Mandibular advancement devices (MADs) are an effective treatment for obstructive sleep apnoea (OSA), though individual responses to therapy can vary.

This study aims to: (1) examine how craniofacial characteristics are associated with MAD effectiveness to refine patient selection and improve outcomes; and (2) assess the association of skeletal facial patterns with treatment efficacy and mandibular advancement.

This retrospective study used data from a previous quasi-experimental study. Analysis was conducted with two-piece adjustable devices, following a standardised protocol. K-means clustering analysis categorised the sample into subtypes using clinical, polysomnographic, and anatomical data to evaluate MAD treatment response. Patients were also classified by growth pattern, and treatment response and mandibular advancement were compared across facial patterns.

The study included 112 patients. Of these, 41 patients (36.61%) were assigned to Cluster 1 and 71 patients (63.39%) to Cluster 2. Cluster 1 patients had more severe OSA, with higher ESS, BMI, T90%, and AHI, along with a vertical facial pattern and narrower airways. Treatment response rates were significantly lower in Cluster 1 compared to Cluster 2. Among facial pattern groups, 32 patients were hyperdivergent, 46 were neutral, and 34 were hypodivergent. The responder rate was significantly lower in the hyperdivergent group, indicating reduced treatment effectiveness.

This study suggests that the efficacy of OSA treatment with MADs may be associated with anatomical subtypes. Cluster 1 patients showed a lower response rate compared to Cluster 2. Additionally, patients with hyperdivergent patterns may have a less favourable response to MAD treatment.

Obstructive sleep apnoea hypopnea syndrome (OSAHS) is a sleep disorder associated with significant cardiovascular complications, characterized by intermittent hypoxia (IH). IH causes endothelial dysfunction, an early event in cardiovascular disease. We investigated the role of dual-specificity phosphatase 8 (DUSP8), a key negative regulator of the mitogen-activated protein kinase (MAPK) signalling pathway, in IH-induced endothelial cell damage, and the therapeutic effects of N-acetylcysteine (NAC) by establishing IH models in human umbilical vein endothelial cells and C57BL/6 mice. DUSP8 and MAPK signalling pathway-related proteins were analysed by western blotting, and DUSP8 mRNA and miR-21-5p expression was assessed by RT-qPCR. Inflammatory cytokines were detected by an enzyme-linked immunosorbent assay, apoptosis-related proteins were analysed by western blotting, and apoptosis was assessed using flow cytometry. IH stimulation induced inflammation and apoptosis in endothelial cells, downregulated DUSP8 expression, and upregulated the phosphorylation of key molecules involved in the MAPK signalling pathway. However, DUSP8 overexpression alleviated IH-induced inflammation and apoptosis in endothelial cells and reduced the phosphorylation of key molecules in the MAPK signalling pathway. Bioinformatic analysis and dual-luciferase reporter assays confirmed that DUSP8 is a direct target of miR-21-5p. DUSP8 overexpression effectively reversed the damage caused by miR-21-5p upregulation under IH conditions. Furthermore, in cell and animal models of IH, NAC demonstrated protective effects against inflammation, apoptosis, and oxidative stress through a mechanism linked to the miR-21-5p/DUSP8/MAPK signalling pathway. Overall, this study elucidated the protective role of DUSP8 against IH-induced endothelial injury and confirmed the potential of NAC as a therapeutic agent for OSAHS-related diseases.

Cardiovascular, kidney and metabolic (CKM) conditions are interrelated, significantly contributing to morbidity, mortality and healthcare burden. Despite therapeutic advances, traditional disease-specific approaches often fail to address their complex interplay. Key therapeutic agents-including glucagon-like peptide-1 receptor agonists (GLP-1 RAs), dual GLP-1/glucose-dependent insulinotropic polypeptide RAs, sodium glucose co-transporter inhibitors and the nonsteroidal mineralocorticoid receptor antagonist (MRA) finerenone-offer multi-organ benefits. Emerging therapies, such as triple receptor agonists and second-generation MRAs, target new pathways further expanding treatment options for CKM conditions. A holistic CKM management approach must address and recognise that conditions such as metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction-associated steatohepatitis, obstructive sleep apnoea and obesity are part of the CKM spectrum. Frailty assessment is also important alongside CKM conditions, warranting comprehensive geriatric assessment and deprescribing when appropriate. Multidisciplinary care-including lifestyle interventions, pathway redesign, pharmacological advances and novel technologies-is essential for improving outcomes. As the CKM landscape evolves, future strategies should prioritise early intervention, personalised treatment and addressing unmet needs in high-risk populations. This review advocates for an integrated CKM framework, exploring treatment strategies, emerging therapies and technological innovations. It also examines the role of artificial intelligence and digital health tools in risk stratification, early diagnosis and long-term condition management, alongside ethical and regulatory considerations.

This systematic review and meta-analysis aimed to evaluate the efficacy and adherence of different mandibular advancement devices (MADs) designed to treat obstructive sleep apnea, focusing on titratable vs nontitratable and custom-made vs ready-made devices.

Registered with the International Register of Systematic Review (PROSPERO CRD42024557402), a comprehensive literature search was conducted across Ovid MEDLINE, Ovid Embase, and Web of Science up to June 2024. Randomized controlled trials and nonrandomized studies comparing MAD designs were included. The primary outcome was apnea-hypopnea index (AHI) reduction. Secondary outcomes included improvements in Epworth Sleepiness Scale scores, adherence rates, and patient preference. The risk of bias was assessed using the risk-of-bias tool for randomized trials, and the Risk-Of-Bias In Nonrandomized Studies of Intervention tools. Meta-analyses were performed with weighted mean differences (WMD) and 95% confidence intervals (CI).

A total of 22 studies were included, comprising 15 randomized controlled trials and 7 nonrandomized studies. Meta-analysis showed significant AHI reduction with both titratable and nontitratable MADs, with no significant difference between groups (WMD: 1.16; 95% CI, -1.29 to 3.61; P = 0.35). Custom-made MADs demonstrated a marginally significantly greater reduction in AHI compared with ready-made MADs (WMD: 1.51; 95% CI, -0.08 to 3.11; P = 0.06). Custom-made MADs also showed higher adherence rates and longer wearing times (WMD: 1.19; 95% CI, 0.65-1.73; P <0.0001) and higher adherence rates.

Both titratable and nontitratable MADs, as well as custom-made and ready-made MADs, effectively treated obstructive sleep apnea, with no clear preference for one design over another. Custom-made MADs, however, generally had fewer side effects and offered potential adherence advantages. Further high-quality studies with longer follow-ups are recommended.

To quantify the contribution of sleep onset latency (SOL), wake after sleep onset (WASO), and wake after sleep offset (WASF) to the discrepancy between total recording time (TRT) and total sleep time (TST) in home-based polysomnography (PSG) using patient-activated and deactivated monitoring devices.

This observational study enrolled patients with a high pretest probability of obstructive sleep apnea who underwent unattended home-based PSG. We measured the duration of SOL, WASO, and WASF to quantify the discrepancy between TRT and TST. TRT was defined as the interval from device activation to deactivation by the patients. SOL represented the time from device activation to the first epoch of any sleep, WASO was the total amount of time spent awake after the sleep onset epoch until the last epoch of any sleep, and WASF was defined as the time from the last epoch of any sleep until the patient-initiated device deactivation. We also assessed differences in the apnea-hypopnea index between home-based PSG and type 3 sleep studies by reanalyzing home-based PSG recordings as simulated type 3 studies after omitting type 2 signals.

