Prader-Willi syndrome (PWS) is a rare genetic disorder that can increase risk of pediatric obstructive sleep apnea (OSA), caused by the combination of increased viscosity of secretions, craniofacial abnormalities, hypotonia, and obesity. While first-line treatment of pediatric OSA is typically adenotonsillectomy, the complex pathophysiology of OSA in PWS patients may lead to less success with this therapy.

The TriNetX database was queried for patients 18 years old or younger based on the diagnoses of PWS and OSA and the surgical interventions of adenotonsillectomy, tonsillectomy, and adenoidectomy. The primary endpoint was the removal of the diagnosis of OSA 6 months postoperatively. Pediatric patients without PWS were used as a control. Secondary endpoints were the risk of OSA with common medical interventions for children with PWS.

A total of 2163 patients were found to have PWS, with 1035 (47 %) diagnosed with OSA. PWS patients undergoing surgery had a total success rate of 39.0 %, compared to 79.6 % in controls (p < 0.001). Total success for these surgeries was also significantly lower compared to controls matched by demographics and obesity status (36.8 % versus 82.1 %, p < 0.001). Use of growth hormone (RR 1.43, p < 0.001) and testosterone (RR 1.39, p < 0.001) were both associated with increased risk of OSA.

Adenotonsillectomy has significantly lower rates of success at treating pediatric OSA in patients with PWS. These patients would likely benefit from multidisciplinary care to treat their OSA and mitigate the effects of untreated disease, and further studies determining best practices for caring for these patients are necessary.

Sleep is a vital function, taking about one-third of a human lifetime, and is essential for achieving and maintaining brain health. From homeostatic neurophysiology to emotional and procedural memory processing to clearance of brain waste, sleep and circadian alignment remain paramount. Yet modern lifestyles and clinical practice often dismiss sleep, resulting in profound long-term repercussions. This chapter examines the roles of sleep and circadian rhythms in memory consolidation, synaptic plasticity, and clearance of metabolic waste, highlighting recent advances in neuroscience research. We explore how insufficient and disordered sleep-a public health concern-can impair cognition, escalate neurodegenerative risks, and compromise neurovascular integrity, thereby impacting brain health. These findings underscore the need for comprehensive screening for disturbed sleep and targeted interventions in clinical practice. Emerging interventions and AI-driven technologies may allow early detection and personalized and individualized treatments and improve outcomes. Overall, this chapter reaffirms that healthy sleep is indispensable at any level of neurological disease prevention-on par with the role of diet and exercise in cardiovascular health-and represents the foundation of brain health.

Study Objectives: This review aims to explore the epidemiology, pathophysiology, risk factors, and diagnostic approaches of obstructive sleep apnea syndrome and small airway disease, emphasizing their interrelationship and implications for clinical management. Methods: A comprehensive analysis of the literature was conducted to examine shared and distinct characteristics of obstructive sleep apnea syndrome and small airway disease. Risk factors, clinical presentations, diagnostic tools, and management strategies were reviewed to identify potential areas for improvement in care. Results: Obstructive sleep apnea syndrome, characterized by intermittent upper airway obstruction during sleep, contributes to fragmented sleep and systemic diseases. Small airway disease involves inflammation and obstruction of the small airways, impairing airflow and gas exchange. Shared risk factors, such as obesity, smoking, and age, were identified as contributors to the development and progression of both conditions. The co-occurrence of obstructive sleep apnea syndrome and small airway disease exacerbates respiratory symptoms and increases the risk of comorbidities, such as pulmonary hypertension, heart failure, and respiratory failure. Recognition of their interplay highlights the need for integrated diagnostic and therapeutic strategies. Conclusions: The interrelationship between obstructive sleep apnea syndrome and small airway disease underscores the importance of integrated management approaches to improve patient outcomes. Addressing shared risk factors and understanding the interplay between these conditions are crucial for optimizing care. This review identifies key knowledge gaps, including the need for precise diagnostic tools and targeted therapies, which are essential for advancing personalized treatment strategies for individuals with obstructive sleep apnea syndrome and small airway disease.

Effective management of obstructive sleep apnoea requires accurate patient selection, integrated data analysis and multidisciplinary approaches, with machine learning enhancing disease prediction and treatment outcomes https://bit.ly/4altpxr.

Unrecognised obstructive sleep apnoea (OSA) has been associated with adverse cardiorespiratory perioperative outcomes. However, with changing anaesthetic and perioperative management, there is ongoing uncertainty about the importance of OSA as a risk factor for post-operative complications.

A cohort study involving subjects undergoing elective surgery was conducted. OSA was diagnosed with a limited channel sleep monitor. In subjects undergoing routine perioperative care, complications were identified based on the assessment of the attending clinical team. The primary outcome was a composite end-point of cardiorespiratory outcomes comprising myocardial infarction, atrial fibrillation, other arrhythmias, bradycardia, need for inotropic support, unplanned intensive care unit admission, pneumonia or respiratory failure.

Four hundred seventy-two subjects were recruited, with 356 being included in the analyses; 281 (79%) had OSA and 66 (19%) had severe OSA. Subjects with OSA did not have a significantly higher incidence of complications (5.7%) compared to those without (2.7%, adjusted relative risk 1.89 (0.23-15.67)). Additionally, complications were not increased in those with severe OSA.

Unrecognised OSA was not associated with an increase in clinically evident cardiorespiratory complications in this cohort. The lower complication rates compared with earlier studies suggest that increased use of less invasive surgical techniques, improved pain management and increased awareness of OSA have had an impact in reducing postoperative complications in this group. Further research is needed to clarify the impact of severe OSA on post-operative outcomes in different surgical cohorts with varying risk profiles in order to develop optimal perioperative pathways.

Conventional metrics such as the apnea-hypopnea index (AHI) may not fully capture the diverse clinical manifestations of obstructive sleep apnea (OSA). This study aims to establish a novel OSA subtype classification based on the patterns of apneic and hypopneic hypoxic burden (HB), a potential biomarker that more accurately reflects the severity and duration of respiratory events. We further examined the associations of these HB-based subtypes with cardiometabolic risk and brain health outcomes.

We retrospectively analyzed polysomnography data from 1000 participants including normal, mild, moderate, and severe OSA patients. We performed hierarchical clustering based on apneic and hypopneic HB to identify OSA subtypes. We then compared the prevalence of cardiometabolic syndrome (CMS) and brain health outcomes using the brain age index (BAI) among these subtypes.

Five distinct subtypes were identified: 'good sleepers' (subtype 1), 'light hypopneic HB' (subtype 2), 'mild HB' (subtype 3), 'moderate HB' (subtype 4), and 'severe HB with marked apneic HB' (subtype 5). The prevalence of CMS (particularly hypertension) was significantly higher in subtypes 2-5 (p < 0.001) compared to subtype 1. BAI was higher in subtypes 4 (3.2 years, p < 0.0001) and 5 (11.1 years, p < 0001) compared to subtype 1. Greater daytime sleepiness was observed in HB-based subtypes 2 and 5 compared to subtype 1 (p < 0.001), whereas no significant differences were found among groups classified by OSA severity using AHI.

Our study demonstrates that the HB-based subtypes of OSA are significantly associated with various clinical features and outcomes. These insights could be utilized to improve risk stratification and guide the design of future OSA studies.

