Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia/hypercapnia (IHC), affects predominantly obese individuals, and increases atherosclerosis risk. Since we and others have implicated gut microbiota and metabolites in atherogenesis, we dissected their contributions to OSA-induced atherosclerosis. Atherosclerotic lesions were compared between conventionally-reared specific pathogen free (SPF) and germ-free (GF) Apoe-/- mice following a high fat high cholesterol diet (HFHC), with and without IHC conditions. The fecal microbiota and metabolome were profiled using 16S rRNA gene amplicon sequencing and untargeted tandem mass spectrometry (LC-MS/MS) respectively. Phenotypic data showed that HFHC significantly increased atherosclerosis as compared to regular chow (RC) in both aorta and pulmonary artery (PA) of SPF mice. IHC exacerbated lesions in addition to HFHC. Differential abundance analysis of gut microbiota identified an enrichment of Akkermansiaceae and a depletion of Muribaculaceae (formerly S24-7) family members in the HFHC-IHC group. LC-MS/MS showed a dysregulation of bile acid profiles with taurocholic acid, taurodeoxycholic acid, and 12-ketodeoxycholic acid enriched in the HFHC-IHC group, long-chain N-acyl amides, and phosphatidylcholines. Interestingly, GF Apoe-/- mice markedly reduced atherosclerotic formation relative to SPF Apoe-/- mice in the aorta under HFHC/IHC conditions. In contrast, microbial colonization did not show a significant impact on the atherosclerotic progression in PA. In summary, this research demonstrated that (1) IHC acts cooperatively with HFHC to induce atherosclerosis; (2) gut microbiota modulate atherogenesis, induced by HFHC/IHC, in the aorta not in PA; (3) different analytical methods suggest that a specific imbalance between Akkermansiaceae and Muribaculaceae bacterial families mediate OSA-induced atherosclerosis; and (4) derived bile acids, such as deoxycholic acid and lithocholic acid, regulate atherosclerosis in OSA. The knowledge obtained provides novel insights into the potential therapeutic approaches to prevent and treat OSA-induced atherosclerosis.

To investigate the prevalence and clinical characteristics of primary aldosteronism (PA) in patients with hypertension and obstructive sleep apnoea (OSA) in a newly established cohort, given inconsistencies in previous studies and intolerance to drug washout in some cases.

A single-centre cross-sectional study enrolled 316 hypertensive patients diagnosed with OSA via polysomnography. All participants underwent PA screening, followed by confirmatory testing for positive cases. Patients with confirmed PA underwent further subtype diagnosis and were assigned to the OSA and PA group. Those unable to undergo antihypertensive drug washout but with a high clinical suspicion of PA were categorised into the OSA and suspected PA group.

Among 316 patients, 41 (13.0%) were PA. The prevalence was 4.8% in OSA alone, and 50.0% in OSA with hypokalaemia. Compared to the OSA group, the OSA and PA group had a lower proportion of current smokers, a longer duration of hypertension, lower serum triglycerides, lower serum potassium, higher plasma aldosterone concentration, urinary aldosterone excretion, and lower renin. Multivariable logistic regression showed that the diagnosis of PA in OSA patients was positively associated with hypertension duration, and negatively associated with serum potassium levels and smoking.

PA screening may be considered in patients with hypertension and OSA; however, given the relatively low prevalence in those with OSA alone, routine screening may not be cost-effective. In contrast, the presence of hypokalaemia was strongly associated with a higher prevalence of PA, suggesting that targeted screening is warranted in this subgroup.

Pediatric obstructive sleep apnea (OSA) involves repeated breathing interruptions during sleep and is linked to neurocognitive impairment and cardiovascular issues. Early diagnosis is crucial, but the current gold-standard -overnight polysomnography-is expensive, complex, and scarce, causing long wait times. This underscores the need for a more efficient screening tool for pediatric OSA.

This cross-sectional study recruited children aged 3-18 years referred for polysomnography for suspected OSA (2019-2024). Parents recorded 3-min videos of their children sleeping. Two blinded pediatric sleep physicians scored videos for OSA using clinical impressions and the Monash score. Inter-rater reliability was evaluated with Cohen's Kappa. Monash score's ability to predict OSA was evaluated with receiver operating characteristic (ROC) analysis.