A total of 78 patients were included in the study. The mean TRT exceeded the mean TST by 19%, with TRT at 457 ± 78 minutes and TST at 383 ± 68 minutes. The mean difference between TRT and TST was 74 ± 53 minutes, attributed to SOL (30%), WASO (45%), and WASF (25%). There was considerable variability in the difference between TRT and TST among study participants, ranging from as little as 14 minutes to as much as 233 minutes. The mean apnea-hypopnea index in simulated type 3 studies (41 ± 29 events/h) was, on average, 23% lower than the mean apnea-hypopnea index recorded in home-based PSG (53 ± 30 events/h) (P < .001).

There was significant variability in the gap between TRT and TST among patients at increased risk of obstructive sleep apnea undergoing unattended home-based PSG. WASO was identified as the largest contributor to this discrepancy, with notable contributions from SOL and WASF. Additionally, simulated type 3 studies underestimated the true apnea-hypopnea index compared to type 2 studies.

Nikolopoulos A, Tatsis K, Tselepi C, et al. Quantifying the sources of discrepancy between total recording time and total sleep time in home sleep apnea testing: insights from home-based polysomnography. J Clin Sleep Med. 2025;21(6):1065-1072.

Obstructive sleep apnea (OSA) is prevalent among critically ill patients and associated with increased mortality. This study investigates the red blood cell distribution width (RDW)-to-peripheral oxygen saturation ratio (RSR) as a predictor of all-cause mortality in critically ill OSA patients using the MIMIC-IV database.

We extracted clinical data from 3237 critically ill OSA patients in MIMIC-IV (version 3.1). The Boruta algorithm was employed for feature selection, and patients were stratified into quartiles based on RSR values. Primary and secondary outcomes were all-cause mortality at 365-day and 30-day, respectively. Kaplan-Meier survival analysis, restricted cubic splines (RCS), and Cox regression were applied to analyze RSR's relationship with outcomes. ROC curves compared RSR with classical prognostic scores, and Delong test assessed AUC differences.

Higher RSR levels were associated with increased 365-day and 30-day mortality (Kaplan-Meier, log-rank P < 0.01). Cox regression confirmed higher mortality risk in the highest RSR quartile. RCS analysis revealed an S-shaped relationship, with inflection points at 19.89 for both outcomes. Below the inflection point, higher RSR levels increased 30-day mortality risk by 30.68 % (HR 1.31, 95 %CI: 1.23-1.38) and 365-day mortality by 35.30 % (HR 1.35, 95 %CI: 1.30-1.41). For 365-day mortality, RSR outperformed SOFA and OASIS (Delong test P < 0.01), and was comparable to SAPS II, APS III, and Charlson scores (Delong test P > 0.05).

RSR significantly associates with all-cause mortality in critically ill OSA patients, particularly those with elevated RSR, serving as a promising prognostic indicator for short- and long-term mortality risk assessment.

Residual sleepiness can occur in adult patients with obstructive sleep apnea (OSA) despite adequate treatment with continuous positive airway pressure (CPAP). Various wake-promoting agents (WPAs) have been shown to reduce residual sleepiness in CPAP-treated patients with OSA. This systematic review and network meta-analysis aimed to compare the efficacy and safety of WPAs in this setting.

We searched MEDLINE, Scopus, and ClinicalTrials.gov up to 9 January 2025 for randomized controlled trials (RCTs) examining WPAs for treating sleepiness in patients with OSA. Included were all RCTs that explored the efficacy and/or safety of any approved WPAs (i.e., modafinil, armodafinil, solriamfetol, or pitolisant) in patients with OSA (aged ≥ 18 years) treated with CPAP but who are still sleepy [Epworth sleepiness scale (ESS) score ≥10]. Studies that were conducted in patients whose comorbidities cause daytime somnolence [i.e., psychiatric conditions (other than depression), other sleep disorders, medical or surgical conditions], open label extension studies, and studies published in a language other than English were excluded. The primary outcomes included ESS, maintenance of wakefulness test (MWT), and adverse events. Two authors independently assessed the risk of bias using the revised Cochrane risk-of-bias tool for randomized trials 2.0.

In total, 14 RCTs studying four WPAs (total N = 2969) including modafinil (six RCTs; 200-400 mg/day), armodafinil (four RCTs; 150-250mg/day), solriamfetol (two RCTs; 37.5-300 mg/day), and pitolisant (two RCTs; 5-40 mg/day) were included. Solriamfetol, modafinil, and armodafinil were efficacious in reducing subjective sleepiness as measured by ESS [mean difference (95% confidence interval) at ≤ 4 weeks: -3.84 (-5.60, -2.07), -2.44 (-3.38, -1.49), and -2.41 (-3.60, -1.21) for solriamfetol, modafinil, and armodafinil, respectively; at > 4 weeks: -4.11 (-6.14, -2.08), -2.88 (-3.85, -1.91), -2.46 (-3.68, -1.24) for solriamfetol, armodafinil, and modafinil, respectively] and clinical global impression of change, as well as the objective MWT [at ≤ 4 weeks: 11.66 min (9.70, 13.61), 3.61 min (2.48, 4.73), and 2.52 min (1.27, 3.76) for solriamfetol, modafinil, and armodafinil, respectively; at > 4 weeks: 10.34 min (4.16, 16.52) for solriamfetol]. Pitolisant showed later improvements in ESS [at > 4 weeks: -2.70 (-3.66, -1.73)], with limited data on MWT. Sensitivity analyses restricted to U.S. Food and Drug Administration-approved solriamfetol dosages (37.5-150 mg/day) still showed higher efficacy, but lower anxiety risk.

Among all WPAs, solriamfetol demonstrated the highest efficacy on ESS and MWT, with the latter being significant. Modafinil demonstrated the best clinician impression, albeit not statistically significant. All four WPAs were associated with a low risk of serious or adverse events.

PROSPERO registration number, CRD42022359237.

We sought to identify preoperative cardiac abnormalities with routine preoperative transthoracic echocardiography (TTE) associated with postoperative mortality in elderly patients undergoing hip fractures surgery, in order to provide reference for focused TTE.

In this retrospective study, a total of 669 elderly patients (age over 65 years) undergoing hip fractures surgery were included, of which 58 (8.7%) died within one-year after discharge. Cox regression analysis models were used to identify the prognostic cardiac abnormalities of postoperative mortality.

Univariate analysis showed that age (HR 1.065, 95%CI 1.030-1.101; P<0.001), ASA score (III, IV vs. I, II) (HR 1.855, 95%CI 1.098-3.067; P=0.022), history of chronic obstructive pulmonary disease (COPD) (HR 4.446, 95%CI 1.909-10.355; P=0.001) and atrial fibrillation (AF) (HR 3.803, 95%CI 1.803-8.024; P<0.001), presence of left ventricular ejection fraction (LVEF)<50% (HR 5.009, 95%CI 2.151-11.665; P<0.001), left ventricular dilatation (HR 3.813, 95%CI 1.730-8.403; P=0.001), pulmonary arterial systolic pressure (PASP)>25mmHg (HR 4.388, 95%CI 2.492-7.725; P<0.001), moderate-severe aortic valve stenosis (AS) (HR 4.702, 95%CI 1.471-15.035; P=0.009) were the dominant predictors of mortality within one-year. The presence of LVEF<50%, left ventricular dilatation and elevated PASP were proved to be the independent predictors of one-year mortality in elderly patients in multivariate analysis.