Respiration is governed by a central rhythm and pattern generator, which has the pre-Bötzinger complex as the inspiratory oscillator initiating the coordinated activity of several respiratory muscles, including the diaphragm, intercostals, and upper airway muscles. The diaphragm is the main inspiratory pump muscle driving inflow, whereas dilator upper airway muscles, such as tongue muscles, reduce airway resistance during inspiration. Breathing exhibits a marked state-dependent pattern attributed to changes in neuromodulatory tone in respiratory-related brain regions, including decreases in noradrenaline and serotonin and increases in acetylcholine levels during rapid eye movement (REM) sleep. Here, we discuss respiratory modulation by acetylcholine acting on its metabotropic muscarinic receptors, focusing on the regulation of upper airway muscle activity during sleep and wakefulness and its changing effects with postnatal maturation. We focus on experimental data examining muscarinic receptor distribution patterns, the ion channels they modulate, and how these distribution patterns change with postnatal maturation. We also consider experimental data highlighting cholinergic cellular and synaptic effects on hypoglossal motoneurons and pre-Bötzinger complex neurons and how they might explain changes in the effects of cholinergic modulation with development. Overall, this discussion is critical to comprehending the postnatal maturation in the cholinergic modulation of the respiratory control system leading to opposing effects of muscarinic receptors on upper airway muscle activity in neonate (excitatory) and adult (inhibitory) preparations. The changes in cholinergic pathways associated with dysfunctional upper airway patency control are also discussed in the context of pathologies such as sleep-disordered breathing.

Untreated obstructive sleep apnea (OSA) in patients with acute ischemic stroke (AIS) is associated with increased morbidity and mortality. However, diagnosing and treating OSA in AIS is challenging. We aimed to determine the feasibility of portable monitoring (PM) for diagnosis and positive airway pressure therapy for treatment of OSA in an inpatient stroke population.

We recruited inpatients with AIS from Cleveland Clinic. Those who consented underwent PM; participants with a respiratory event index (REI) ≥ 10 were offered auto-titrating positive airway pressure therapy (APAP). Ease-of-use questionnaires were completed. We summarized categorical variables using n(%) and continuous variables using mean ± SD or median [IQR].

27 participants (age 59.8 ± 11.8, 51.9% female, 51.9% Black, BMI 33.4 ± 8.5) enrolled. The study ended early due to Medicare contracting that forced most patients to complete stroke rehabilitation outside the Cleveland Clinic health system. 59.3% had large vessel occlusions and 53.8% had moderate/severe disability (Modified Rankin score ≥ 2). PM was attempted in 21 participants, successful in 18. Nurses and patients rated the PM device as highly easy to use. 13 of 18 (72%) patients who had an REI ≥ 10 consented to APAP titration, but only eight (61.5%) of those 13 used APAP for more than one night, and only five (27.8%) used APAP up to 90 days with data captured for only one participant. Five required troubleshooting at titration, and only one had adherent APAP usage by objective assessment after discharge.

This study demonstrates the real-world challenges of assessing and treating OSA in an AIS population, highlighting the necessity for further research into timely and feasible screening and treatment.

Sleep disordered breathing (SDB) is considered a risk factor for cardiovascular disease (CVD). Obstructive sleep apnoea (OSA) can be treated with continuous positive airway pressure (CPAP), and central sleep apnoea (CSA), in patients with heart failure with reduced ejection fraction (HFrEF), by peak flow-triggered adaptive servo-ventilation. Presently, there is equipoise as to whether treating SDB prevents cardiovascular events. Some propose treatment for this indication, based on observational data, while others argue against because of the lack of randomised trial evidence. This review evaluates literature concerning the cardiovascular effects of treating SDB with PAP devices in individuals with and without CVDs. Nine observational studies report significantly lower cardiovascular event rates in those treated, than in those not treated, for SDB. Conversely, 12 randomised trials in which excessive daytime sleepiness was generally an exclusion criterion showed no reduction in cardiovascular event rates. The SERVE-HF trial showed an increase in mortality with use of minute ventilation-triggered adaptive servo-ventilation for CSA in patients with HFrEF. In the ADVENT-HF trial, treating HFrEF patients with coexisting OSA or CSA using peak flow-triggered adaptive servo-ventilation was safe and improved sleep structure and heart failure-related quality of life but did not reduce all-cause mortality or cardiovascular events. More evidence is required to determine whether treating CSA in patients with HFrEF prevents cardiovascular events and improves survival. Presently, the rationale for treating SDB with PAP remains improving sleep structure and quality of life, as well as relieving excessive daytime sleepiness, but not reducing cardiovascular events.

Sleep deficiency in patients with obstructive sleep apnea (OSA) includes abnormal quality, timing and duration of sleep, and the presence of other comorbid conditions. These include insomnia, circadian misalignment disorders, and periodic limb movements of sleep, among others. The co-occurrence of these conditions with OSA likely plays a role in pathogenesis, clinical presentation, and management of OSA. Considering these conditions and their treatment in evaluating sleep deficiency in OSA may help improve patient outcomes. However, future research is needed to understand the intersection between OSA and these disorders.

We aimed to assess the extent to which people with type 2 diabetes or pre-diabetes, obesity (BMI 30-45 kg/m2) and moderate obstructive sleep apnoea (OSA) requiring continuous positive airway pressure ventilation (CPAP) were able to discontinue CPAP following EndoBarrier-related weight loss. We assessed sleep and metabolic parameters before, during and after EndoBarrier in 12 participants with moderate OSA requiring CPAP (75% female, 8/12 [66%] type 2 diabetes, 4/12 [34%] prediabetes, mean ± SD age 52.6 ± 9.7 years, BMI 37.4 ± 3.5 kg/m2, median duration of OSA while on CPAP 9.0 [7.0-15.0] months). With EndoBarrier in-situ, mean ± SD Apnoea Hypopnoea Index (AHI) fell by 9.1 ± 5.0 events/h from 18.9 ± 3.8 to 9.7 ± 3.0 events/h (p < .001) with an associated reduction in symptoms of daytime sleepiness (mean Epworth Sleepiness Score) such that all the 12 participants no longer required CPAP according to National Institute for Health and Care Excellence criteria. After EndoBarrier removal, 10/12 (83%) patients attended follow-up and at 12 months after removal, AHI remained below 15 in 5/10 (50%) patients but in other five the AHI rose above 15 such that restarting CPAP was recommended as justified by their symptoms. Rather than restart CPAP, two patients lost the regained weight and their AHI dropped below 15 again. Thus, 7/10 (70%) of patients were able to remain off CPAP 12 or more months after EndoBarrier removal. These results demonstrate major benefit of EndoBarrier in moderate OSA, allowing all patients to discontinue CPAP during treatment, and with maintenance of improvement at follow-up in 70%. They confirm previously demonstrated metabolic improvements in diabetes and obesity.

To develop and validate machine learning (ML) and deep learning (DL) models using drug-induced sleep endoscopy (DISE) images to predict the therapeutic efficacy of hypoglossal nerve stimulator (HGNS) implantation.

Patients who underwent DISE and subsequent HGNS implantation at a tertiary care referral center were included. Six DL models and five ML algorithms were trained on images from the base of tongue (BOT) and velopharynx (VP) from patients classified as responders or non-responders as defined by Sher's criteria (50% reduction in apnea-hypopnea index (AHI) and AHI < 15 events/h). Precision, recall, F1 score, and overall accuracy were evaluated as measures of performance.

