Effects Of Obstructive Sleep Apnea Research Articles

Effects of obstructive sleep apnea on nocturnal changes in blood pressure - a retrospective study.

To explore the effects of obstructive sleep apnea (OSA) on nocturnal changes in blood pressure (BP), we enrolled 2037 participants who underwent polysomnography (PSG) between 2019 and 2020 and examined BP changes before and after sleep. BP was measured in the evening and the following morning using an electronic wrist sphygmomanometer in the supine position. The severity of OSA was determined by PSG and graded based on the apnea/hypopnea index (AHI). Participants with OSA (AHI ≥ 5 events/h) had significantly higher morning systolic BP (SBP) and diastolic BP (DBP) compared to their evening measurements. BP values, whether measured in the evening or the morning, as well as the nocturnal changes (differences between morning and evening values), showed significant correlations with the AHI for both SBP and DBP, even after adjusting for confounders such as age, sex, body mass index, and the presence of comorbidities, including hypertension, heart failure, coronary artery disease, diabetes, renal disorder, and cerebrovascular attack. After standardization, the extent of nocturnal changes in DBP was greater than SBP, especially among participants with severe OSA. In a logistic regression model with serial multivariate adjustments, OSA was found to be independently associated with morning hypertension, particularly in individuals with moderate to severe OSA.

L-type Calcium Channel Blockade Worsens Glucose Tolerance and β-Cell Function in C57BL6/J Mice Exposed to Intermittent Hypoxia.

Intermittent hypoxemia (IH), a pathophysiologic consequence of obstructive sleep apnea (OSA), adversely affects insulin sensitivity, insulin secretion, and glucose tolerance. Nifedipine, an L-type calcium channel blocker frequently used for treatment of hypertension, can also impair insulin sensitivity and secretion. However, the cumulative and interactive repercussions of IH and nifedipine on glucose homeostasis have not been previously investigated. Adult male C57BL6/J mice were exposed to either nifedipine or vehicle concurrently with IH or intermittent air (IA) over five days. IH exposure entailed cycling fractional inspired oxygen levels between 0.21 and 0.055 at a rate of 60 events per hour. Nifedipine (20 mg/kg/day) or vehicle was administered via subcutaneous osmotic pumps resulting in four groups of mice: IA-vehicle (control), IA-nifedipine, and IH-vehicle, IH-nifedipine. Compared to IA (control), IH increased fasting glucose (Mean Δ:33.0 mg/dl; p<0.001) and insulin (mean Δ: 0.53 ng/ml; p<0.001) with nifedipine having no independent effect. Furthermore, glucose tolerance was worse with nifedipine alone, and IH further exacerbated the impairment in glucose disposal (p=0.013 for interaction). Nifedipine also decreased glucose-stimulated insulin secretion and the insulinogenic index, with addition of IH attenuating those measures further. There were no discernible alterations in insulin biosynthesis/processing, insulin content, or islet morphology. These findings underscore the detrimental impact of IH on insulin sensitivity and glucose tolerance, while highlighting that nifedipine exacerbates these disturbances through impaired β- cell function. Consequently, cautious use of L-type calcium channel blockers is warranted in OSA patients, particularly in those at risk for type 2 diabetes.

L-type calcium channel blockade worsens glucose tolerance and β-cell function in C57BL6/J mice exposed to intermittent hypoxia.