Cardiac abnormalities derived from preoperative TTE, namely LVEF<50%, AS, left ventricular dilatation and elevated PASP had prognostic value for elderly patients undergoing hip fracture surgery. We consider that these indices would be clinically important regarding the preoperative cardiac risk assessment of elderly hip fracture, which may be assessed in the focused TTE.

A high prevalence of non-dipping diastolic blood pressure (DBP) patterns has been observed in Obstructive Sleep Apnea (OSA), suggesting that diminished circadian blood pressure variability may significantly contribute to hypertensive end-organ damage.

This study aimed to evaluate cardiovascular complications in non-dipper OSA patients using a combination of 24-hour Ambulatory Blood Pressure Monitoring (ABPM), Holter electrocardiography, and transthoracic echocardiography (TTE).

This cross-sectional study assessed 64 adult non-dipper OSA patients. The patients, with an average age of 46.5 years, underwent clinical assessments via sphygmomanometer, resting electrocardiogram (ECG), TTE, 24-hour ABPM, and 24-hour Holter ECG. The average age of the patients was 46.5 years, with 50% exhibiting grade 2 obesity. OSA severity was classified as follows: 42.2% moderate; 32.8% severe; and 25% mild. A positive correlation was identified between OSA severity and body mass index (BMI), diabetes, and hypertension. ABPM revealed masked hypertension in 45% of participants. TTE showed that severe OSA was linked to regional wall motion abnormalities, ischemic changes, and increased interventricular septal thickness. Elevated pulmonary artery systolic pressure is predominantly observed in patients with severe OSA. Holter monitoring detected intermittent atrial fibrillation in 15.6% and infrequent extrasystoles in 31.2%. The multivariate logistic regression analysis identified BMI, age, male gender, and the presence of hypertension and diabetes mellitus as significant risk factors for severe OSA. Higher BMI, age, male gender, and these comorbidities increased the likelihood of severe OSA, with odds ratios of 1.22, 1.03, 2.80, and 1.85, respectively.

The 24-hour ABPM is an effective tool for detecting masked hypertension in non-dipper OSA patients. Additionally, the severity is directly associated with an increased risk of cardiovascular disease (CVD). Regular cardiovascular assessments are recommended for patients with OSA to mitigate potential complications.

ZUIRB#9417/2042022 Registered 20 April 2022, email IRB_123@medicine.zu.edu.eg.

Previous observational studies have suggested a potential link between obstructive sleep apnea (OSA) and interstitial lung disease (ILD), however, the casual relationship between OSA and ILD remains uncertain.

This study aims to rigorously assess the potential causal relationship between OSA and ILD.

The study utilized genome-wide association studies (GWAS) data on OSA and ILD. Univariable and multivariable Mendelian randomization (MR) were employed to explore the causal relationship. Multiple MR methods such as MR Egger, weighted median, inverse variance weighting (IVW), and weighted mode were used.

Univariate MR analyses using IVW analysis indicates a potential association between ILD and an increased risk of OSA (Odds ratio (OR) = 1.071, 95 % CI: 1.018 to 1.126, P = 0.007). However, no compelling evidence supports a reverse causal relationship in the findings above. A thorough analysis further validates the reliability of the present study. Following adjustment for the effects of smoking and BMI in multivariate MR analyses, ILD still has a positive independently association with OSA risk (OR = 1.117, 95 % CI: 1.018 to 1.225, P = 0.020).

Our study identifies ILD as a causal risk factor for OSA, providing the evidence for the prevention and treatment of the disease.

The association between the microbiota and obstructive sleep apnea (OSA) remains understudied. In this study, we conducted a comprehensive systematic review and meta-analysis of studies investigating the diversity and relative abundance of microbiota in the gut, respiratory tracts and oral cavity of patients with OSA, aiming to provide an in-depth characterization of the microbial communities associated with OSA.

A comprehensive literature search across PubMed, the Cochrane Library, Web of Science, and Embase databases were conducted to include studies published prior to Dec 2024 that compared the gut, respiratory and oral microbiota between individuals with and without OSA. The findings regarding alpha-diversity, beta-diversity, and relative abundance of microbiota extracted from the included studies were summarized. This meta-analysis was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and the study protocol was registered with PROSPERO (CRD42024525114).

We identified a total of 753 articles, out of which 27 studies were ultimately included in the systematic review, involving 1,381 patients with OSA and 692 non-OSA populations, including 1,215 OSA patients and 537 non-OSA populations in adults and 166 OSA patients and 155 non-OSA populations in children. The results of alpha diversity revealed a reduction in the Chao1 index (SMD = -0.40, 95% CI = -0.76 to -0.05), Observed species (SMD = -0.50, 95% CI = -0.89 to -0.12) and Shannon index (SMD = -0.27, 95% CI = -0.47 to -0.08) of the gut microbiota in patients with OSA. Beta diversity analysis indicated significant differences in the gut, respiratory and oral microbial community structure between individuals with OSA and those without in more than half of the included studies. Furthermore, in comparison to the non-OSA individuals, the gut environment of patients with OSA exhibited an increased relative abundance of phylum Firmicutes, along with elevated levels of genera Lachnospira; conversely, there was a decreased relative abundance of phylum Bacteroidetes and genus Ruminococcus and Faecalibacterium. Similarly, within the oral environment of OSA patients, there was an elevated relative abundance of phylum Actinobacteria and genera Neisseria, Rothia, and Actinomyces.

Patients with OSA exhibit reduced diversity, changes in bacterial abundance, and altered structure in the microbiota, especially in the gut microbiota. The results of this study provide basic evidence for further exploration of microbiome diagnostic markers and potential intervention strategies for OSA.

Chronic intermittent hypoxia (IH), a major feature of obstructive sleep apnea syndrome (OSA), is associated with greater severity of myocardial infarction. In this study, we performed RNA sequencing of cardiac samples from mice exposed to IH, which reveals a specific transcriptomic signature of the disease, relative to mitochondrial remodeling and cell death. Corresponding to its activation under chronic IH, we stabilized the Hypoxia Inducible Factor-1α (HIF-1α) in cardiac cells in vitro and observed its association with an increased autophagic flux. In accordance, IH induced autophagy and mitophagy, which are decreased in HIF-1α+/- mice compared to wild-type animals, suggesting that HIF-1 plays a significant role in IH-induced mitochondrial remodeling. Next, we showed that the AMPK metabolic sensor, typically activated by mitochondrial stress, is inhibited after 3 weeks of IH in hearts. Therefore, we assessed the effect of metformin, an anti-diabetic drug and potent activator of AMPK, on myocardial response to ischemia-reperfusion (I/R) injury. Daily administration of metformin significantly decreases infarct size without any systemic beneficial effect on insulin resistance under IH conditions. The cardioprotective effect of metformin was lost in AMPKα2 knock-out mice, demonstrating that AMPKα2 isoform promotes metformin-induced cardioprotection in mice exposed to IH. Mechanistically, we found that metformin inhibits IH-induced mitophagy in myocardium and decreases HIF-1α nuclear expression in mice subjected to IH. In vitro experiments demonstrated that metformin induced HIF-1α phosphorylation, decreased its nuclear localization, and HIF-1 transcriptional activity. Collectively, these results identify the AMPKα2 metabolic sensor as a novel modulator of HIF-1 activity. Our data suggest that metformin could be considered as a cardioprotective drug in OSA patients independently of their metabolic status.