109 children (median age: 7.2 years, 61 % male) participated, including 66 healthy children, 21 with Down syndrome, 9 with obesity, and 13 with autism. Inter-rater reliability was high for both Monash score severity and dichotomized Monash score (kappa 0.94 and 0.79, both p < 0.001), with strong agreement on clinician impression of OSA presence and severity (kappa 0.84 and 0.70, both p < 0.001). Inter-rater reliability was highest in healthy children, with no significant differences between groups. The Monash score effectively discriminated OSA presence (area under curve 0.99 (95 % CI: 0.98, 1.00), with excellent performance across groups.

Video assessments showed high inter-rater reliability for OSA presence and severity. Although videos are promising for OSA screening, further research comparing them to polysomnography is needed to confirm clinical validity.

Sleep-disordered breathing (SDB) is characterized by recurrent reductions or interruptions in airflow during sleep, termed hypopneas and apneas, respectively. SDB impairs sleep quality and is linked to substantive health issues including cardiovascular and metabolic disorders, as well as cognitive decline. Recent evidence suggests a link between gut microbiota (GM) composition and sleep apnea. Indeed, GM, a community of microorganisms residing in the gut, has emerged as a potential player in various diseases, and several studies have identified associations between sleep apnea and GM diversity along with shifts in bacterial populations. Additionally, the concept of "leaky gut," a compromised intestinal barrier with potentially increased inflammation, has emerged as another key player in the potential bidirectional relationship between GM and sleep apnea. One of the potential effectors could be extracellular vesicles (EVs) underlying gut-brain communication pathways that are relevant to sleep regulation and function. Thus, therapeutic implications afforded by targeting the GM or exosomes for sleep apnea management have surfaced as promising areas of research. This review explores current understanding of the relationship between GM, exosomes and sleep apnea, highlighting key research dynamics and potential mechanisms. A comprehensive review of the literature was conducted, focusing on studies investigating GM composition, intestinal barrier function and gut-brain communication in relation to sleep apnea.

To investigate the independent predictive value of insomnia for resistant hypertension (RH) in uncontrolled hypertensive patients with obstructive sleep apnea (OSA).

This prospective follow-up study enrolled 386 OSA patients with uncontrolled blood pressure (BP) using 1 or 2 classes of antihypertensive drugs visiting Sleep Medicine Center from April 2021 to August 2022. Information on demographic characteristics, comorbidities, BP control and classes of antihypertensive medication, sleep related symptoms and sleep parameters was collected. Insomnia was assessed using DSM-V criteria and the Insomnia Severity Index (ISI). RH incidence according to the BP control and classes of antihypertensive drugs data during the 5 months follow-up was collected. Logistic regression models were used to assess the association between insomnia and RH, adjusting for potential confounders.

After 5 months follow-up, 301 participants were included for final data analysis. Insomnia was prevalent in 23.9 % of the participants and was associated with a higher risk of RH (adjusted ORs around 2.0, all P < 0.05). Participants with clinical insomnia (ISI >14) had a 4-6 times higher risk of RH compared to those without insomnia. Insomnia treatment improved ISI score significantly, but didn't reduce the incidence of RH significantly. Effective insomnia treatment was associated with antihypertensive drugs reduction (OR, 5.57; 95 % CI, 1.24-25.01).

Insomnia is an independent predictor of RH in uncontrolled hypertensive patients with OSA. Addressing insomnia may be crucial for managing RH in this patient population.

This study aimed to investigate the effects of intermittent hypoxia (IH) on auditory thresholds, auditory brainstem response (ABR) latency, and neuronal activity in the auditory cortex using a novel recurrent airway obstruction device.

Twenty-four male Sprague-Dawley rats (300-350 g) were randomly assigned to experimental or control groups. A custom 3D-printed mask with one-way valves and a ventilation system was used to induce IH in the experimental group via periodic airflow cessation. The control group wore the same apparatus without hypoxic exposure. Blood oxygen saturation was continuously monitored using a pulse oximeter. A three-dimensional gas dynamics model was constructed to validate the oxygen and carbon dioxide dynamics within the mask. After 3 h of exposure, ABR and the spontaneous firing rate (SFR) of auditory cortical neurons were recorded.

The experimental group showed periodic desaturation, with minimum and maximum oxygen saturation values of 80.19 ± 0.34 % and 97.68 ± 0.31 %, respectively. ABR thresholds at 24 and 32 kHz significantly increased to 19.17 ± 1.54 dB and 25.00 ± 1.83 dB (P<0.05). ABR wave III-V latency at 32 kHz was significantly shortened from 2.79 ± 0.17 ms to 2.27 ± 0.16 ms (P<0.05). Additionally, the SFR of auditory cortical neurons increased to 2.67 ± 0.18 Hz in the experimental group versus 1.02 ± 0.11 Hz in controls (P<0.01).