In total, 25,040 images from 127 patients were included, of which 16,515 (69.3%) were from responders and 8,262 (30.7%) from non-responders. Models trained on the VP dataset had greater overall accuracy when compared to BOT alone and combined VP and BOT image sets, suggesting that VP images contain discriminative features for identifying therapeutic efficacy. The VCG-16 DL model had the best overall performance on the VP image set with high training accuracy (0.833), F1 score (0.78), and recall (0.883). Among ML models, the logistic regression model had the greatest accuracy (0.685) and F1 score (0.813).

Deep neural networks have potential to predict HGNS therapeutic efficacy using images from DISE, facilitating better patient selection for implantation. Development of multi-institutional data and image sets will allow for development of generalizable predictive models.

NA Laryngoscope, 134:5210-5216, 2024.

While your nightly symphony may be testing your loved one's patience, it could also be giving your own heart reasons to complain [...].

Obstructive sleep apnea (OSA) can have many adverse effects on people's health, including cognitive decline and high blood pressure. Typical surgical treatment methods include the commonly performed uvulopalatopharyngoplasty and the highly successful maxillomandibular advancement (MMA). These surgical methods are more effective than non-surgical methods because they widen the airway where a collapse has occurred through direct treatment. However, few studies has shown that moving the upper and lower jaws in a specific manner is the most efficient way to treat OSA during an MMA surgery. In this study, the airway of an OSA patient was reproduced digitally, and computational fluid dynamics analysis was performed on various models with changed airway shapes, including the original model based on an actual CT image and three resizing models of the retropalatal (RP) and retroglossal (RG) regions of the airway. Consequently, it was possible to provide more quantitative predicted flow data, which could be helpful in performing sophisticated OSA surgery. Among the four airway models of the OSA patient, a reduction in the epiglottis regional pressure difference of up to 40.2% was evident in the model with an expanded RG region, and a reduction in the wall shear stress of up to 25.8% was confirmed. The proposed process could be an important aid for surgeons in determining the optimal surgical method suitable for an individual patient's uniquely-shaped airway.

NO previous studies have examined the simultaneous effects of obstructive sleep apnea (OSA), hypertension, and the SNP rs68430822 on stroke. We aimed to explore whether these elements together, play a role as risk factors for stroke. Data was obtained from the Taiwan Biobank and the National Health Insurance database. We used logistic regression analysis to investigate the effect of OSA and hypertension as a risk factor for stroke in different genotypes. We found that OSA and hypertension was associated with stroke in those with the rs6843082 genotype. People with OSA and hypertension together with the rs6843082 genotype (GA + AA) showed a statistically significant difference as a risk for stroke (OR,2.57; 95% CI,1.53 to 4.33). However, there was no statistically significant difference in those people with OSA but without hypertension (OR, 0.53; 95% CI,0.13 to 2.25). After further stratification by combination of OSA and hypertension, those with genotype rs6843082 (GG) had higher risk odds than those with OSA and those with hypertension alone (OR,5.46, 95% CI,3.46 to 8.60). Individuals with genotype rs6843082(GA + AA), OSA and hypertension together had the highest risk for stroke (OR,6.25, 95% CI,3.63 to 10.76) and those with OSA and no hypertension (OR,0.57, 95% CI,0.14 to 2.36) had no significant risk. Our findings showed that people with genotype rs6843082 (GG), with or without hypertension had OSA as a risk factor for stroke. For individuals with the genotype rs6843082 (GA + AA), those with hypertension, OSA is a risk factor for stroke, and for those without hypertension, OSA is not associated with stroke.

Obstructive sleep apnea (OSA) is a prevalent clinical disorder characterized by intermittent airway obstruction during sleep, resulting in hypoxemia and hypercapnia. Although OSA is associated with increased cardiovascular disease (CVD) risk, such as hypertension, the precise nature of this relationship remains uncertain. This systematic review and meta-analysis aim to evaluate the potential links between OSA and cardiovascular outcomes by synthesizing data from recent prospective studies. A systematic literature search was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, utilizing electronic databases, including PubMed/MEDLINE, Scopus, and the Cochrane Library. The PICTS (patients, index test, comparator/reference test, target condition, study design) framework was used to structure the primary research question and define the investigation's scope. The Newcastle-Ottawa Scale (NOS) was employed for quality appraisal, and a meta-analysis was performed using Review Manager 5.4 software (Cochrane Collaboration, London, UK). The analysis included 12 studies, focusing on the association between OSA and various cardiovascular outcomes, including hypertension, coronary artery disease, congestive heart failure, cardiac arrhythmias, and cardiovascular events. The pooled relative risk (RR) from the random-effects model was 0.79 (95% CI: 0.56-1.03), indicating a non-significant reduction in cardiovascular risk associated with OSA. The results were heterogeneous, with individual studies showing both increased and decreased risk. Subgroup analyses based on study design, patient characteristics, and follow-up duration suggested that the observed associations were stable across different subsets of studies. However, the overall findings did not establish a definitive causal link between OSA and increased cardiovascular risk. This meta-analysis underscores the complex relationship between OSA and CVD, highlighting the need for further research to elucidate the underlying mechanisms and confirm the potential causal association. Despite the lack of significant findings, the high prevalence of OSA and its association with cardiovascular risk factors warrant routine screening and early intervention, particularly through continuous positive airway pressure (CPAP) therapy, which may mitigate the cardiovascular risks linked to OSA. Future studies should focus on high-quality prospective data and explore the impact of OSA management on cardiovascular outcomes.

Exercise improves chronic inflammation and is recommended as a first-line medical or behavioral treatment for OSA with obesity. We examined whether the effects of an exercise program on inflammatory blood markers differed according to severity of OSA among obese adults. Overweight (BMI > 27 kg/m2) adults were evaluated for OSA using overnight polysomnography and subsequently classified as exhibiting no-to-mild OSA (AHI < 15 events/hour) or moderate-to-severe OSA (AHI ≥ 15 events/hour). Cardiorespiratory fitness, body composition assessed by DXA, fasting metabolic parameters and adipokines (i.e., glucose, insulin, leptin and adioponectin), and multiple markers of inflammation (i.e., CRP, IL-4, IL-8 and TNF-α) were measured at baseline (Pre) and following a 6-week (3 days per week) comprehensive exercise program (Post). Ten adults (Age: 48 ± 8 years; W:6; M:4) with no/mild OSA and 12 adults (Age: 54 ± 8 years; W:5; M:7) with moderate/severe OSA completed all aspects of the trial. No significant differences in age, cardiorespiratory fitness, body composition, fasting metabolic parameters and most inflammatory markers were observed between groups at baseline. Exercise training decreased total fat mass (Pre: 41,167 ± 13,315 g; Post: 40,311 ± 12,657 g; p = 0.008), leptin (Pre: 26.7 ± 29.6 pg/ml; Post: 22.7 ± 19.4 pg/ml; p = 0.028) and adiponectin (Pre: 16.6 ± 10.9 µg/ml; Post: 11.0 ± 10.6 µg/ml; p = 0.004) in those with moderate/severe OSA. Among those with no/mild OSA, exercise training resulted in a decrease in total fat mass (Pre = 37,332 ± 20,258 g; Post: 37,068 ± 18,268 g, p = 0.037). These data suggest that while 6 weeks of exercise reduced adipokines in those with moderate-to-severe OSA, it was not sufficient to improve common markers of inflammation among overweight adults with OSA.