Sleep-disordered breathing (SDB) links to various cardiovascular diseases (CVDs), but comprehensive insights and detailed profiles remain scarce. This study examined the clinical characteristics of CVD patients complicated by SDB in the enrolled all consecutive 5765 patients who underwent screening tests for SDB during hospitalization from January 2014 to December 2019, using the database of Cardiovascular Medicine, Kurume University Hospital. Desaturation during sleep in SDB was significantly worse in terms of age, sex, daytime resting oxygen saturation (SpO2), systolic blood pressure (SBP), pulse pressure, body mass index (BMI), white blood cell count, hemoglobin A1c, serum creatinine, N-terminal pro-B-type natriuretic peptide (NT-proBNP), cardiothoracic ratio on chest X-ray, and left ventricular ejection fraction on echocardiography (all p-values < 0.001, except for SBP p = 0.002, and NT-proBNP p = 0.004). Coronary artery disease and heart failure, but not pulmonary hypertension, were associated with a higher prevalence and a greater risk of moderate to severe SDB, typically in older patients. Notably, low SpO2 during daytime and elevated BMI were indicative of SDB across all age categories for both sexes. Heatmaps of daytime SpO2 and BMI can effectively predict the severe SDB in patients with CVDs, suggesting the potential for efficient therapeutic interventions for SDB.

The relationship between the Triglyceride-Glucose (TyG) index and Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) remains unclear. This study aimed to investigate the association between TyG index-related parameters (TyG, TyG-Body Mass Index (BMI), TyG-Waist Circumference (WC)) and OSAHS. Consecutive subjects referred to our sleep center were enrolled in this study and categorized into four groups based on the severity of OSAHS, as determined by the apnea-hypopnea index (AHI). Multivariate regression analysis was performed to identify independent risk factors associated with TyG index-related parameters in OSAHS. The study included 1250 participants, categorized into 114 without OSAHS, 212 with mild OSAHS, 257 with moderate OSAHS, and 667 with severe OSAHS. Significant differences were observed in fasting glucose levels, TyG, TyG-BMI, and TyG-WC across increasing severity of OSAHS. Multivariate regression showed that TyG-BMI and TyG-WC were independently associated with oxygen desaturation index (ODI), mean oxygen saturation (MSO2), and age (all p < 0.05). TyG was significantly associated with BMI, ODI, and sex (all p < 0.05). FPG was linked to BMI, age and MSO2, while insulin was associated with lowest oxygen saturation (LaSO2) and AHI (all p < 0.05). OSAHS-induced intermittent hypoxia is independently associated with increased TyG index-related parameters. These findings suggest that intermittent hypoxia may contribute to metabolic disturbances and insulin resistance, highlighting the need for further investigation into its clinical implications.

Sleep is regarded as one of the most crucial factors in keeping a healthy lifestyle. To function normally, a person needs at least 6-8 h of sleep per day. Sleep influences not only our mood but also the efficiency with which we complete tasks. Sleep disorders exhibit diverse etiologies across different conditions and populations, with genetic and environmental factors playing a significant role in their development. Many issues emerge as a result of inadequate sleep. Unhealthy food and lifestyle choices have increased our susceptibility to sleep disorders. A well-balanced diet rich in essential vitamins and minerals can have a profound impact on sleep patterns, enhancing both the duration and quality of rest. The primary categories of sleep disorders include insomnia, sleep apnea (SA), narcolepsy, parasomnias, circadian rhythm disorders, and restless legs syndrome (RLS). The drugs used to treat sleep disorders are primarily habit-forming and have a history of withdrawal effects. This insufficiency in medication has prompted the hunt for newer, better options. Nutraceuticals are well-suited to the treatment of such illnesses. Its non-toxic, non-habit-forming properties, and practical efficiency have made it an outstanding choice. This review provides nutraceuticals used in sleep disorders. A comprehensive literature search was conducted utilizing several databases, including Google Scholar, Elsevier, Springer Nature, Wiley, PubMed, and EKB. Nutraceuticals are products that employ food or dietary components to treat or prevent disease. In the therapy of sleep disorders, nutraceuticals such as Artemisia annua, valerian, rosemary, jujube, Passionflower, lemon balm, ashwagandha, kava-kava, lavender, and chamomile have been shown to have remarkable benefits. These remedies exert their effects through multiple mechanisms, both directly by modulating neurotransmitter and hormonal pathways within sleep circuits, and indirectly by enhancing sleep quality through the alleviation of stress, inflammation, and oxidative stress. Clinical studies were piloted to validate the efficacy of natural sleep aids. Future research should focus on elucidating the precise mechanisms through which natural products influence sleep.

The 10th Cardiovascular Outcome Trial (CVOT) Summit: Congress on Cardiovascular, Kidney, and Metabolic Outcomes was held virtually on December 5-6, 2024. This year, discussions about cardiovascular (CV) and kidney outcome trials centered on the recent findings from studies involving empagliflozin (EMPACT-MI), semaglutide (STEP-HFpEF-DM and FLOW), tirzepatide (SURMOUNT-OSA and SUMMIT), and finerenone (FINEARTS-HF). These studies represent significant advances in reducing the risk of major adverse cardiovascular events (MACE) and improving metabolic outcomes in heart failure with preserved ejection fraction (HFpEF), chronic kidney disease (CKD), and obstructive sleep apnea (OSA). The congress also comprised sessions on novel and established therapies for managing HFpEF, CKD, and obesity; guidelines for managing CKD and metabolic dysfunction-associated steatotic liver disease (MASLD); organ crosstalk and the development of cardio-kidney-metabolic (CKM) syndrome; precision medicine and person-centered management of diabetes, obesity, cardiovascular disease (CVD) and CKD; early detection of type 1 diabetes (T1D) and strategies to delay its onset; continuous glucose monitoring (CGM) and automated insulin delivery (AID); cardiovascular autonomic neuropathy (CAN) and the diabetic heart; and the role of primary care in the early detection, prevention and management of CKM diseases. The contribution of environmental plastic pollution to CVD risk, the increasing understanding of the efficacy and safety of incretin therapies in the treatment of CKM diseases, and the latest updates on nutrition strategies for CKM management under incretin-based therapies were also topics of interest for a vast audience of endocrinologists, diabetologists, cardiologists, nephrologists and primary care physicians, who actively engaged in online discussions. The 11th CVOT Summit will be held virtually on November 20-21, 2025 ( http://www.cvot.org ).

COPD is an established risk factor for lung cancer. Sleep apnoea is prevalent in COPD and the inflammation caused by intermittent hypoxaemia may increase this lung cancer risk. Females have more systemic inflammation for a similar apnoea-hypopnoea index than males. Therefore, this study aims to investigate sex-specific associations between sleep apnoea and lung cancer in COPD.