Short-term IH induces high-frequency hearing loss, reduces ABR latency, and enhances cortical neuronal excitability, implicating both peripheral and central auditory pathways.

Keratoconus (KC) is a multifactorial disease characterized by progressive corneal thinning and structural deformation. Despite being an ophthalmological disorder, KC is proposed to have systemic implications. The aim of this study was to evaluate cardiac functions in KC patients by two-dimensional (2D) speckle-tracking echocardiography (STE) and three-dimensional (3D) echocardiography.

The study included 45 consecutive patients with KC (mean age: 37.6 ± 12.6 years, 23 male) and 42 healthy controls (mean age: 38.1 ± 8.6 years, 23 male). All participants underwent standard transthoracic echocardiography, 3D echocardiography, and 2D STE to evaluate cardiac functions.

Although there were no significant differences in the conventional echocardiographic markers regarding left ventricular (LV) and right ventricular (RV) functions except tricuspid annular plane systolic excursion; patients with KC had significantly lower LV global longitudinal strain (GLS) compared to controls (-17.75 ± 2.43% vs. -19.71 ± 1.97%, p < 0.001). They also had lower RV GLS, left and right atrial reservoir, and conduit strains, although the differences were not statistically significant. LV GLS negatively correlated with corneal densitometry in KC patients. Linear regression analysis showed that KC was independently associated with LV GLS when adjusted for age and sex.

Patients with KC had significantly lower LV GLS, suggesting the presence of a subclinical LV dysfunction in these patients, which supports that KC may be a component of a systemic disease.

Obstructive sleep apnea (OSA), is associated with dysfunction in the cardiovascular, metabolic and neurological systems. However, the relationship between OSA and memory impairment, intervention effects, and underlying pathways are not well understood. This review summarizes recent advances in the clinical characterization, treatment strategies, and mechanisms of OSA-induced memory impairments. OSA patients may exhibit significant memory declines, including impairments in working memory from visual and verbal sources. The underlying mechanisms behind OSA-related memory impairment are complex and multifactorial with poorly understood aspects that require further investigation. Neuroinflammation, oxidative stress, neuronal damage, synaptic plasticity, and blood-brain barrier dysfunction, as observed under exposures to intermittent hypoxia and sleep fragmentation are likely contributors to learning and memory dysfunction. Continuous positive airway pressure treatment can provide remarkable relief from memory impairment in OSA patients. Other treatments are emerging but need to be rigorously evaluated for cognitive improvement. Clinically, reliable and objective diagnostic tools are necessary for accurate diagnosis and clinical characterization of cognitive impairments in OSA patients. The complex links between gut-brain axis, epigenetic landscape, genetic susceptibility, and OSA-induced memory impairments suggest new directions for research. Characterization of clinical phenotypic clusters can facilitate advances in precision medicine to predict and treat OSA-related memory deficits.

Obstructive sleep apnea (OSA) is a common sleep disorder associated with repetitive episodes of nocturnal intermittent hypoxia (IH), obesity and elevated leptin. Newly diagnosed OSA patients have a history of significant recent weight gain. While IH is implicated in OSA pathophysiology, the factors contributing to weight gain in OSA are not completely understood. Leptin is an adipokine with a central role in energy homeostasis and appetite control. Increases in leptin suppress appetite, while decreases in leptin increase appetite and may consequently cause weight gain. Using an in vitro approach, we examined the role of acute and chronic IH exposure on leptin secretion in differentiated human white preadipocytes. We show that acute 24-h exposure to IH and sustained hypoxia both increased leptin secretion, compared to normoxic controls (p = 0.01). In contrast, chronic repetitive IH exposure for 7 days decreased leptin secretion, compared to normoxic controls (p = 0.02). The decrease in leptin secretion during chronic IH exposure suggests a mechanism which may contribute to increased appetite and thereby predispose patients with untreated OSA to weight gain and obesity in early stages. As obesity progresses, leptin levels likely rise secondary to the increase in body fat. Elevated leptin levels in patients with longstanding OSA may be indicative of increased fat mass and not a consequence of IH-mediated effects on adipocytes.