Obstructive sleep apnea (OSA) has been linked to various pathologies, including arrhythmias such as atrial fibrillation. Specific treatment options for OSA are mainly limited to symptomatic approaches. We previously showed that increased production of reactive oxygen species (ROS) stimulates late sodium current through the voltage-dependent Na+ channels via Ca2+/calmodulin-dependent protein kinase IIδ (CaMKIIδ), thereby increasing the propensity for arrhythmias. However, the impact on atrial intracellular Na+ homeostasis has never been demonstrated. Moreover, the patients often exhibit a broad range of comorbidities, making it difficult to ascertain the effects of OSA alone.

We analyzed the effects of OSA on ROS production, cytosolic Na+ level, and rate of spontaneous arrhythmia in atrial cardiomyocytes isolated from an OSA mouse model free from comorbidities.

OSA was induced in C57BL/6 wild-type and CaMKIIδ-knockout mice by polytetrafluorethylene (PTFE) injection into the tongue. After 8 weeks, their atrial cardiomyocytes were analyzed for cytosolic and mitochondrial ROS production via laser-scanning confocal microscopy. Quantifications of the cytosolic Na+ concentration and arrhythmia were performed by epifluorescence microscopy.

PTFE treatment resulted in increased cytosolic and mitochondrial ROS production. Importantly, the cytosolic Na+ concentration was dramatically increased at various stimulation frequencies in the PTFE-treated mice, while the CaMKIIδ-knockout mice were protected. Accordingly, the rate of spontaneous Ca2+ release events increased in the wild-type PTFE mice while being impeded in the CaMKIIδ-knockout mice.

Atrial Na+ concentration and propensity for spontaneous Ca2+ release events were higher in an OSA mouse model in a CaMKIIδ-dependent manner, which could have therapeutic implications.

Obesity is a global health concern that has been increasing over the years, and it is associated with several pathophysiological changes affecting the respiratory system, including alveolar hypoventilation. Obesity hypoventilation syndrome (OHS) is one of the six subtypes of sleep-hypoventilation disorders. It is defined as the presence of obesity, chronic alveolar hypoventilation leading to daytime hypercapnia and hypoxia, and sleep-disordered breathing. The existence of a sleep disorder is one of the characteristics that patients with OHS present. Among them, 90% of patients have obstructive sleep apnea (OSA), and the remaining 10% of patients with OHS have non-obstructive sleep hypoventilation without OSA or with mild OSA. This review aims to provide a comprehensive understanding of the epidemiological and pathophysiological impact of OHS and to highlight its clinical features, prognosis, and severity, as well as the available treatment options.

Obstructive Sleep Apnea Syndrome (OSA) is a common sleep disorder characterized by recurrent episodes of partial or complete upper airway obstruction during sleep. Floppy Eye Syndrome (FES) is a condition in which the upper eyelids easily evert with upward traction due to underlying tarsal plate laxity and is associated with chronic, reactive papillary conjunctivitis; this causes the eye to be vulnerable to discomfort and visual symptoms. A 49-year-old man with an 8-year history of snoring, sleep fragmentation, and daytime sleepiness was admitted as an outpatient in our sleep clinic. The patient had complied ocular symptoms such as burning eyes, redness, and irritative ocular symptoms in the past five years, arising upon waking up. The symptoms did not regress with the use of artificial tears and proper ointment. The patient was diagnosed with OSA and began using continuous positive airway pressure (CPAP). CPAP therapy significantly corrected the symptoms of FES associated with OSA . This would help to sensibilize ocular findings in patients with OSA and identify hidden sleeping diseases needing a more appropriate investigation and possible treatment. We must look beyond our approach to sleep clinic patients and avoid being kept to the common symptoms patients represent.

The pathophysiological interplay between sleep-disordered breathing (SDB) and pulmonary hypertension (PH) is complex and can involve a variety of mechanisms by which SDB can worsen PH. These mechanistic pathways include wide swings in intrathoracic pressure while breathing against an occluded upper airway, intermittent and/or sustained hypoxemia, acute and/or chronic hypercapnia, and obesity. In this review, we discuss how the downstream consequences of SDB can adversely impact PH, the challenges in accurately diagnosing and classifying PH in the severely obese, and review the limited literature assessing the effect of treating obesity, obstructive sleep apnea, and obesity hypoventilation syndrome on PH.

The authors sought to correlate the complex sequel of obesity with various parameters known to develop metabolic syndrome viz. insulin resistance, dyslipidemia, hypertension etc., as these anomalies are linked to vascular atherosclerosis and outbreak of cardiovascular and cerebrovascular diseases.  A comprehensive online survey using MEDLINE, Scopus, PubMed and Google Scholar was conducted for relevant journals from 1970 till present time (2023) with key search terms like: 'obesity', 'leptin', type-2 diabetes', 'atherosclerosis', 'cardiovascular and cerebrovascular diseases'. The findings of the reports were compared and correlated. The information was then collated for developing this review. Reports showed that in human obesity, hyper-leptinemia could induce hyperglycemia, which in turn templates hypercholesterolemia. Persisting hypercholesterolemia over a period of time may en-route atherosclerosis in blood vessels. Thus obesity has been considered as a template for originating hyperglycemia, hypercholesterolemia and outbreak of vascular atherogenesis or in other words, obesity in long run can trigger atherosclerosis and its related disorders e.g. heart attack and stroke. Literature survey shows that primarily, co-morbidities of human obesity start with leptin and insulin resistance and then multiplies with metabolic irregularities to an extreme that results in pathogenesis of heart attack and stroke. Atherosclerosis associated cardiovascular and cerebrovascular events are independent risks of obese subjects and particularly in the cases of persisting obesity.

Restless legs syndrome (RLS) and periodic limb movements of sleep (PLMS) have been variably implicated in risk for cardiovascular disease (CVD), but there is lack of consensus on these relationships. We sought to assess subclinical CVD measures and RLS/PLMS in a large cohort to further evaluate these associations. The Emory Center for Health Discovery and Well Being cohort is composed of employed adults, with subclinical CVD measures including endothelial function (flow-mediated vasodilation), microvascular function (reactive hyperemia index, RHI), arterial stiffness (pulse wave velocity and augmentation index), and carotid intima-media thickness (cIMT). Participants were grouped based on presence (N = 50) or absence (N = 376) of RLS and subclinical CVD measures compared between groups. A subset of participants (n = 40) underwent ambulatory monitoring for PLMS and obstructive sleep apnea. PLMS association with subclinical CVD measures was assessed. RLS status was significantly associated with flow-mediated dilation in univariate analyses but not after controlling for potential confounders; RLS was not associated with other subclinical CVD measures. PLMS were significantly correlated with the RHI, augmentation index, and cIMT in univariate analyses; only the association between PLMS and cIMT remained significant (p = 0.04) after controlling for RLS status, age, apnea-hypopnea index, hyperlipidemia, and hypertension. The observed association between higher PLMS and greater cIMT suggests that PLMS may be a marker of subclinical CVD. Further work is needed to determine the relationship between PLMS and CVD risk.