The sex-specific absolute and relative risk of sleep apnoea on newly diagnosed lung cancer was estimated in a nationwide observational study of Belgian patients with COPD (≥55 years), between 2017 and 2022, using an Aalan-Johanson estimator and a cause-specific Cox regression model adjusted for age, socioeconomic status, smoking status, alcoholism, frailty, comorbidities, and comedication.

The study consisted of 62,903 COPD patients (42·80% female), of whom 2898 (4·60%) developed lung cancer. We found a significant sex interaction of sleep apnoea on lung cancer hazard ( χ -squared: 13·239, P-interaction < 0·01). In females, sleep apnoea was associated with a higher lung cancer risk (cumulative incidence: 1545 vs 1350 per 100,000 PY; aHR: 1·31 (95% CI: 1·05-1·63)). For males, sleep apnoea patients had a lower lung cancer risk (cumulative incidence: 1632 and 2305 per 100,000 PY; aHR: 0·82 (95% CI: 0·70-0·95)). The impact of sleep apnoea on lung cancer development was especially strong in female COPD patients with hypoxia-related comorbidities e.g., with a history of emphysema (aHR: 2·65 (95% CI: 1·11-6·34)).

Sleep apnoea was associated with a higher risk of lung cancer in female COPD patients while, in males, there was a lower risk. Especially in female COPD patients with hypoxia, sleep apnoea is strongly associated with an increased lung cancer risk.

Emmanuel van der Schueren cancer research fellowship "Kom Op Tegen Kanker".

Sleep disordered breathing, represented by sleep apnea syndrome, not only significantly reduces the quality of daily life but is also known to contribute to the development of various cardiovascular diseases. Since 2000, sleep apnea syndrome has become widely recognized by the general public. However, the number of suspected patients who seek medical consultation remains low, and even fewer receive a proper diagnosis and treatment. One reason for this is the lack of information that apnea is linked to cardiovascular disease, even among individuals experiencing typical sleep apnea syndrome symptoms such as daytime sleepiness and general fatigue. Additionally, healthcare providers may not be effectively guiding patients while providing sleep hygiene education. Furthermore, the limited number of medical facilities and technicians capable of conducting overnight polysomnography tests for diagnosing sleep disordered breathing is another factor preventing more patients from benefiting from treatment. This article explores the relationship between sleep disordered breathing and the onset of cardiovascular diseases, as well as the latest treatment approaches.

The authors evaluated patients who received a diagnosis of obstructive sleep apnea (OSA) and were treated with a mandibular advancement appliance (MAA) for more than 10 years.

In a cohort of 839 patients who received a diagnosis of OSA and initiated MAA therapy for a period exceeding 10 years, a subset of 298 patients underwent both pretreatment and posttitration polysomnography. These patients participated in a survey conducted through an electronically distributed, questionnaire-based method. The analysis encompassed participants' perceived enhancement in symptoms of OSA and the satisfaction levels reported by the participants. In addition, the authors investigated the factors affecting adherence to and discontinuation of the treatment through a stepwise forward binary logistic regression analysis.

A total of 121 patients (54.5%) returned the questionnaire. The main reason for seeking treatment was that their snoring was disturbing a bed partner (77.6%). Factors associated with long-term adherence included experiencing morning headaches before treatment (odds ratio [OR], 32.11; 95% CI, 2.52 to 404.13; P = .007), perception that MAA therapy improves sleep (OR, 6.58; 95% CI, 1.58 to 27.38; P = .01), bed partner satisfaction with MAA therapy (OR, 4.12; 95% CI, 1.64 to 10.36; P = .003), and perception of irritability as a motivating factor for seeking treatment (B = -3.64; OR, 0.026; 95% CI, 0.002 to 0.412; P = .009).

Results of long-term MAA therapy for OSA, with more than a decade of use, showed significant benefits in improving self-perception of OSA symptoms, reducing daytime sleepiness, and enhancing partner satisfaction.

Understanding the factors influencing long-term adherence or nonadherence to OSA treatment with MAA is essential for sustaining the health and quality of life of the patients affected.

A dysregulated circadian system is independently associated with both Obstructive Sleep Apnea (OSA) and cardiovascular disease (CVD). OSA and CVD coexistence is often seen in patients with prolonged untreated OSA. However, the role of circadian dysregulation in their relationship is unclear. Half of the human genes, associated biological pathways, and physiological functions exhibit circadian rhythms, including blood pressure and heart rate regulation. Mechanisms related to circadian dysregulation and heart function are potentially involved in the coexistence of OSA and CVD. In this article, we provide a comprehensive overview of circadian dysregulation in OSA and associated CVD. We also discuss feasible animal models and new avenues for future research to understand their relationship. Oxygen-sensing pathways, inflammation, dysregulation of cardiovascular processes, oxidative stress, metabolic regulation, hormone signaling, and epigenetics are potential clock-regulated mechanisms connecting OSA and CVD.

Heart failure is the leading cardiovascular cause of hospitalization with an increasing prevalence, especially in older patients. About 50% of patients with heart failure have preserved ventricular function, a form of heart failure that, until a few years ago, was orphaned by pharmacological treatments effective in reducing hospitalization and mortality. New trials, which have tested the use of gliflozins in patients with heart failure with preserved ejection fraction (HFpEF), have for the first time demonstrated their effectiveness in changing the natural history of this insidious and frequent form of heart failure. Therefore, diagnosing those patients early is crucial to provide the best treatment. Moreover, the diagnosis is influenced by the patient's comorbidities, and some HFpEF patients have symptoms common to other rare diseases that, if unrecognized, develop an unfavourable prognosis. This position paper aims to provide the clinician with a useful tool for diagnosing and treating patients with HFpEF, guiding the clinician towards the most appropriate diagnostic and therapeutic pathway.

Although continuous positive airway pressure (CPAP) effectively prevents sleep apnea and reduces blood pressure, many patients do not use CPAP every night. This trial investigates cardiovascular effects after sleeping five nights without CPAP.

We randomized 100 patients (67 men and 33 women with a mean age 64 ± 9 years) using CPAP treatment for moderate-to-severe sleep apnea to either withdraw treatment for five nights ( n  = 50) or to continue with CPAP ( n  = 50). The primary outcomes were arterial stiffness and 24 h blood pressure.

The 24 h SBP increased by a mean of 2.8 mmHg [95% confidence interval (CI) 0.2-5.4 mmHg] ( P  = 0.035) and DBP increased by a mean of 1.7 mmHg (95% CI 0.1-3.3 mmHg) ( P  = 0.032) in the group without CPAP compared to the CPAP group. There was a significant effect on blood pressure in women but not in men. In women, SBP increased by 5.1 mmHg (95% CI 1.0-9.5 mmHg) ( P  = 0.017) and DBP by 2.9 mmHg (95% CI 0.4-5.6 mmHg) ( P  = 0.029). Arterial stiffness remained unaffected. Secondary outcomes that worsened in patients without CPAP included apnea-hypopnea index, oxygen desaturation index, hemoglobin levels, and daytime sleepiness.