Characterized by intermittent hypoxia (IH), sleep fragmentation, and enhanced sympathetic nervous system activity, obstructive sleep apnea (OSA) precipitates oxidative stress, systemic inflammation, and metabolic perturbations. These disturbances manifest as alterations in serum uric acid (SUA) and high-density lipoprotein cholesterol (HDL-C) levels. Recently, the ratio of SUA to HDL-C (UHR) has emerged as a potential biomarker reflecting both inflammatory and metabolic status. This study investigates the association between UHR and OSA.

Using a cross-sectional design, data were extracted from adults aged 20 years and older in the National Health and Nutrition Examination Survey (NHANES) database, covering the period from 2015 to March 2020. OSA was determined via the NHANES Sleep Disorders Questionnaire. The investigation employed weighted logistic regression alongside trend tests to evaluate the relationship between UHR and OSA. Nonlinear relationships were examined with restricted cubic spline analysis and threshold effect analysis. Receiver operating characteristic (ROC) curves were utilized to compare the predictive capacities of UHR, SUA, and HDL-C for OSA, with the area under the curve (AUC) calculated to assess the models' predictive accuracy. In addition, mediation analyses were conducted to explore the role of body mass index (BMI) in this association, and sensitivity analyses confirmed the robustness of the findings. Subgroup analyses further assessed the impact of various covariates.

Among the 9985 adults included, 4906 were identified as individuals with OSA. A positive association between UHR and the risk of OSA was observed (OR = 1.02; 95% CI: 1.01, 1.04; P = 0.014). Moreover, a nonlinear relationship was confirmed (P for nonlinearity = 0.024), with an inflection point at a UHR level of 10.23. UHR demonstrated greater predictive accuracy for OSA (AUC = 0.591) compared to SUA (AUC = 0.568) and HDL-C (AUC = 0.580). Additionally, BMI was found to partially mediate the relationship between UHR and OSA, with a mediation proportion of 61.99%. This association remained significant within specific subpopulations (P < 0.05) and was further modulated by factors such as age, alcohol consumption, and diabetes status (P for interaction < 0.05). Sensitivity analyses underscored the stability of these results.

UHR is positively correlated with the risk of OSA in adults, with BMI serving as a partial mediator. The findings support UHR as a viable biomarker for early detection and risk assessment in patients with OSA. Strategies focusing on weight management may reduce the risk of OSA among individuals with elevated UHR levels.

Pulmonary hypertension (PH) is a common cardiovascular complication of obstructive sleep apnea (OSA), posing a significant threat to the health and life of patients with OSA. However, no clinical prediction model is currently available to evaluate the risk of PH in OSA patients. This study aimed to develop and validate a nomogram for predicting PH risk in OSA patients.

We collected medical records of OSA patients diagnosed by polysomnography (PSG) from January 2016 to June 2024. Transthoracic echocardiography (TTE) was performed to evaluate PH. A total of 511 OSA patients were randomly divided into training and validation sets for model development and validation. Potential predictive factors were initially screened using univariate logistic regression and Lasso regression. Independent predictive factors for PH risk were identified via multivariate logistic regression, and a nomogram model was constructed. Model performance was assessed in terms of discrimination, calibration, and clinical applicability.

Eight independent predictive factors were identified: age, recent pulmonary infection, coronary atherosclerotic heart disease (CHD), apnea-hypopnea index (AHI), mean arterial oxygen saturation (MSaO2), lowest arterial oxygen saturation (LSaO2), alpha-hydroxybutyrate dehydrogenase (α-HBDH), and fibrinogen (FIB). The nomogram model demonstrated good discriminative ability (AUC = 0.867 in the training set, AUC = 0.849 in the validation set). Calibration curves and decision curve analysis (DCA) also indicated good performance. Based on this model, a web-based nomogram tool was developed.

We developed and validated a stable and practical web-based nomogram for predicting the probability of PH in OSA patients, aiding clinicians in identifying high-risk patients for early diagnosis and treatment.

A tendency to obstruct the upper airway is markedly increased in supine sleep. Positional obstructive sleep apnea (OSA) (POSA) occurs predominantly in the supine position. The implication of POSA in terms of future cardiovascular (CV) risk is unknown. We hypothesized that patients with POSA have decreased future CV risks compared to OSA patients without POSA (non-POSA).