Intermittent hypoxemia (IH), a pathophysiologic consequence of obstructive sleep apnea (OSA), adversely affects insulin sensitivity, insulin secretion, and glucose tolerance. Nifedipine, an L-type calcium channel blocker frequently used for the treatment of hypertension, can also impair insulin sensitivity and secretion. However, the cumulative and interactive repercussions of IH and nifedipine on glucose homeostasis have not been previously investigated. Adult male C57BL6/J mice were exposed to either nifedipine or vehicle concurrently with IH or intermittent air (IA) over 5 days. IH exposure entailed cycling fractional-inspired oxygen levels between 0.21 and 0.055 at a rate of 60 events/h. Nifedipine (20 mg/kg/day) or vehicle was administered via subcutaneous osmotic pumps resulting in four groups of mice: IA-vehicle (control), IA-nifedipine, IH-vehicle, and IH-nifedipine. Compared with IA (control), IH increased fasting glucose (mean Δ: 33.0 mg/dL; P < 0.001) and insulin (mean Δ: 0.53 ng/mL; P < 0.001) with nifedipine having no independent effect. Furthermore, glucose tolerance was worse with nifedipine alone, and IH further exacerbated the impairment in glucose disposal (P = 0.013 for interaction). Nifedipine also decreased glucose-stimulated insulin secretion and the insulinogenic index, with addition of IH attenuating those measures further. There were no discernible alterations in insulin biosynthesis/processing, insulin content, or islet morphology. These findings underscore the detrimental impact of IH on insulin sensitivity and glucose tolerance while highlighting that nifedipine exacerbates these disturbances through impaired β-cell function. Consequently, cautious use of L-type calcium channel blockers is warranted in patients with OSA, particularly in those at risk for type 2 diabetes.NEW & NOTEWORTHY The results of this study demonstrate the interaction between intermittent hypoxemia (IH) and nifedipine in a murine model. IH raises fasting glucose and insulin levels, with nifedipine exacerbating these disturbances. Glucose tolerance worsens when nifedipine is administered alone, and IH magnifies the impairment in glucose disposal. These findings raise the possibility of potential deleterious effects of L-type calcium channel blockers in patients with obstructive sleep apnea (OSA).

Effects of gestational intermittent hypoxia on the respiratory system: A tale of the placenta, fetus, and developing offspring.

Obstructive sleep apnea (OSA) is a common sleep disorder that is associated with a wide variety of health conditions, including cardiovascular, cerebrovascular, metabolic, neoplastic, and neurocognitive manifestations. OSA, as a chronic condition, is mainly characterised by repeated upper airway obstructions during sleep that cause episodes of intermittent hypoxia (IH), resulting in tissue hypoxia-reoxygenation cycles. Decreased arterial oxygen pressure (PaO2) and haemoglobin saturation (SatO2) stimulate reflex responses to overcome the obstruction. The prevalence of OSA is significant worldwide, and an underrated problem when focussing on women during pregnancy. The physiological changes associated with pregnancy, especially during its latest stages, are related to a higher prevalence of OSA events in pregnant mothers, and associated with an increased risk of hypertension, pre-eclampsia and diabetes, among other deleterious consequences. Furthermore, OSA during pregnancy can interfere with normal fetal development and is associated with growth retardation, preterm birth, or low birth weight. Carotid body overstimulation and hypoxia-reoxygenation episodes contribute to cardiovascular disease and oxidative stress, which can harm both mother and fetus and have long-lasting effects that can reach into adulthood. Because IH is the hallmark of OSA, this review examines the literature available about the impact of gestational intermittent hypoxia (GIH) on the respiratory system at maternal, fetal, and offspring levels. Offering the latest scientific data about OSA during pregnancy, we may help to tackle this condition with lifestyle changes and therapeutic approaches, that could influence the mothers, but also impact adult health problems, mostly unknown, inherited from these hypoxic episodes in the uterus.

Association of Positive Airway Pressure Adherence with Clinical Outcomes in Patients with Type 2 Diabetes and Obstructive Sleep Apnea.

Background/Objectives: There are controversies regarding the effect of obstructive sleep apnea (OSA) treatment with positive airway pressure (PAP) on diabetes-related outcomes. Therefore, we aimed to explore the association of PAP adherence with diabetes-related outcomes in patients with type 2 diabetes mellitus (T2DM) and OSA. Methods: In this prospective study, we included T2DM patients diagnosed with OSA during an 8-year period (2015-2023). PAP adherence (optimal usage for > 6 h/night for ≥ 70% of nights), hemoglobin A1c (HbA1c), body mass index (BMI), systolic (SBP) and diastolic blood pressure (DBP), daytime sleepiness (Epworth Sleepiness Scale-ESS) and cardiovascular (CVD) events were recorded. Comparisons of the change in diabetes-related outcomes (follow-up to baseline) in the adherent and non-adherent groups were assessed by analysis of covariance to adjust for relevant confounders. Results: Of the 355 patients included, 199 (56%) were PAP adherent. The mean follow-up period was 5.5 years. At the end of the follow up period, the PAP adherent group achieved a greater decrease in HbA1c levels (-1.4 vs. -0.3), SBP (-10.1 vs. -5.5), DBP (-2.9 vs. -0.55) and ESS (-5.9 vs. -4.2) compared to the non-adherent groups. Conclusions: Achieving optimal PAP adherence in patients with T2DM and OSA was associated with improved diabetes-related outcomes. Therefore, current practices need to be modified to incorporate systematic assessment and treatment of OSA in these patients.