The online version contains supplementary material available at 10.1007/s41105-023-00497-7.

Sleep-disordered breathing (SDB) can be a sequela of stroke caused by vascular injury to vital respiratory centers, cerebral edema, and increased intracranial pressure of space-occupying lesions. Likewise, obstructive sleep apnea (OSA) contributes to increased stroke risk through local mechanisms such as impaired ischemic cerebrovascular response and systemic effects such as promoting atherosclerosis, hypercoagulability, cardiac arrhythmias, vascular-endothelial dysfunction, and metabolic syndrome. The impact of OSA on stroke outcomes has been established, yet it receives less attention in national guidelines on stroke management than hyperglycemia and blood pressure dysregulation. Furthermore, whether untreated OSA worsens stroke outcomes is not well-described in the literature. This scoping review provides an updated investigation of the correlation between OSA and stroke, including inter-relational pathophysiology. This review also highlights the importance of OSA treatment and its role in stroke outcomes. Knowledge of pathophysiology, the inter-relationship between these common disorders, and the impact of OSA therapy on outcomes affect the clinical management of patients with acute ischemic stroke. In addition, understanding the relationship between stroke outcomes and pre-existing OSA will allow clinicians to predict outcomes while treating acute stroke.

Sleep disorders are the most widespread mental disorders after stroke and hurt survivors' functional prognosis, response to restoration, and quality of life. This review will address an overview of the progress of research on the biological mechanisms associated with stroke-complicating sleep disorders. Extensive research has investigated the negative impact of stroke on sleep. However, a bidirectional association between sleep disorders and stroke exists; while stroke elevates the risk of sleep disorders, these disorders also independently contribute as a risk factor for stroke. This review aims to elucidate the mechanisms of stroke-induced sleep disorders. Possible influences were examined, including functional changes in brain regions, cerebrovascular hemodynamics, neurological deficits, sleep ion regulation, neurotransmitters, and inflammation. The results provide valuable insights into the mechanisms of stroke complicating sleep disorders.

This study aimed to conduct a cost-utility analysis of continuous positive airway pressure (CPAP) therapy compared with usual care as treatment of moderate to severe cases of obstructive sleep apnea (OSA) in Brazil, where decentralized policies of CPAP provision are in place.

Markov cohort model comparing CPAP therapy with usual care, that is, no specific treatment for OSA, for moderate to severe cases was used. The payer perspective from the Unified Health System, Brazil, was adopted. Effectiveness parameters and costs related to health states were informed by literature review. Resource use related to CPAP therapy was defined by specialists and costs informed by recent purchase and leasing contracts. Incremental cost-effectiveness ratios were generated for purchase and leasing contracts to reflect current practices. A conservative willingness-to-pay threshold was set at 1 gross domestic product per capita per quality-adjusted life-year (QALY) (Brazilian reais [BRL] 40 712/QALY). Uncertainties were explored in deterministic and probabilistic sensitivity analyses.

Incremental cost-effectiveness ratio for the purchase modality was 8303 BRL/QALY and for leasing 45 192 BRL/QALY. Considering the adopted willingness-to-pay threshold, provision of CPAP by the purchase modality was considered cost-effective but not the leasing modality. The parameter related to the greatest uncertainty was the reduction in the risk of having a stroke attributable to CPAP. Probabilistic analysis confirmed the robustness of results.

CPAP therapy is a cost-effective alternative compared with usual care for moderate to severe OSA for the purchase modality. These results should help underpinning the decision making related to a uniform policy of CPAP provision across the country.

Obstructive sleep apnea syndrome (OSAS) leads to many cardiovascular, neurologic, metabolic, and neurocognitive consequences. Conduction deficits, deviations in electrical axis, and changes in QRS morphology reflect the impairments in cardiac muscle activity and underlie the cardiovascular complications of OSAS. Here we aimed to determine the relationship between OSAS and changes in the cardiac conduction system in children and adolescents. During the 6-month duration of the study, all children having the diagnosis of OSAS in Sleep and Disorders Unit following a full-night polysomnography (PSG) were consecutively evaluated. ECGs were performed and analyzed in the Division of Pediatric Cardiology, Department of Pediatrics. The maximum spatial vector size (QRSmax), QRS electrical axis (EA), left and right ventricular hypertrophy, and the presence of fragmented QRS (fQRS) or prolonged R or S wave were examined in detail. A total of 17 boys with OSAS and 13 healthy boys participated in the study. The mean QRSmax and the QRSmax on V5 derivative were significantly lower in the patient group compared to those in the control group (p = 0.011 and p = 0.017, respectively). EA was similar between the two groups. While none of the patients with OSAS nor the control group had left ventricular hypertrophy, only one boy with OSAS had right ventricular hypertrophy according to ECG-derived analysis. The percentage of fQRS or notched R or S waves was significantly higher in patients with OSAS compared to healthy controls (p = 0.035), especially in children below the age of 5 years (p = 0.036).  Conclusion: This study demonstrated that male children and adolescents with OSAS have a combination of QRS complex changes characterized by low QRS voltages, and increased frequency of fragmented QRS. These findings reflect that the electrical remodeling and structural remodeling of the myocardium are considerably affected by OSAS in children and adolescents, leading to ventricular changes and intraventricular conduction problems. What is Known: • Pediatric obstructive sleep apnea syndrome (OSAS) characterized by recurrent intermittent hypoxemia, hypercapnia, and sleep fragmentation results in sympathetic nervous system activation, increased inflammation, and hypoxic endothelial dysfunction. When left untreated, OSAS leads to many cardiovascular, neurologic, metabolic and neurocognitive consequences, and also to sudden infant death syndrome in young children, probably due to the involvement of the cardiac conduction system. What is New: • This study demonstrated that mean QRSmax was significantly lower in male children and adolescents with OSAS, reflecting the structural and electrical remodeling of the myocardium, and one boy with OSAS had RVH according to ECG-derived analysis. The percentage of fQRS or notched R or S waves was much higher in boys with OSAS, especially in children below the age of five years. These finding showed that myocardium was considerably affected to impair the intraventricular conduction in younger children with OSAS.

Treatment of obstructive sleep apnea (OSA) has historically been centered on outpatients given sleep testing is performed on an outpatient basis. Much of this practice originates from insurers only covering sleep testing on an outpatient basis. Over the last decade, there have been innovations made in the portability of sleep monitors which have allowed sleep testing on inpatients to be facilitated. There is also emerging data that inpatient sleep testing may reduce readmissions and healthcare costs in certain cardiovascular conditions. Accordingly, this review aims to provide comprehensive coverage of recent advances in the practice of inpatient sleep medicine and its effect on reducing the burden of cardiovascular disease.

Chief cardiovascular diseases that intersect with OSA in inpatients are stroke, atrial fibrillation, and heart failure. There is data from the National Inpatient Sample comparing arrhythmia burdens in patients with OSA and HFpEF showing that OSA patients have higher mortality rates, hospital durations, and medical costs. Also, OSA is associated with higher burdens of arrhythmia. It is currently unknown whether treatment of inpatients with PAP therapy lowers the occurrence of arrhythmias. Recent data suggests that costs for heart failure patients with OSA that are readmitted are higher than those for heart failure patients without OSA. A recent analysis of patients with HFpEF (heart failure with preserved ejection fraction) and OSA showed that the PAP adherent patients had fewer healthcare related costs, lower readmission rates, and fewer emergency room visits than those that were nonadherent. In broader terms, rapid initiation of PAP therapy in a large administration database query of 23 million Medicare patients appears to reduce annual healthcare costs and reduce readmissions although further study is required.