This single-center study included patients who underwent clinically indicated polysomnography. POSA was defined as an apnea-hypopnea index (AHI) ≥ 5 events/hour and supine AHI at least twice as high as non-supine AHI (nsAHI). Exclusive POSA (ePOSA) includes the additional requirement that the nsAHI normalizes to an AHI of < 5/hour. A Cox proportional hazard model was used to assess the future risk of new CV events in patients with POSA compared to non-POSA (reference group).

There were 3,779 patients (mean age 51, female 59.7%), consisting of 35.9% POSA, 38.4% non-POSA, and 25.7% no OSA. Using the ePOSA definition, 17.3% had ePOSA, 57.1% had non-ePOSA, and 25.7% had no OSA. Over a median 8.4 years, there were 1,297 composite events. Patients with POSA had a lower risk of CV events compared to non-POSA (HR 0.85, CI:0.74-0.96; p = 0.010). There was a non-significant trend towards lower risk of CV events in patients with ePOSA compared to non-ePOSA (HR 0.86, CI:0.73-1.01; p = 0.061).

POSA is associated with lower CV risk than non-POSA. Future studies should consider POSA as a distinct subtype when studying OSA and CV outcomes.

To determine the influence of type D personality on the prevalence of cardiovascular diseases (CVD), anxiety, depression, sleep quality and insomnia in OSA patients.

Patients planned for a polysomnography filled out the DS-14 questionnaire, Hospital Anxiety and Depression Scale (HADS), Insomnia Severity Index (ISI) and Pittsburgh Sleep Quality Index (PSQI). History of cardiovascular diseases and current medication intake were assessed.

In a cohort of 948, OSA patients with type D personality did not have CVD more often (40%) compared to OSA patients without type D personality (42%) (P = 0.625). Out of 395 patients with OSA and CVD, 70% were treated for isolated arterial hypertension (AHT) and 30% for cerebrovascular and/or cardiac pathologies. Cerebrovascular and/or cardiac pathologies were significantly more prevalent in OSA patients with type D personality vs. without (39% vs. 26%; P = 0.001). In OSA patients with CVD and type D personality, medication intake was significantly higher (> 2 cardiovascular medications (P = 0.009), anxiolytics (P = 0.001), antidepressants (P = 0.011), sleep medication (P = 0.002)) as well as scores of HADS for anxiety (P < 0.0001) and depression (P < 0.0001), ISI (P = < 0.0001) and PSQI (P < 0.0001).

The prevalence of CVD in OSA patients was not related to the presence of type D personality. Apart from arterial hypertension, cerebrovascular and/or cardiac pathologies were more frequently observed in OSA patients with type D personality. In OSA patients with CVD, the presence of type D personality was associated with more depression, anxiety, insomnia, poor sleep quality and more medication intake.

Purpose: The relationship between regional fat and obstructive sleep apnea (OSA) remains poorly understood. This study seeks to explore the link between regional fat and OSA, utilizing data from the National Health and Nutrition Examination Survey (NHANES). Methods: This cross-sectional analysis used NHANES 2015-2018 data. OSA symptoms were assessed through sleep questionnaires. Regional fat mass (FM) was measured using dual-energy X-ray absorptiometry, including trunk, arm, leg, android, gynoid, and abdominal FM. The fat mass index (FMI) was calculated by dividing FM by the square of height. Logistic regression evaluated the association between regional FMI and OSA, with univariate and stratified analyses to identify potential effect modifiers. Results: A total of 3,099 participants were included, with 1,595 classified into the OSA group. Significant associations were found between OSA and several regional FMIs, including trunk, arm, leg, android, gynoid, and abdomen. These associations were consistent in males, and in females, leg and gynoid FMI were not linked to OSA. Stratified analyses by race revealed significant associations between OSA and regional FMI indices (trunk, arm, leg, android, gynoid, and abdominal FMI) in non-Hispanic Whites and between OSA and trunk, android, and abdominal FMI in other Hispanics. No associations were observed in the Mexican American or non-Hispanic Black groups. Stratification by body mass index (BMI) indicated distinct profiles: obese individuals (BMI ≥30) showed associations limited to trunk, arm, android, and abdominal FMIs, while nonobese participants (BMI <30) displayed broader associations encompassing all regional FMIs. Both univariate and stratified analyses highlighted abdominal FMI as the strongest predictor of OSA. Conclusion: Higher regional FMI, particularly abdominal fat, is associated with an increased risk of OSA, with stronger associations observed in male, White, and nonobese populations.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with heart failure (HF), independent of shared risk factors. Our aim was to describe the incidence of HF in patients with biopsy-proven MASLD.