Roles of BMI in mediating the causal effect of obstructive sleep apnea on psoriasis: a two-step mendelian randomization study.

Observational studies have reported an association between obstructive sleep apnea (OSA) and psoriasis. Nonetheless, the presence of a causal relationship within this observed association remains to be confirmed. Consequently, we utilized the Mendelian Randomization (MR) method to assess the causal effects between OSA on psoriasis.Single-nucleotide polymorphisms associated with OSA were extracted from the FinnGen study. statistics for psoriasis were obtained from the publicly available IEU GWAS database. Inverse-variance weighted (IVW) method was chosen as the primary analysis, combined with several sensitivity analyses to evaluate the robustness of results. The study design included two-sample MR and two-step MR.Our primary MR analysis revealed that genetically predicted OSA was positively linked to psoriasis (OR = 1.26, 95% confidence interval [CI]: 1.12-1.42, p < 0.001), while no significant causal relationships were observed between psoriasis and OSA (p > 0.05). The two-step MR suggests that BMI might act as a mediating factor in the effect of OSA on psoriasis, with a mediated portion estimated at 23%.Our findings provide support for a causal relationship between genetically predicted OSA and psoriasis. Furthermore, our results suggest that BMI may play a role in mediating the influence of OSA on psoriasis.

Distribution patterns of obstructive and central apnea in adults with obstructive sleep apnea-hypopnea syndrome

Objective: This study aimed to investigate the distribution patterns of obstructive and central apnea events in adults with obstructive sleep apnea-hypopnea syndrome (OSAHS). Methods: Utilizing polysomnography (PSG) data, we selected patients with a habitual snoring condition and categorized them into OSAHS and non-OSAHS groups. The OSAHS group was further stratified into mild, moderate, and severe subgroups based on disease severity. We compared the distribution of obstructive sleep apnea (OSA) and central sleep apnea (CSA) events between the groups, analyzing their correlation with the apnea-hypopnea index (AHI), age, gender, and other factors. Results: A total of 460 patients were enrolled for the study, 374 patients were in the OSAHS group and 86 patients in the non-OSAHS group. (1) There were statistical differences in AHI and obstructive apnea index (OAI) in all groups (P &lt; 0.05), with the OSAHS group having a higher AHI and OAI than the non-OSAHS group. (2) In the OSAHS group, OAI and AHI had the highest correlation (r = 0.884, P &lt; 0.01), and central apnea index (CAI) and AHI had the lowest correlation (r = 0.237, P &lt; 0.01); in the non-OSAHS group, OAI and AHI had the highest correlation (r = 0.520, P &lt; 0.01), and CAI and AHI had the lowest correlation (r = 0.312, P &lt; 0.01). (3) In the OSAHS group, OAI was significantly correlated with the severity of patient disease (r = 0.828, P &lt; 0.01), whereas CAI was marginally correlated with the severity of patient disease (r = 0.235, P &lt; 0.01), but it increased as the condition became more severe. Conclusion: Patients with OSAHS exhibited both CSA and OSA, with OAI having a significantly greater impact. OAI can serve as a valuable index for evaluating OSAHS severity, while CSA appears to be primarily influenced by the overall disease severity. Notably, patients with OSAHS had a higher CAI compared to those without OSAHS.

Sequential exploratory mixed-method research of an eHealth intervention on blood pressure, sleep quality and physical activity in obstructive sleep apnoea: rationale and methodology of the Moore4Medical trial protocol

IntroductionThe management of a chronic and frequent pathology, such as obstructive sleep apnoea (OSA), requires personalised programmes that implement new technology-based tools to improve the comprehensive treatment of the patient...

The association of objective daytime sleepiness with impaired glucose metabolism in patients with obstructive sleep apnea: a multi-omics study.