OSA is globally underdiagnosed, with an estimated one billion individuals affected. OSA's pathogenesis involves a combination of risk factors, such as obesity, age, and increased neck circumference that contribute to fragmented sleep patterns and in turn, numerous cardiovascular comorbidities, such as stroke, atrial fibrillation, and coronary artery disease. Recently, inpatient sleep medicine programs have emerged as a promising avenue for improving diagnosis, patient safety, and potentially reducing readmissions. Integrating inpatient sleep medicine into healthcare systems to address the significant health and economic burden associated with undiagnosed OSA. Improved coverage of inpatient sleep testing and services will be a key driver of addressing inpatient gaps in sleep medicine care. The current research findings provide a bedrock from which further investigations may proceed in a prospective and randomized, controlled fashion to further clarify the effects of treatment of OSA on cardiovascular outcomes of inpatients.

Objectives: Obstructive sleep apnea (OSA) is a prevalent sleep disorder that can increase the risk of hypertension, diabetes, obesity, and cardiovascular diseases. Hypoglossal nerve stimulation (HGNS) is an alternative therapy for OSA in patients who cannot tolerate continuous positive airway pressure. Understanding the impact of HGNS on blood pressure, hemoglobin A1C (A1C), and body mass index (BMI) currently remains limited. Methods: A retrospective review study of HGNS outcomes at a single practice from January 2020 to November 2022 was conducted. Inclusion/exclusion criteria were based on HGNS eligibility and postoperative titration study. Statistical analysis and data management were performed using statistical software, R (v.4.2.1; R Core Team). Paired Student's T test, Fisher's exact test, and McNemar's exact test were utilized for statistical analysis. P values less than .05 were considered statistically significant. Results: Sixty-three patients were included in this study. A significant decrease in mean apnea-hypopnea index was noted following HGNS (mean change -28; P < .0001). Similar significant decreases were also seen in mean arterial pressures (mean change -8.4, P < .0001). There was a significant change in overall antihypertensive medication requirements and in requirements ≥3 medications (P < .0005, P = .03). There was a trend toward reduction in A1C; however, there was no change in BMI or number of diabetes medications taken. Conclusions: Our results reinforce previous findings that HGNS is an effective treatment option for carefully selected patients with OSA. In addition, our findings suggest that HGNS may improve patients' quality of life while minimizing OSA associated morbidity.

Obstructive sleep apnea (OSA) is common but under-recognized after stroke. The aim of this study was to determine whether post-stroke phenotypic OSA subtypes are associated with stroke outcome in a population-based observational cohort.

Ischemic stroke patients (n = 804) diagnosed with OSA (respiratory event index ≥10) soon after ischemic stroke were identified from the Brain Attack Surveillance in Corpus Christi (BASIC) project. Functional, cognitive, and quality of life outcomes were assessed at 90 days post-stroke and long-term stroke recurrence was ascertained. Latent profile analysis was performed based on demographic and clinical features, pre-stroke sleep characteristics, OSA severity, and vascular risk factors. Regression models were used to assess the association between phenotypic clusters and outcomes.

Four distinct phenotypic clusters provided the best fit. Cluster 1 was characterized by more severe stroke; cluster 2 by severe OSA and higher prevalence of medical comorbidities; cluster 3 by mild stroke and mild OSA; and cluster 4 by moderate OSA and mild stroke. Compared to cluster 3 and after adjustment for baseline stroke severity, cluster 1 and cluster 2 had worse 90-day functional outcome and cluster 1 also had worse quality of life. No difference in cognitive outcome or stroke recurrence rate was noted by cluster.

Post-stroke OSA is a heterogeneous disorder with different clinical phenotypes associated with stroke outcomes, including both daily function and quality of life. The unique presentations of OSA after stroke may have important implications for stroke prognosis and personalized treatment strategies.

Sleep-disordered breathing, ranging from habitual snoring to severe obstructive sleep apnea, is a prevalent public health issue. Despite rising interest in sleep and awareness of sleep disorders, sleep research and diagnostic practices still rely on outdated metrics and laborious methods reducing the diagnostic capacity and preventing timely diagnosis and treatment. Consequently, a significant portion of individuals affected by sleep-disordered breathing remain undiagnosed or are misdiagnosed. Taking advantage of state-of-the-art scientific, technological, and computational advances could be an effective way to optimize the diagnostic and treatment pathways. We discuss state-of-the-art multidisciplinary research, review the shortcomings in the current practices of SDB diagnosis and management in adult populations, and provide possible future directions. We critically review the opportunities for modern data analysis methods and machine learning to combine multimodal information, provide a perspective on the pitfalls of big data analysis, and discuss approaches for developing analysis strategies that overcome current limitations. We argue that large-scale and multidisciplinary collaborative efforts based on clinical, scientific, and technical knowledge and rigorous clinical validation and implementation of the outcomes in practice are needed to move the research of sleep-disordered breathing forward, thus increasing the quality of diagnostics and treatment.

Obstructive sleep apnea syndrome (OSAS) is associated with cerebrovascular disease, which can lead to life-threatening outcomes. The purpose of the study was to investigate the relationship between OSAS and comorbid intracranial aneurysms. We retrospectively reviewed 564 patients who underwent a polysomnography and brain magnetic resonance angiography as part of their health checkup. We calculated the prevalence of an intracranial aneurysm and OSAS in patients and measured the size of the intracranial aneurysm if present. The mean patient age was 55.6 ± 8.5 years, and 82.3% of them were men. The prevalence of an intracranial aneurysm in patients with OSAS was 12.1%, which is significantly higher than patients with non-OSAS (5.9%, p = 0.031). Patients with OSAS had a much higher prevalence of intracranial aneurysms, after adjusting all possible confounding factors such as age, sex, smoking status, alcohol drinking, and body mass index (odds ratio: 2.32; 95% confidence interval: 1.07-5.04). Additionally, the OSAS group had noticeably larger aneurysms compared with those of the non-OSAS group (3.2 ± 2.0 mm vs. 2.0 ± 0.4 mm, p = 0.013). We found a significant association between OSAS and intracranial aneurysms. OSAS could be another risk factor for the development of intracranial aneurysms.

To evaluate craniofacial measurements on 3D-stereophotogrammetry and see if particular measurements are more typical in obstructive sleep apnea (OSA) and have a correlation with its severity.

Subjects included were adults undergoing a diagnostic polysomnography. Age, BMI, neck, abdominal and hip circumference (cm) were recorded. 3D-stereophotogrammetry was performed and landmarks were placed on the 3D-image. Different linear, angular and volume measurements were performed to gauge facial and neck anatomy. The relationship between these measurements and the severity of OSA, based on the obstructive apnea/hypopnea index (OAHI, events/h), was assessed by multiple linear regression, and adjusted for BMI and sex.