We followed patients with biopsy-proven MASLD from the prospective Duke NAFLD Biorepository and Clinical Database from liver biopsy (2007-2013) until death or 5 January 2023. Clinical and echocardiographic data were abstracted via manual chart review. Incident HF was defined as one of the following: (1) hospitalization for HF, (2) medical record diagnosis of HF, (3) ≥1 sign/symptom of HF and elevated natriuretic peptide, or (4) diastolic dysfunction on transthoracic echocardiography with ≥1 sign/symptom of HF. Univariable and multivariable logistic regression models were evaluated. Overall, 570 patients with biopsy-proven MASLD were included. The mean age was 49.5 years, 42.5% were male and 87.0% were non-Hispanic White. Ten patients (1.8%) had baseline HF, leaving 560 patients to assess for incident HF. Over a median follow up of 4009 days (11.0 years) (interquartile range 2270-4672 days), 100 (17.9%) patients developed incident HF while 268 (47.9%) met criteria for HF suspicion. In a multivariable model, increasing age (odds ratio [OR] 1.05, 95% confidence interval [CI] 1.02-1.08, p < 0.001) and female sex (OR 1.85, 95% CI 1.12-3.04, p = 0.02) were associated with incident HF.

We found a high incidence of HF in patients with biopsy-proven MASLD. Despite nearly half of patients having suspected HF, very few carried a chart diagnosis. Screening for HF in high-risk patients and establishment of formal care pathways to address early HF may reduce morbidity and mortality.

Obstructive sleep apnea (OSA) impacts approximately 70% of stroke patients, often causing fatigue and sleepiness. Although continuous positive airway pressure (CPAP) reduces sleepiness, systematic OSA screening is not standard in post-stroke care, and the effect of untreated OSA on fatigue is unclear. This study investigated changes in sleepiness and fatigue among OSA patients following ischemic stroke or transient ischemic attack (TIA) who underwent CPAP treatment.

This prospective multi-center cohort study, ischemic stroke and TIA patients were screened for OSA using respiratory polygraphy. CPAP-eligible patients (Apnea-Hypopnea Index ≥15) were assessed with the Epworth Sleepiness Scale (ESS) and Visual Analogue Scale-Fatigue (VAS-F) at baseline and seven to eight months post-stroke. CPAP compliance was classified into high (≥70%), moderate (50-69%), and low (<50%) compliance based on nights using CPAP more than four hours per night. Poisson regression models analyzed differences in ESS and VAS-F between compliance groups, with low-compliance as the reference.

Of 2605 patients, 1518 (mean age: 70 ± 12 years; 61% male) were screened, and 648 were CPAP-eligible. At follow-up, 333 patients were assessed (49% lost to follow-up). Sleepiness significantly decreased in the high-compliance group compared to low-compliance (p<0.001). Fatigue levels decreased across all compliance groups, b no differences were observed between groups.

High CPAP compliance in post-stroke or TIA patients with OSA was associated with a reduction in sleepiness but not fatigue. These findings support the recommendation to systematically screen post-stroke patients for OSA and encourage CPAP compliance to mitigate sleepiness.

Currently, beta-blockers are recommended for non-ST elevation acute coronary syndrome (NSTE-ACS). However, there is still a lack of studies evaluating the use of beta-blockers in patients with NSTE-ACS complicated by obstructive sleep apnea (OSA).

This is the sub-analysis of OSA-ACS project (NCT03362385), a prospective, observational study recruited ACS patients undergoing portable sleep monitoring between June 2015 and January 2020. Patients with NSTE-ACS were selected in this analysis. The primary endpoint was major adverse cardiovascular events (MACE), including cardiovascular death, myocardial infarction or ischemia-driven revascularization.

After exclusion, 1452 NSTE-ACS patients were enrolled, and 75.3 % of patients received beta-blockers at discharge. The proportion of beta-blockers users in the OSA group was 77.4 % and 73.2 % in the non-OSA group, with no significant difference (P = 0.068). In OSA group, beta-blocker users had higher rate of MACE (18.2 % versus 9.0 %, adjusted hazard ratio [HR] 1.90, 95 % confidence interval [CI] 1.04-3.45, p = 0.037) but not in non-OSA group (14.1 % versus 9.9 %, adjusted HR 1.45, 95 % CI 0.80-2.62, p = 0.219). After propensity score matching, beta-blocker users were still at higher risk of MACE (19.3 % versus 9.3 %, adjusted HR 2.18, 95 % CI 1.09-4.35, p = 0.028) in OSA group, in contrast the risk was comparable in non-OSA group (13.2 % versus 9.9 %, adjusted HR 1.27, 95 % CI 0.63-2.57, p = 0.501). Sensitivity analysis was consistent with the main results. Subgroup analysis showed no significant interactions (P > 0.10, for all comparisons).