To examine the joint effect of obstructive sleep apnea (OSA) and objective excessive daytime sleepiness (EDS) on glucose metabolism and the underlying mechanisms. We included 127 patients with OSA. The multiple sleep latency test (MSLT) and Epworth sleepiness scale (ESS) were used to assess objective and subjective EDS, respectively. Disordered glucose metabolism was defined as either a physician diagnosis or having fasting blood glucose levels ≥ 5.6 mmol/L. Values of fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) higher than the median values of our sample were defined as high fasting insulin and insulin resistance. Serum metabolomics and fecal microbiota were used to explore underlying mechanisms. Lower MSLT values were associated with higher levels of fasting blood glucose, fasting insulin, and HOMA-IR. Furthermore, objective EDS was associated with increased odds of disordered glucose metabolism, elevated fasting insulin, and insulin resistance. Dysregulation of serum valine degradation and dysbiosis of fecal Bacteroides thetaiotaomicron were associated with impaired glucose metabolism in OSA with objective EDS. No association between subjective EDS and impaired glucose metabolism was observed. OSA with objective, but not subjective, EDS is associated with an increased risk of disordered glucose metabolism and insulin resistance. Dysregulation of valine degradation and dysbiosis of Bacteroides thetaiotaomicron appear to link objective EDS and disordered glucose metabolism in OSA.

Cardiovascular effects of obstructive sleep apnoea and effects of continuous positive airway pressure therapy: evidence from different study models

INTRODUCTIONCardiovascular consequences of obstructive sleep apnoea (OSA) and the effects of continuous positive airway pressure (CPAP) therapy on blood pressure, endothelial dysfunction, and MACE (major adverse cardiovascular events) have been studied over decades using different study designs. However, clinical findings from different study models on cardiovascular outcomes are sometimes contradictory.METHODSA literature search was conducted in PubMed for randomised controlled trials, meta-analyses, population-based epidemiological studies and OSA cohort studies up to September 2023 investigating the cardiovascular effect of OSA and CPAP in adults with OSA on the following cardiovascular endpoints: blood pressure, arterial hypertension, endothelial function, and MACE (myocardial infarction, stroke, transient ischemic attack, cardiovascular death). The level of evidence for these outcomes was discussed on the basis of different study models.RESULTS AND CONCLUSIONSThere is high-level evidence of a causal relationship between OSA and arterial hypertension and endothelial dysfunction, as well as on higher MACE incidence among subgroups of patients with untreated OSA. The cardiovascular effects of OSA depend on the severity of OSA, symptoms, phenotype, and comorbidities. The blood pressure-lowering effect of CPAP is mainly observed in uncontrolled and treatment-resistant hypertension. The MACE risk reduction in OSA depends on good long-term CPAP adherence. Younger, sleepy patients with more severe OSA, higher hypoxaemic burden and without overt cardiovascular end-organ disease may particularly benefit from CPAP treatment in terms of cardiovascular risk reduction. Randomised controlled trials of CPAP or other effective OSA treatments in primary cardiovascular prevention and in patients at highest risk are lacking.

Pediatric Obstructive Sleep Apnea: Clinical Manifestations and Consequences

Obstructive sleep apnea (OSA) significantly impacts the quality of life in children, affecting their physical and mental health. The pathophysiology involves a complex interaction between anatomical factors (such as enlarged tonsils, adenoids, and structural abnormalities) and obesity, along with neuromuscular compensations. Clinical manifestations include loud snoring, breathing pauses, restless sleep, unusual sleeping positions, and frequent awakenings. OSA can lead to enuresis, growth impairment, poor academic performance, and neurocognitive and behavioral difficulties. Long-term consequences are cardiovascular morbidity, metabolic dysfunction, and neurocognitive impairment. Many studies have explored these associations and the impact of adenotonsillectomy. This review provides an overview of clinical manifestations and consequences of OSA, aiming to enhance diagnosis and treatment strategies for pediatric OSA.

Obstructive sleep apnea and genotype rs6843082 as a risk factor for cerebrovascular accident

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.