Of 91 subjects included (61 male), mean age was 46 ± 12 years, BMI 30.1 ± 6.5 kg/m2, OAHI 19.3 ± 18.8/h. BMI was higher (p = 0.0145) in females (32.9 ± 7.7) than in males (28.6 ± 5.3). This was also true for hip circumference (118 ± 15 vs 107 ± 10, p = 0.0006), while the neck circumference was higher (p < 0.0001) in males (41 ± 4 vs 37 ± 4). The following parameters could predict the logOAHI (r2-adjusted = 0.51): sex (p < 0.0001), BMI (p = 0.0116), neck-depth/mandibular-length (p = 0.0002), mandibular-width angle (p = 0.0118), neck-depth euclidean distance/surface distance (E/S) (p = 0.0001) and the interaction terms between sex and neck-depth/mandibular-length (p = 0.0034), sex and neck-depth E/S (p = 0.0276) and BMI and neck-depth E/S (p = 0.0118). The interaction between sex and neck-depth/mandibular-length showed a steeper linear course in females. This is also true for the interaction term BMI with neck-depth E/S in patients with a higher BMI. With a same neck-depth ratio, the OAHI is larger in men.

Measurements involving the width of the face and addressing the soft tissue in the upper neck were found to have a significant relation with OSA severity. We found remarkable differences between non-obese/obese subjects and between males and females.

Whether obstructive sleep apnea (OSA) increases the risk of cognitive decline and how sex and age influence this association is not clear. Here, we characterized the sex- and age-specific associations between OSA risk and 3-year cognitive change in middle-aged and older adults.

We included 24,819 participants aged 45-85 (52% women) from the Canadian Longitudinal Study on Aging. OSA risk was measured at baseline using the STOP combined to body mass index (STOP-B). Neuropsychological tests assessed memory, executive functioning, and psychomotor speed at baseline and at 3-year follow-up. We conducted age- and sex-specific linear mixed models to estimate the predictive role of baseline STOP-B score on 3-year cognitive change.

Men at high-risk for OSA aged 45-59 years showed a steeper decline in psychomotor speed (+13.2 [95% CI: -1.6, 27.9]) compared to men at low-risk. Men at high-risk for OSA aged 60-69 showed a steeper decline in mental flexibility (-1.2 [-1.9, -0.5]) and processing speed (+0.6 [0.3, 0.9]) than those at low-risk. Women at high-risk for OSA aged 45-59 showed a steeper decline in processing speed (+0.1 [-0.2, 0.4]) than women at low-risk, while women at high-risk ≥70 years had a steeper decline in memory (-0.2 [-0.6, 0.1]) and processing speed (+1.0 [0.4, 1.5]).

Associations between OSA risk and cognitive decline over 3 years depend on age and sex. Being at high-risk for OSA is associated with a generalized cognitive decline in attention and processing speed, while a memory decline is specific to older women (≥70 years).

The effect of continuous positive airway pressure (CPAP) on secondary cardiovascular disease prevention is highly debated.

To assess the effect of CPAP treatment for obstructive sleep apnea (OSA) on the risk of adverse cardiovascular events in randomized clinical trials.

PubMed (MEDLINE), EMBASE, Current Controlled Trials: metaRegister of Controlled Trials, ISRCTN Registry, European Union clinical trials database, CENTRAL (Cochrane Central Register of Controlled Trials), and ClinicalTrials.gov databases were systematically searched through June 22, 2023.

For qualitative and individual participant data (IPD) meta-analysis, randomized clinical trials addressing the therapeutic effect of CPAP on cardiovascular outcomes and mortality in adults with cardiovascular disease and OSA were included.

Two reviewers independently screened records, evaluated potentially eligible primary studies in full text, extracted data, and cross-checked errors. IPD were requested from authors of the selected studies (SAVE [NCT00738179], ISAACC [NCT01335087], and RICCADSA [NCT00519597]).

One-stage and 2-stage IPD meta-analyses were completed to estimate the effect of CPAP treatment on risk of recurrent major adverse cardiac and cerebrovascular events (MACCEs) using mixed-effect Cox regression models. Additionally, an on-treatment analysis with marginal structural Cox models using inverse probability of treatment weighting was fitted to assess the effect of good adherence to CPAP (≥4 hours per day).

A total of 4186 individual participants were evaluated (82.1% men; mean [SD] body mass index, 28.9 [4.5]; mean [SD] age, 61.2 [8.7] years; mean [SD] apnea-hypopnea index, 31.2 [17] events per hour; 71% with hypertension; 50.1% receiving CPAP [mean {SD} adherence, 3.1 {2.4} hours per day]; 49.9% not receiving CPAP [usual care], mean [SD] follow-up, 3.25 [1.8] years). The main outcome was defined as the first MACCE, which was similar for the CPAP and no CPAP groups (hazard ratio, 1.01 [95% CI, 0.87-1.17]). However, an on-treatment analysis by marginal structural model revealed a reduced risk of MACCEs associated with good adherence to CPAP (hazard ratio, 0.69 [95% CI, 0.52-0.92]).

Adherence to CPAP was associated with a reduced MACCE recurrence risk, suggesting that treatment adherence is a key factor in secondary cardiovascular prevention in patients with OSA.

Obstructive sleep apnea (OSA) may be linked with oral health issues. This study evaluated the associations between OSA, dental pain, and chewing discomfort. Big data from a nationwide survey involving 6984 participants aged ≥ 40 years were analyzed. The STOP-Bang questionnaire was used to assess the OSA risk, categorizing the participants into low-, intermediate-, and high-risk groups. The associations of OSA risk with dental pain and chewing discomfort were evaluated using multivariate logistic regression analyses (α = 0.05). Results revealed that 50.33%, 37.50%, and 12.17% of the population belonged to the low-, intermediate-, and high-risk groups, respectively. After adjusting for covariates, a significant association emerged between OSA risk and dental pain, with adjusted odds ratios (95% confidence intervals) of 1 (reference), 1.208 (1.003-1.455), and 1.472 (1.131-1.916) for the low-, intermediate-, and high-risk groups, respectively (p = 0.0156). The adjusted odds ratio for chewing discomfort in the high-risk OSA group was 1.307 (0.977-1.748), although not significantly different from that of the low-risk group (p > 0.05). A high risk of OSA was associated with 1.472-fold increased risk of dental pain compared to those at low risk, implicating OSA as a potential risk indicator of poor oral health.

The oral microbiota is closely associated with systemic health, but few studies have investigated the oral microbiota in patients with obstructive sleep apnea (OSA). This study aimed to identify the variation of oral microbiota among patients with severe OSA, and the change of oral microbiota after treatment with continuous positive airway pressure (CPAP).

Participants were enrolled in the study from November 2020 to August 2021. Sleep parameters using full nocturnal polysomnography (PSG) were collected on healthy controls, patients with severe OSA, and patients with severe OSA after CPAP treatment for 3 months. Oral samples were also collected by rubbing disposable medical sterile swabs on the buccal mucosa. Routine blood tests and biochemical indicators were measured using the fully automated biochemical analyzer. Oral microbial composition of oral samples were determined using whole-genome metagenomic analysis in all participants. Correlations were analyzed between the oral microbiota and blood lipids.