Blood pressure is affected after five nights of CPAP interruption, along with a rapid return of sleep apneas, nocturnal hypoxic events, daytime sleepiness and increased hemoglobin levels, but arterial stiffness was not affected. Blood pressure was affected in women only, suggesting a sex-related CPAP effect on blood pressure.

Some observational studies found that there is an epidemiological association between type 2 diabetes (T2D) and sleep apnea (SA) and glucose-lowering drugs may lower SA risk. However, the causative relationship among them remains unclear.

Linkage Disequilibrium Score Regression (LDSC) was utilized to assess the genetic correlation between T2D and SA. Mendelian Randomization (MR) was applied, primarily using the inverse variance weighted (IVW) method, to evaluate the causal relationship between T2D and SA. Additionally, we performed Drug-target MR analysis to evaluate the impact of Glucagon-like Peptide-1 Receptor Agonists (GLP-1RAs) on SA. We used two kinds of genetic instruments to proxy the exposure of GLP-1RAs, including expression quantitative trait loci of drugs target genes, and genetic variants within drugs target genes associated with glycated hemoglobin A1c(HbA1c) from genome wide association study. Summary-data-based MR (SMR) and IVW were used to calculate the effect estimates. A two-step MR analysis was further employed to explore potential mediating factors in the T2D-SA relationship.

A genetic correlation and bidirectional causal association were found between T2D and SA. GLP-1RAs-mediated reductions in HbA1c levels showed associations with decreased SA risk in two independent datasets: (odds ratio (OR)1 = 0.48 [95% confidence interval (CI) 0.28-0.83], P1 = 9.21 × 10-3; OR2 = 0.21 [95% CI 0.05-0.92], P2 = 3.89 × 10-2); a higher expression of GLP-1R was associated with a decreased risk of SA (OR1 = 0.98 [95% CI 0.96-1.00], P1 = 4.55 × 10-2; OR2 = 0.95 [95% CI 0.92-0.99], P2 = 1.71 × 10-2). Body mass index (BMI) and current tobacco smoking mediated 20.28% and 6.65%, respectively, of the total effect of GLP-1RAs on SA risk.

This study suggested a bidirectional causal relationship between T2D and SA, with GLP-1-RAs potentially serving as a therapeutic target for SA. The reduction of SA risk by GLP-1RAs may be partially mediated by decreases in BMI and current tobacco smoking.

This study reviewed the global prevalence, health and socioeconomic impact, and management approaches of obstructive sleep apnea. The narrative review examined three key dimensions: (1) worldwide OSA prevalence across different regions, accounting for variations in diagnostic standards; (2) OSA's effects on health outcomes and socioeconomic conditions across diverse populations and healthcare systems; and (3) current global approaches to OSA diagnosis, treatment, and public health management. Despite advances in diagnosis and treatment, a large proportion of OSA cases remain undiagnosed or inadequately managed. The findings show that untreated OSA significantly increases public safety risks, particularly regarding motor vehicle and occupational accidents, while also creating a substantial pool of patients at high risk for systemic complications with severe impacts on overall health. There is a critical need for increased public awareness, universal screening approaches, and integrated care strategies to address this global health challenge and reduce its considerable socioeconomic burden. Our review uniquely addresses global disparities in OSA prevalence, clarifies the health and socioeconomic impacts that remain underexplored in the current literature, and suggests concrete strategies for public health and clinical management improvement worldwide.

Obstructive sleep apnea (OSA) is increasingly recognized as a chronic condition that is closely interrelated to olfactory disorders, with a significant contribution to quality of health and overall quality of life. This narrative review aims to provide a thorough overview of the emerging evidence that now integrates these two previously considered distinct physiologic systems. Studies published recently have reported a significantly higher frequency of olfactory dysfunction among OSA patients compared to the general population, which raises the possibility of a causal relationship. We explore the postulated mechanisms behind this association, namely, the chronic intermittent hypoxia, local inflammatory effect, and neuroanatomical changes attributed to OSA. The review further explores the clinical impacts of this relationship through proposing the potential for an olfactory assessment to be used as a diagnostic modality for OSA and the effects of OSA treatment on olfactory function. Thus, we explore the difficulties in treating patients who experience both and suggest future areas for research. This review attempts to bridge the gap between the existing literature and impending investigation necessary for a better management of the interaction of sleep apnea and the human sense of smell.

To establish a simple and noninvasive screening test for sleep apnea (SA) that imposes less burden on potential patients. The specific objective of this study was to verify the effectiveness of past and future single-lead electrocardiogram (ECG) data from SA occurrence sites in improving the estimation accuracy of SA and sleep apnea syndrome (SAS) using machine learning.

The Apnea-ECG dataset comprising 70 ECG recordings was used to construct various machine-learning models. The time window size was adjusted based on the accuracy of SA detection, and the performance of SA detection and SAS diagnosis (apnea‒hypopnea index ≥ 5 was considered SAS) was compared.

Using ECG data from a few minutes before and after the occurrence of SAs improved the estimation accuracy of SA and SAS in all machine learning models. The optimal range of the time window and achieved accuracy for SAS varied by model; however, the sensitivity ranged from 95.7 to 100%, and the specificity ranged from 91.7 to 100%.

ECG data from a few minutes before and after SA occurrence were effective in SA detection and SAS diagnosis, confirming that SA is a continuous phenomenon and that SA affects heart function over a few minutes before and after SA occurrence. Screening tests for SAS, using data obtained from single-lead ECGs with appropriate past and future time windows, should be performed with clinical-level accuracy.

The peculiar expression of N6-methyladenosine (m6A) in Circular RNAs (circRNAs) is closely linked to the occurrence of many diseases. However, roles of m6A-modified circRNAs in OSA-induced cardiovascular disease are unknown. Here, we use bioinformatics analysis to investigate the expression profiles of m6A-modified circRNAs and reveal their potential functional roles in the mouse models of chronic intermittent hypoxia (CIH).

Firstly, the expression profiles of m6A-modified circRNA in left ventricular tissue of the CIH mouse model were examined using circRNA microarray analysis. Then, the expression level of selected circrRNA was compared by folding change filtration, and the consistency between them and microarray results was verified by MeRIP-qPCR. GO analyses and KEGG analyses were conducted to predict the potential functions of these m6A-modified circRNAs. Finally, we conducted a ceRNA analysis, and a network was constructed to clarify the relationship between the selected circRNAs and miRNAs as well as the targeted genes.

In total, 255 circRNAs with m6A peaks in CIH-treated cardiac tissues were identified. 250 were up-regulated, 5 were down-regulated. The results of MeRIP-qPCR were consistent with the microarray results. 73 pathways were detected in the up-regulated transcripts and no relevant pathways were detected in the down-regulated transcripts. Finally, three circRNAs (mmu_circRNAs_22543, mmu_circRNAs_29768, and mmu_circRNAs_34841) were selected for ceRNA analysis, and the circRNA-miRNA-mRNA network was constructed.

Our findings are the first to show that m6A-modified circRNAs play a key role in OSA-induced cardiovascular disease. This study highlights the pivotal role of m6A-modified circRNAs in regulating gene expression and their potential implications in understanding the molecular pathogenesis of OSA-induced cardiac injury.