Pentraxin-3 marker as a predictor of cardiovascular events in obstructive sleep apnea; a cross-sectional study

Introduction A large population suffers from obstructive sleep apnea (OSA). Most of these individuals (almost 90%) are either unrecognized or untreated OSA. These patients are at increased risk of cardiovascular diseases. Aim The aim of this study was to assess the prognostic value of Pentraxin 3 (PTX3) in OSA compared with the clinically relevant biological markers (HbA1c, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), uric acid, and fibrinogen) and to evaluate the relationship between PTX3 levels and risk of cardiovascular diseases. Patients and methods This research used a cross-sectional design and enrolled 100 participants with suspected OSA. All the participants underwent a full clinical history, a STOP-Bang questionnaire, and a polysomnography (PSG) study, and the serum biomarkers were also analyzed. Results The apnea-hypopnea index (AHI) from PSG was used to measure the OSA severity, and the individuals were distributed into three groups accordingly. Our findings showed that there was a significant difference in Pentraxin 3 and fibrinogen levels between patients with mild or moderate OSA and those with severe OSA. Pentraxin 3, at a cutoff point of greater than 4.25 ng/ml, had the highest prognostic accuracy in OSA (96%), with an AUC of 0.96. Regression analysis revealed that Pentraxin 3, with a cutoff point greater than 4.25, and CRP were significant predictors of cardiovascular disease in individuals with OSA. Furthermore, Pentraxin 3 (with a cutoff point of greater than 4.25 ng/ml) and fibrinogen were significant predictors of pulmonary embolism in patients with OSA. Conclusion Serum PTX3 was higher in patients with severe OSA than in those with mild- to moderate OSA. Furthermore, we found that OSA severity as indicated by the AHI was significantly correlated with serum PTX3. PTX3 and CRP are useful markers of cardiovascular risk in OSA.

Cardiopulmonary exercise testing in patients with obstructive sleep apnea

Background The cardiopulmonary exercise testing (CPET) is a noninvasive process aiming to evaluate the respiratory and cardiovascular system during exercise. Aim To study the effect of obstructive sleep apnea (OSA) on cardiovascular system and exercise capacity and to correlate the severity of OSA with CPET parameters. Patients and methods Fifty patients (30 males and 20 females) were enrolled in this study, diagnosed as OSA based on polysomnography (apnea–hypopnea index ≥5). All patients were given a thorough medical history, a thorough physical examination, an arterial blood gas analysis before and after exercise, a pulmonary-function test, polysomnography, and a CPET. Results Patients with mild/moderate OSA had significantly higher oxygen consumption (VO2) at peak (ml/min) and predicted value. Predicted VO2/kg was significantly higher among patients with mild/moderate OSA. Also, patients with mild/moderate OSA had significantly higher LT. Out of enrolled patients, three (6%), 15 (30%), and 32 (64%) patients had mild, moderate, and severe exercise impairment, respectively. Majority (90%) of the patients with severe OSA had severe exercise impairment, while majority (70%) of those with mild/moderate OSA had moderate exercise impairment. Conclusions OSA causes exercise impairment, which has a positive correlation with the severity of the disease.

Identification biomarkers in disease progression of obstructive sleep apnea from children serum based on WGCNA and Mfuzz.

Obstructive sleep apnea (OSA) syndrome is a prevalent form of respiratory sleep disorder, with an increasing prevalence among children. The consequences of OSA include obesity, diabetes, cardiovascular disease, and neuropsychological diseases. Despite its pervasive impact, a significant proportion of individuals especially children remain unaware that they suffer from OSA. Consequently, there is an urgent need for an accessible diagnostic approach. In this study, we conducted a bioinformatic analysis to identify potential biomarkers from a proteomics dataset comprising serum samples from children with OSA in the progression stage. In the Gene Set Enrichment Analysis (GSEA), we observed that the complement and immune response pathways persisted throughout the development of OSA and could be detected in the early stages. Subsequent to soft clustering and WGCNA analysis, it was revealed that the Hippo pathway, including ITGAL and FERMT3, plays a role in mild OSA. The analysis revealed a significant alteration of the complement and coagulation pathways, including TFPI and MLB2, in moderate OSA. In severe OSA, there was an association between hypoxia and the extracellular matrix (ECM) receptor interaction and collagen binding. In summary, it can be posited that the systemic inflammation may persist throughout the progression of OSA. Furthermore, severe OSA is characterized by abnormal vascular endothelial function, which may be attributed to chronic hypoxia. Finally, four potential biomarkers (ITGAL, TFPI, TTR, ANTXR1) were identified based on LASSO regression, and a prediction model for OSA progression was constructed based on the biomarkers.