The administration of beta-blockers is associated with higher risk of adverse cardiovascular outcomes in NSTE-ACS patients with concomitant 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.

Background and Objectives: The association between syncope and sleep apnea (SA) has been scarcely investigated. Dysfunction of the autonomic nervous system (ANS) may represent a shared pathophysiological mechanism. This study aimed to determine the prevalence of SA in patients with syncope of unclear cause (SUC), identify potential associated factors, and evaluate nocturnal heart rate variability (HRV) as a marker of ANS function. Materials and Methods: A prospective cohort study was conducted in adult patients diagnosed with SUC. Nocturnal cardiorespiratory polygraphy was performed to detect the presence of SA. A range of variables potentially associated with SA was collected. Both SA diagnosis and HRV parameters were assessed using the Embletta® MPR polygraph system. Results: A total of 156 patients were enrolled (57% male), with a mean age of 64 years and a mean body mass index of 27.5 kg/m2 (range: 24.8-32.2). Hypertension was present in 46% of the cohort. The overall prevalence of SA was 78.2% (95% CI: 71.7-84.4%), with 28.7% classified as severe. Age (OR = 1.04; 95% CI: 1.01-1.07) and BMI (OR = 1.17; 95% CI: 1.06-1.28) were independent predictors of SA. Mean RR interval was significantly lower in patients with SA compared to those without (942 ms vs. 995 ms; p = 0.04). No significant differences in HRV parameters were observed between the two groups. Conclusions: This study found a high prevalence (nearly 78%) of SA among adult patients with SUC, particularly in individuals over 50 years of age and those who were overweight. However, this association could not be predicted based on clinical variables alone. No significant differences in nocturnal HRV were detected between patients with SUC with and without SA.

Multilevel upper airway surgery is effective for some patients with obstructive sleep apnea (OSA), but predicting the response to surgery remains a challenge. The underlying endotypes of OSA include upper airway collapsibility, muscle compensation, loop gain, and the arousal threshold. This study aimed to explore the effect of surgery on polysomnography (PSG)-derived OSA endotypes and establish a surgical response prediction model.

Our study included 54 Chinese patients with OSA who underwent multilevel upper airway surgery. Participants underwent PSG before and after surgery with a median follow-up time of 6.5 months. Using AHIBaseline/AHIpost-surgery ≥ 2 and AHIpost-surgery < 10 events/h as criteria, participants were classified as surgery responders and non-responders. The surgical success rate was 26%. These endotypic traits were derived from a standard PSG data by validated methods.

The surgery altered both anatomical and non-anatomical endotypic traits, including increased Vpassive (baseline vs post-surgery: 51.5 [18.7-84.2] vs 86.8 [67.4-93.7] %Veupnea, p < .001), decreased loop gain (baseline vs post-surgery: 0.7 [0.7-0.8] vs 0.6 [0.5-0.6]; p < .001), and a higher arousal threshold (baseline vs post-surgery: 202.9 [183.7-222.0] vs 160.7 [143.9-177.4] %Veupnea; p < .001). However, it did not significantly affect muscle compensation. Fully adjusted logistic regression analyses indicated that a favorable response to surgery was independently associated with a lower LG (OR [CI 95%], 0.1 [0.0-0.5], p = .032). In patients with improved muscle compensation or a more collapsible airway (lower Vpassive), a lower loop gain was more strongly indicative of success. However, when muscle compensation was lower or collapsibility was less severe (higher Vpassive), a lower loop gain was less predictive of success.

This study demonstrated that multilevel upper airway surgery altered both anatomical and non-anatomical endotypes in Chinese patients with OSA. An endotype based regression model may meaningfully predict surgical success.