The cardiometabolic index (CMI) reflects an individual's cardiometabolic health and is linked to the risk of dyslipidemia, obesity, hyperglycemia, and hypertension. These risk factors not only increase the likelihood of cardiovascular disease but are also strongly associated with sleep issues such as sleep apnea and insomnia. However, the relationship between CMI and the risk of sleep disorders remains unclear. This study aimed to investigate the association between CMI and sleep disorder-related morbidity and mortality. This cross-sectional study utilized data from 6220 adults aged ≥ 20 years from the National Health and Nutrition Examination Survey (2007-2014). The CMI was calculated as [waist circumference (cm)/height (cm)] × [triglycerides (mmol/L)/high-density lipoprotein-C (mmol/L)], reflecting metabolic risk. Participants were categorized into 3 CMI tertiles (Q1-Q3). Based on survey data, participants were classified into sleep disorder and non-sleep disorder groups. The analysis included logistic regression, subgroup analysis, forest plots, and survival analysis. The average age of participants was 49 ± 18.00 years; 49% were male. The high-CMI group had older participants, more males, higher body mass index, higher triglycerides, and more hypertension (P < .001). Higher CMI was significantly associated with an increased risk of sleep disorders (odds ratio [OR] = 1.11, 95% CI: 1.02 to 1.21, P = .017), with the prevalence being greater in Q3 than in Q1 (OR = 1.46, 95% CI: 1.27 to 1.68, P ≤ .001). After adjusting for demographics, the association persisted (OR = 1.13, 95% CI: 1.03-1.24, P = .014). The mortality rate was also higher in the high-CMI group (P≤.001), with a 34% increased risk of death (OR = 1.34, 95% CI: 1.08-1.67, P = .021). The study found that a higher CMI is associated with increased risks of sleep disorders and mortality. Understanding this relationship may help in monitoring cardiometabolic health and assessing sleep disorder severity. CMI could serve as a cost-effective indicator for sleep disorder assessment.

This systematic review and meta-analysis aimed to evaluate the dental and skeletal effects of the long-term oral appliance (OA) treatment in patients with obstructive sleep apnea (OSA) and provide insights for clinicians in treatment planning and decision-making for OSA patients undergoing OA treatment.

A comprehensive literature search was conducted in major databases up to April 2024. Studies were included if they assessed long-term OA treatment (≥6 months) in adults with OSA using any type of mandibular advancement device (MADs) or tongue retaining device (TRD). Dental and skeletal changes, measured by dental cast and cephalometric analysis, were the primary outcomes.

A total of 42 studies were included in the systematic review, with 23 included in the meta-analysis. Long-term OA treatment was associated with a significant decrease in overbite (0.87 mm, 95% CI: 0.69-1.05) and overjet (0.86 mm, 95% CI: 0.69-1.03). Subgroup analyses showed the decrease of overbite and overjet progressively changed over the years intervals. There was a significant retroclination of the upper incisors (U1-SN, 2.58°, 95% CI: 1.07-4.08) and proclination of the lower incisors (L1-MP, -2.67° (95% CI: -3.78-1.56). Skeletal changes were not significant.

Overbite and overjet gradually decreased in the long-term OA treatment, which might predominantly result from the retroclination of the upper incisors and the proclination of the lower incisors. The skeletal patterns in the anteroposterior and vertical direction might remain relatively stable over time. There was a tendency for the clockwise rotation of the mandible.

Sleep apnea is a common respiratory disorder in humans and consists of recurrent episodes of cessation of breathing or decrease in airflow during sleep. Sleep apnea can be classified as central or obstructive, based on its origin. Central sleep apnea results from an impaired transmission of the signal for inspiration from the brain to inspiratory muscles, while obstructive sleep apnea occurs in the presence of an obstruction of the upper airways during inspiration. This condition leads to repetitive episodes of reduced oxygen and elevated carbon dioxide levels in the bloodstream, which entail both direct and indirect adverse effects on vital organs, especially the brain and heart. Basic research on animal models has been instrumental in advancing the understanding of disease mechanisms and pathophysiology, and in expediting the development of targeted therapies in several medical fields. Among animal models, mice are the mammalian species of choice for functional genomics of integrative functions such as sleep. Mice have long been known to show sleep apneas, but the classification of sleep apneas as central or obstructive in mice is technically challenging due to the small size of these animals. Here we present a method aimed at identifying central and obstructive sleep apneas in mice. This method involves the surgical implantation of electrodes for recording the electroencephalogram and nuchal muscle electromyogram, which are the gold standard to study the wake-sleep cycle, and for recording the diaphragm electromyogram, which allows the detection of diaphragm contraction. The method also includes the simultaneous recording of the above-mentioned biological signals and breathing inside a whole-body plethysmograph and the data analysis allows to score wake-sleep states and to detect sleep apneas and categorize them into central and obstructive events.

Obstructive sleep apnea (OSA) is a common condition affecting around one billion people worldwide. Emerging evidence from recent studies suggests that Glucagon-like peptide 1 receptor (GLP-1) agonists may reduce OSA severity. Hence, this meta-analysis aims to evaluate the efficacy and safety of GLP-1 agonists in patients with OSA.

Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we searched four electronic databases (PubMed, EMBASE, Cochrane Library, Scopus, and Web of Science) to identify eligible studies reported up to 24 June 2024. Using Review Manager software, we reported outcomes as risk ratios (RRs) or mean difference (MD) and confidence intervals (CIs). The protocol for this review has been registered and published in PROSPERO with the ID (CRD42024562853).

The meta-analysis included three randomized controlled trials with 828 patients. Pooled analysis of patients administered GLP-1 agonists or tirzepatide showed improvement in Apnea/Hypopnea Index (MD -16.57 events per hour, 95% CI [-27.41, -5.73], p = 0.003), weight reduction (MD -12.71%, 95% CI [-21.38, -4.03], p = 0.004), and systolic blood pressure (MD -4.93 mmHg,95% CI [-7.67, -2.19], p = 0.0004). Tirzepatide showed a reduction in high-sensitivity C-reactive protein (MD -0.89 mg/dl, 95% CI [-1.25, -0.54], p < 0.0001) and sleep apnea-specific hypoxic burden (MD -66.21%/min, 95% CI [-81.75, -50.67], p < 0.0001). Despite the heterogeneity observed in the AHI and weight, it was resolved, and the results were consistent. GLP-1 agonists/tirzepatide showed comparable outcomes concerning diastolic blood pressure (MD -1.34 mmHg, 95% CI [-2.80, 0.12], p = 0.07). No significant serious adverse events were observed for GLP-1 agonists/tirzepatide, but it was associated with a higher incidence of gastrointestinal adverse events.

GLP-1 agonists, including tirzepatide, improved Apnea/Hypopnea Index, weight, and systolic blood pressure in adults with moderate-to-severe OSA. However, the evidence remains limited to two published studies comprising three randomized controlled trials using different pharmacological agents. Consequently, further research is needed before firm conclusions can be drawn.