Multicenter comparative study of polysomnography outcomes in children with the monogenic disorder sickle cell disease.

Sleep-disordered breathing (SDB) is prevalent in children with sickle cell disease (SCD) and is associated with worse outcomes. This study aims to compare the outcomes of polysomnography (PSG) performed for pediatric patients with SCD at three United States centers. We included children with SCD aged 0-21 who underwent PSG at three American Academy of Sleep Medicine accredited centers: the University of Alabama at Birmingham (UAB), the University of Florida (UF), and Duke University Hospital (DUH), between 2012 and 2022. Descriptive statistics were used as appropriate to compare the baseline characters and PSG outcomes among the different centers. A total of 210 children with SCD from the three centers were included, with comparable sex, SCD genotypes, hemoglobin, hematocrit levels, and chronic transfusion. Children from the different centers exhibited variations in age (P < .001), BMI (P < .05), mean corpuscular volume (P < .05), and hydroxyurea use (P < .05) at the time of the PSG. Overall, the three centers showed significantly different PSG outcomes. Patients from UF had worse obstructive sleep apnea, oxygenation, and periodic leg movement events, together with lower hydroxyurea usage. While those from DUH showed higher hypoventilation and arousal indices. This multicenter study underscores variations in PSG outcomes among pediatric SCD patients at different centers in the Southeast United States. These findings emphasize the need for standardized approaches to screen for SDB, refer to PSG, and interpret the results in children with SCD. These conclusions may apply to other genetic disorders associated with an increased risk of sleep-disordered breathing.

Machine-learning-based classification of obstructive sleep apnea using 19-channel sleep EEG data

ObjectiveThis study aimed to investigate the neurophysiological effects of obstructive sleep apnea (OSA) using multi-channel sleep electroencephalography (EEG) through machine learning methods encompassing various analysis methodologies including power spectral analysis, network analysis, and microstate analysis. MethodsTwenty participants with apnea-hypopnea index (AHI) ≥ 15 and 18 participants with AHI <15 were recruited. Overnight polysomnography was conducted concurrently with 19-channel EEG. Preprocessed EEG data underwent computation of relative spectral power. A weighted network based on graph theory was generated; and indices of strength, path length, eigenvector centrality, and clustering coefficient were calculated. Microstate analysis was conducted to derive four topographic maps. Machine learning techniques were employed to assess EEG features capable of differentiating two groups. ResultsAmong 71 features that showed significant differences between the two groups, seven exhibited good classification performance, achieving 88.3 % accuracy, 92 % sensitivity, and 84 % specificity. These features were power at C4 theta, P3 theta, P4 theta, and F8 gamma during NREM1 sleep and at Pz gamma during REM sleep from power spectral analysis; eigenvector centrality at F7 gamma during REM sleep from network analysis; and duration of microstate 4 during NREM2 sleep from microstate analysis. These seven EEG features were significantly correlated with polysomnographic parameters reflecting the severity of OSA. ConclusionsThe application of machine learning techniques and various EEG analytical methods resulted in a model that showed good performance in classifying moderate to severe OSA and highlights the potential of EEG to serve as a biomarker of functional changes in OSA.

Prognostic effect of obstructive sleep apnea in acute coronary syndrome patients with heart failure

Background and objectiveAcute coronary syndrome (ACS), heart failure (HF) and obstructive sleep apnea (OSA) often overlap and interact, the impact of OSA on ACS patients with HF remains unclear. The study sought to comprehensively evaluate the effects of the interaction between OSA and HF on long-term cardiovascular outcomes in ACS patients. MethodsBetween June 2015 and January 2020, patients hospitalized for ACS were prospectively enrolled and underwent portable sleep monitoring after clinically stabilization. OSA was defined as an apnea hypopnea index ≥15 events/h. HF was defined using medical records. The primary endpoint was major adverse cardiovascular and cerebrovascular event (MACCE), including death, myocardial infarction, stroke, ischemia-driven revascularization, and hospitalization for unstable angina. ResultsAmong all 1927 included patients, 214 (11.1 %) had HF, and 1014 (52.6 %) had OSA. For 2.9 years (1.5, 3.6 years) follow-up, OSA was independently associated with the risk of MACCE in HF patients (adjusted hazard ratio [HR], 2.11; 95%CI, 1.16–3.84; P = 0.014), but not in those without HF (adjusted HR, 1.15; 95%CI, 0.92–1.45; P = 0.228). Further analysis showed OSA exerted more prognostic effect in HF patients with preserved eject fraction (adjusted HR, 2.45; 95 % CI, 1.11–5.41; P = 0.027) than those with reduced eject fraction (adjusted HR, 1.62; 95 % CI, 0.63–4.20; P = 0.319). ConclusionsIn the settings of ACS, OSA was independently associated with poor prognosis in patients with concomitant HF especially those with persevered ejection fraction. Screening and treatment for OSA are highly recommended in ACS patients with HF. Clinical trial registrationURL: www.clinicaltrails.gov; Unique Identifier: NCT03362385.

