOP and visual field changes are more variable. These observations underscore the clinical relevance of the OSA–glaucoma relationship and support a multidisciplinary approach incorporating routine ophthalmic screening for subclinical optic nerve damage. Full article

Obstructive sleep apnea (OSA) is a common condition defined by recurrent upper airway collapse, intermittent hypoxia, and sleep fragmentation that leads to sympathetic activation and adverse cardiometabolic effects. OSA and type 2 diabetes mellitus (T2DM) share a complex, bidirectional relationship driven in part by obesity, but also by overlapping pathophysiologic mechanisms. Diabetes may worsen upper airway collapsibility, while untreated OSA may exacerbate hyperglycemia, contributing to a self-perpetuating cycle of metabolic abnormalities. Continuous positive airway pressure (CPAP) remains the first-line therapy for OSA, and improves symptoms and some cardiometabolic parameters, although effects on glycemic control have been mixed and may depend on patient factors. Alternative therapies play important roles in some patients. Incretin-based therapies, particularly tirzepatide, have emerged as promising treatments for obesity-related OSA following the SURMOUNT-OSA trial, demonstrating significant reductions in apnea–hypopnea index and cardiometabolic risk factors, though their effect in patients with T2DM remains unclear. Considerations such as sarcopenia with weight loss and evolving pharmacologic and procedural strategies further shape management decisions. This review synthesizes current evidence on the pathophysiologic overlap, therapeutic approaches, and future directions in optimizing care for patients with coexisting OSA and diabetes. Full article