Study enrollment included 14 participants, 7 healthy controls and 7 patients with severe OSA. At the species level, the relative abundances of Prevotella, Alloprevotella, Bacteroides, Veillonella_tobetsuensis, Candidatus saccharimonas, and Leptotrichia in the groups with severe OSA were significantly lower than those in the healthy controls (P both < 0.05). The abundances of Capnocytophaga, Veillonella, Bacillus_anthracis, Eikenella, and Kingella were significantly higher whereas the abundances of Gordonia and Streptococcus were significantly lower in the group with severe OSA compared to the severe OSA-CPAP group (P < 0.05 for both). According to the Kyoto Encyclopedia of Genes and Genomes (KEGG), 4 pathways changed in the group with severe OSA compared with healthy controls (P both < 0.05). Pathways related to Novobiocin biosynthesis, 2-Oxocarboxylic acid metabolism, and Histidine metabolism were enriched in the patients with severe OSA. Nine pathways showed significant differences with regard to the relative abundances of phenylalanine metabolism; alanine, aspartate, and glutamate metabolism; one carbon pool by folate; monobactam biosynthesis; 2-oxocarboxylic acid metabolism; arginine biosynthesis and vitamin B6 metabolism; novobiocin biosynthesis; and arginine and proline metabolism, which were significantly higher in the group with severe OSA compared to the severe OSA-CPAP group (P both < 0.05). The Spearman correlation analysis between blood lipid parameters and oral microbiota components showed that negative correlations were observed between total cholesterol and Streptomyces (r =  - 0.893, P = 0.007), and high-density lipoprotein cholesterol (HDL-C) and Gordonia (r = - 0.821, P = 0.023); positive correlations were observed between HDL-C and Candidatus saccharimonas (r = 0.929, P = 0.003), and low-density lipoprotein cholesterol (LDL-C) and Capnocytophaga (r = 0.893, P = 0.007).

There was an apparent discrepancy of the oral microbiota and metabolic pathways between the group with severe OSA and controls, and CPAP significantly changed oral microbial abundance and metabolic pathways in patients with severe OSA. Correlation analysis showed that these oral bacteria were strongly correlated with the blood lipids level.

Obstructive Sleep Apnea (OSA) is exceedingly common but often under-treated. Continuous positive airway pressure (CPAP) has long been considered the gold standard of OSA therapy. Limitations to CPAP therapy include adherence and availability. The 2021 global CPAP shortage highlighted the need to tailor patient treatments beyond CPAP alone. Common CPAP alternative approaches include positional therapy, mandibular advancement devices, and upper airway surgery. Upper airway training consists of a variety of therapies, including exercise regimens, external neuromuscular electrical stimulation, and woodwind instruments. More invasive approaches include hypoglossal nerve stimulation devices. This review will focus on the approaches for modifying upper airway muscle behavior as a therapeutic modality in OSA.

There is currently no way to estimate the period of time a person has had obstructive sleep apnoea (OSA). Such information would allow identification of people who have had an extended exposure period and are therefore at greater risk of other medical disorders; and enable consideration of disease chronicity in the study of OSA pathogenesis/treatment.

The 'age of OSA Onset' algorithm was developed in the Wisconsin Sleep Cohort (WSC), in participants who had ≥2 sleep studies and not using continuous positive airway pressure (n = 696). The algorithm was tested in a participant subset from the WSC (n = 154) and the Sleep Heart Health Study (SHHS; n = 705), those with an initial sleep study showing no significant OSA (apnea-hypopnea index (AHI) < 15 events/hr) and later sleep study showing moderate to severe OSA (AHI≥15 events/hr).

Regression analyses were performed to identify variables that predicted change in AHI over time (BMI, sex, and AHI; beta weights and intercept used in the algorithm). In the WSC and SHHS subsamples, the observed years with OSA was 3.6 ± 2.6 and 2.7 ± 0.6 years, the algorithm estimated years with OSA was 10.6 ± 8.2 and 9.0 ± 6.2 years.

The OSA-Onset algorithm estimated years of exposure to OSA with an accuracy of between 6.6 and 7.8 years (mean absolute error). Future studies are needed to determine whether the years of exposure derived from the OSA-Onset algorithm is related to worse prognosis, poorer cognitive outcomes, and/or poorer response to treatment.

Obstructive sleep apnea syndrome (OSAS) is a common breathing disorder in sleep in which the airways narrow or collapse during sleep, causing obstructive sleep apnea. The prevalence of OSAS continues to rise worldwide, particularly in middle-aged and elderly individuals. The mechanism of upper airway collapse is incompletely understood but is associated with several factors, including obesity, craniofacial changes, altered muscle function in the upper airway, pharyngeal neuropathy, and fluid shifts to the neck. The main characteristics of OSAS are recurrent pauses in respiration, which lead to intermittent hypoxia (IH) and hypercapnia, accompanied by blood oxygen desaturation and arousal during sleep, which sharply increases the risk of several diseases. This paper first briefly describes the epidemiology, incidence, and pathophysiological mechanisms of OSAS. Next, the alterations in relevant signaling pathways induced by IH are systematically reviewed and discussed. For example, IH can induce gut microbiota (GM) dysbiosis, impair the intestinal barrier, and alter intestinal metabolites. These mechanisms ultimately lead to secondary oxidative stress, systemic inflammation, and sympathetic activation. We then summarize the effects of IH on disease pathogenesis, including cardiocerebrovascular disorders, neurological disorders, metabolic diseases, cancer, reproductive disorders, and COVID-19. Finally, different therapeutic strategies for OSAS caused by different causes are proposed. Multidisciplinary approaches and shared decision-making are necessary for the successful treatment of OSAS in the future, but more randomized controlled trials are needed for further evaluation to define what treatments are best for specific OSAS patients.

Wake-up stroke (WUS) is a certain type of ischemic stroke in which a patient wakes up with a new neurological deficit due to cerebral ischemia. Sleep-disordered breathing is an independent risk factor for stroke, but the role of nocturnal oxygen desaturation in the pathophysiology of WUS is still insufficiently explored. According to several studies, patients with WUS have a significantly more severe sleep apnea syndrome and lower mean blood oxygen saturation. This study aimed to assess the severity of nocturnal desaturations in acute WUS and non-WUS patients using nocturnal pulse oximetry.

The cohort of 225 consecutive patients with neuroimaging-verified acute cerebral ischemia was prospectively enrolled. For further analyses, 213 subjects with known WUS/non-WUS status were selected (111 males and 102 females, average age 70.4 ±12.9, median baseline NIHSS = 5, median baseline mRS = 3). Patients were divided into the WUS group (n = 45) and the non-WUS group (n = 168). Overnight pulse oximetry was performed within 7 days of the stroke onset and data of both of the studied groups were compared.

We found oxygen desaturation index (ODI) in the WUS group was 14.5 vs. 16.6 (p = 0.728) in the non-WUS group, basal O2 saturation was 92.2% vs. 92.5% (p = 0.475), average low O2 saturation was 90.3% vs. 89.6% (p = 0.375), minimal O2 saturation was 79.5% vs. 80.6% (p = 0.563), and time with O2 saturation <90% (T90) was 4.4% vs. 4.7% (p = 0.729).

In the studied sample, monitored respiratory parameters including ODI, basal O2 saturation, average low O2 saturation, minimal O2 saturation, and T90 did not significantly differ between groups of WUS and non-WUS patients.