Causal effects of obstructive sleep apnea on chronic kidney disease and renal function: a bidirectional Mendelian randomization study.

Observational studies have suggested an association between obstructive sleep apnea (OSA), chronic kidney disease (CKD), and renal function, and vice versa. However, the results from these studies are inconsistent. It remains unclear whether there are causal relationships and in which direction they might exist. We used a two-sample Mendelian randomization (MR) method to investigate the bidirectional causal relation between OSA and 7 renal function phenotypes [creatinine-based estimated glomerular filtration rate (eGFRcrea), cystatin C-based estimated glomerular filtration rate (eGFRcys), blood urea nitrogen (BUN), rapid progress to CKD, rapid decline of eGFR, urinary albumin to creatinine ratio (UACR) and CKD]. The genome-wide association study (GWAS) summary statistics of OSA were retrieved from FinnGen Consortium. The CKDGen consortium and UK Biobank provided GWAS summary data for renal function phenotypes. Participants in the GWAS were predominantly of European ancestry. Five MR methods, including inverse variance weighted (IVW), MR-Egger, simple mode, weighted median, and weighted mode were used to investigate the causal relationship. The IVW result was considered the primary outcome. Then, Cochran's Q test and MR-Egger were used to detect heterogeneity and pleiotropy. The leave-one-out analysis was used for testing the stability of MR results. RadialMR was used to identify outliers. Bonferroni correction was applied to test the strength of the causal relationships (p < 3.571 × 10-3). We failed to find any significant causal effect of OSA on renal function phenotypes. Conversely, when we examined the effects of renal function phenotypes on OSA, after removing outliers, we found a significant association between BUN and OSA using IVW method (OR: 2.079, 95% CI: 1.516-2.853; p = 5.72 × 10-6). This MR study found no causal effect of OSA on renal function in Europeans. However, genetically predicted increased BUN is associated with OSA development. These findings indicate that the relationship between OSA and renal function remains elusive and requires further investigation.

The Effect of Obstructive Sleep Apnea on Subclinical Target Organ Damage in Patients With Resistant Hypertension

IntroductionAmong all patients with hypertension, those with resistant hypertension (RH) have the highest rates of subclinical organ damage (SOD). The prevalence of obstructive sleep apnea (OSA) is high in RH patients, and it could contribute to SOD. We aimed to investigate how OSA and its treatment are related to SOD in a large cohort of RH patients. MethodsThis is an ancillary analysis to the SARAH study, a multicentre observational cohort aiming to evaluate the impact of OSA on RH. Individuals with RH who were undergoing a sleep study and have information on at least one of the SOD variables (vascular, cardiac or renal damage) were selected. Patients were followed-up for three years. ResultsIn total, 503 subjects were included. The participants were predominantly male, obese, and the median (IQR) apnea–hypopnea index (AHI) was 15.5 (7.90–31.5)events/h. No differences in the presence of vascular or cardiac damage were observed between OSA and non-OSA patients. A lower estimated glomerular filtration rate (eGFR) was observed in participants with OSA than in those without OSA, with an adjusted effect of −8.69mL/min/1.73m2 (−13.59, −3.79; p value<0.001). Kidney damage was also greater in subjects with OSA, with an adjusted OR (95% CI) of 1.77 (1.09, 2.87; p value=0.02). The eGFR showed a linear dose–response relationship with OSA severity. Among patients treated with CPAP, lower eGFR values were observed in noncompliant subjects. ConclusionsOSA could contribute to worsening renal function in patients with RH. No compliance with CPAP was associated with lower values of eGFR.