Hypoxic burden (HB) is a measure incorporating frequency, depth and duration of respiratory event-related desaturations. While HB is associated with cardiovascular disease in adults with obstructive sleep apnea (OSA), it has not been assessed in typically developing (TD) children with OSA, nor in children with Down syndrome (DS), who have a higher incidence of OSA with more severe hypoxia. We assessed whether HB in these children was related to heart rate variability (HRV), an indicator of cardiovascular outcomes. Children (3-19 years, n = 44) with DS and TD children matched for OSA severity, age and sex underwent overnight polysomnography and were grouped into primary snoring (PS), Mild or Moderate/Severe (MS) OSA. HRV was analysed using power spectral analysis of the electrocardiograph. Regression analysis determined whether HB was predictive of HRV. Children with MS OSA in both groups had higher HB compared with children with PS (p < 0.001 for both) and Mild OSA (DS, p < 0.001; TD, p < 0.05). Children with DS and PS or Mild OSA had higher HB compared with TD children (PS p < 0.05; Mild OSA p < 0.001). There was no difference between the MS OSA groups. HB predicted dampened sympathetic and parasympathetic activity only in children with DS (R2 = 0.12, β = -10.6, SE = 4.6, p = 0.03). HB was higher in children with DS and PS or Mild OSA compared to TD children and predicted dampened autonomic function in children with DS. The potential contribution of the adverse effects of HB on autonomic function adds weight to the importance of identifying and treating OSA in children with DS.

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder that is closely associated with metabolic conditions. The Blood Urea Nitrogen to Creatinine Ratio(BUCR) is commonly utilized as a tool for evaluating renal function, particularly in cases where there are concerns about pre-renal or renal causes of azotemia. However, the connection between OSA and BUCR is not yet fully understood.

This study examined the link between BUCR and OSA in adults over 20 using National Health and Nutrition Examination Surveys(NHANES) data from 2005-2008. Logistic regression models adjusted for multiple variables were used to analyze the relationship. The non-direct correspondence relationship were explored with a smooth curve and a two-part linear regression model, which revealed a threshold effect. Subgroup analyses were conducted to assess variations among different populations.

The survey, encompassing a total of 8826 participants, revealed that the median age of all respondents was 48 years, with a notable OSA prevalence of 51.3%. Upon adjusting for pertinent covariates using Model III(age, sex, marital status, education level, BMI, smoking status, drinking, hypertension, and diabetes), our findings indicated a significant association between OSA and BUCR, as evidenced by an odds ratio (OR) of 1.01 (95% CI: 1.00-1.02, P = 0.005). Furthermore, the risk association was found to be non-linear, featuring an inflection point for BUNR at 10.86. This non-linear relationship adds complexity to our understanding of the interplay between OSA and BUCR. In addition, a subgroup analysis underscored the influence of diabetes on the association between BUCR and OSA.

This study reveals a significant correlation between elevated BUCR levels and the incidence of OSA, particularly in the presence of diabetes. This discovery underscores the necessity for additional research to investigate the underlying mechanisms and ramifications of this connection within the diabetic context.

Central sleep apnea, a rare polysomnographic finding in the general population, is prevalent in certain cardiovascular conditions including systolic and diastolic left ventricular dysfunction, atrial fibrillation, coronary artery disease, carotid artery stenosis, stroke, and use of certain cardiac-related medications. Polysomnographic findings of central sleep apnea with adverse cardiovascular impacts include nocturnal hypoxemia and arousals, which can lead to increased sympathetic activity both at night and in the daytime. Among cardiovascular diseases, central sleep apnea is most prevalent in patients with left ventricular systolic dysfunction; a large study of more than 900 treated patients has shown a dose-dependent relationship between nocturnal desaturation and mortality. Multiple small randomized controlled trials have shown mitigation of sympathetic activity when central sleep apnea is treated with nocturnal oxygen, continuous positive airway pressure, and adaptive servoventilation. However, two early randomized controlled trials with positive airway pressure devices have shown either a neutral effect on survival or excess premature mortality in the active treatment arm, compared to untreated central sleep apnea. In contrast, the results of the most recent trial using an advanced adaptive servoventilation device showed improved quality of life and no signal for mortality suggesting that treatment of central sleep apnea was at least safe. In addition to positive airway pressure devices, multiple medications have been shown to improve central sleep apnea, but no long-term trials of pharmacologic therapy have been published. Currently, phrenic nerve stimulation is approved for the treatment of central sleep apnea, and the results of a randomized controlled trial showed significant improvement in sleep metrics and quality of life.

Patients with pulmonary hypertension (PH) often have comorbid sleep apnea (SA), but the prevalence, severity, and clinical characteristics of PH patients with SA have not been well studied.

Using a combination of the keywords "pulmonary hypertension" and "sleep apnea," the PubMed, Embase, Web of Science, and Scopus databases were searched for articles reporting the prevalence, severity, and clinical characteristics of PH patients with SA that were available through June 25, 2024.

Of the 7969 studies, 39 were included in the final analysis. Prevalence of obstructive and central SA was 45.4% [39.2%, 51.6%]) and 9.3% [6%, 14.2%], respectively. The mean apnea hypopnea index (AHI) of patients with obstructive SA and PH was 18 [13.6, 22.4] with a standard error of 2.2. Subgroup analysis revealed that 51.4% [38.4%, 64.2%] had mild SA, 28% [22.5%, 33.6%] had moderate, and 20% [15.2%, 25%] had severe SA. PH patients with SA were characterized by male sex (odds ratio (OR) = 1.86 [1.45, 2.37], P < 0.001), older age (mean difference (MD) = -9.37 [-14.23, -4.43], P < 0.001), and higher body mass index (BMI) (MD = -2.16 [-3.32, -1.00], P < 0.001) compared to those without SA. However, mean pulmonary arterial pressure (mPAP) was not significantly different between SA and non-SA (MD = -2.4 [-5.1, 0.3], P = 0.078). Meta-regression showed no significant association between mPAP and AHI among patients with PH and SA (P = 0.13).

Our study found that SA is common in PH patients with certain clinical characteristics. We recommend conducting sleep studies in all PH patients, especially in older, overweight male patients.

Sleep apnea (SA) is a sleep disorder characterized by frequent interruptions in breathing during sleep and is widely recognized as a significant global public health concern. Although genome-wide association studies (GWAS) have identified several loci associated with SA susceptibility, the underlying genes and biological mechanisms remain largely unknown. A cross-tissue transcriptome-wide association study (TWAS) was performed to integrate SA GWAS summary statistics from 410,385 individuals (43,901 cases and 366,484 controls) and gene expression data from 49 distinct tissues and obtained from 838 post-mortem donors. Functional Summary-based Imputation was employed to validate these findings in whole blood tissue. Additionally, candidate susceptibility genes were further verified using Gene Analysis combined with Multi-marker Analysis of Genomic Annotation. Subsequent Mendelian randomization and colocalization analyses were conducted. In the cross-tissue TWAS analysis, 60 susceptibility genes were identified. Two novel susceptibility genes, GPD2 and L3MBTL2, were validated through both single tissue TWAS and MAGMA analysis. Mitochondrial glycerophosphate dehydrogenase (GPD2) may reduce the SA risk by regulating energy metabolism, while Lethal (3) malignant brain tumor-like protein 2 (L3MBTL2) may increase the risk of SA by disturbing DNA damage repair pathway and by regulating the process of the cell cycle. In summary, two novel biological macromolecules were identified in our study whose expression was predicted to be associated with SA risk, providing new insight into the genetic basis of this condition.