Sleep fragmentation (SF) and intermittent hypoxia (IH), hallmark features of obstructive sleep apnea (OSA), disrupt restorative processes by inducing sympathetic activation and endothelial dysfunction, contributing to cardiovascular risk. While IH has been extensively studied, the independent effects of SF remain underexplored. This study investigated the cardiovascular impact of chronic SF in a murine model mimicking moderate-to-severe OSA. Male C57BL/6J mice were exposed to chronic SF or control conditions for 12 weeks. Mean blood pressure (MBP), cardiac function, pulse wave velocity (PWV), and coronary flow velocity reserve (CFVR) were assessed. Endothelium-dependent relaxation in aortic and coronary vessels was examined ex vivo, and aortic histological analysis evaluated intima-to-media thickness and collagen content. SF significantly elevated MBP (107 ± 8 mmHg vs. 89 ± 5 mmHg; p = 0.0001) and PWV (4.3 ± 0.6 m/s vs. 3.1 ± 0.2 m/s; p = 0.0001), indicating hypertension and arterial stiffness. Endothelium-dependent relaxation was impaired in coronary (67 ± 9 % vs. 86 ± 5 %; p = 0.0004) and aortic (73 ± 12 % vs. 87 ± 7 %; p = 0.045) vessels. Histology revealed increased intima-to-media thickness (128 ± 9 μm vs. 102 ± 14 μm; p = 0.008) and collagen deposition (56 ± 10 μm vs. 41 ± 7 μm; p = 0.027). Cardiac function and CFVR were unaffected. Chronic SF independently drives cardiovascular dysfunction through hypertension, arterial stiffness, endothelial impairment, and vascular remodeling. These findings emphasize SF as a distinct pathological factor in OSA, necessitating adjunctive interventions to mitigate cardiovascular risks.

Obstructive sleep apnea (OSA) is common in type 2 diabetes mellitus (T2DM), but its association with cardiac structure and function in advanced diabetic kidney disease (DKD) remains unclear.

T2DM patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 and albuminuria were assessed for OSA using the apnea-hypopnea index (AHI). Cardiac structure and function were assessed by transthoracic echocardiography following standard guidelines. 39 patients without OSA (AHI < 5) were compared to 34 patients with moderate-severe OSA (AHI ≥ 15).

Mean age was 71.4 ± 9.4 years (73 % male), and eGFR was 32.1 ± 12.3 mL/min/1.73 m2. DKD patients with moderate-severe OSA had a higher left atrial volume index (LAVI: 36.6 ± 13.9 vs. 28.1 ± 10.5 mL/m2, p < 0.01) left ventricular mass index (LVMI: 48.8 ± 11.7 vs. 41.8 ± 9.7 g/m2.7, p < 0.01) and right ventricular diameter (RVD: 34.1 ± 5.8 vs. 28.4 ± 4.4 mm, p < 0.001) than DKD patients without OSA. Left ventricular ejection fraction (LVEF) did not differ, but global longitudinal strain (GLS) was reduced (-15.1 ± 3.0 vs. -16.6 ± 2.8 %, p < 0.05). In multivariable linear regression analyses, moderate-severe OSA remained significantly associated with LAVI, LVMI, RVD, and GLS but not with LVEF.

Moderate-severe OSA is associated with cardiac hypertrophy and chamber dilatation, potentially contributing to cardiovascular risk in advanced DKD.

China bears the highest global burden of obstructive sleep apnea (OSA), yet its spatiotemporal and occupational patterns remain unclear. We quantified OSA prevalence across Chinese subpopulations, focusing on geographic disparities, temporal trends, and occupational risks.

Following PRISMA guidelines, we systematically searched six databases (2000-2024) for population-based OSA studies using polysomnography or validated portable monitoring. Two researchers independently screened studies with third-party adjudication of discrepancies. Risk of bias was assessed using Joanna Briggs Institute criteria. Random-effects models pooled prevalence estimates; meta-regression identified heterogeneity contributors. OSA diagnosis followed 2012 AASM criteria (AHI ≥5; pediatric studies: OAHI ≥1.5).

From 62 studies (N=178,049), pooled OSA prevalence was 11.8% (95% CI:10.1-13.4%), rising from 8.1% (2000-2005) to 26.9% (2021-2024). Prevalence was higher in males vs females (11.1% vs 6.0%, P<0.001), with marked geographic disparities: Northwest China had the highest prevalence (17.8%, 16.3-19.3%) versus Southwest (6.9%, 3.7-10.9%). Drivers exhibited the highest occupational risk (15.3%). Low-quality studies overestimated prevalence (15.0% vs 7.6-10.2% in higher-quality studies), and two-step sampling yielded higher estimates than single-risk-group designs (13.6% vs 7.4%, P<0.001). Meta-regression identified survey period (β=0.036, P=0.025), male sex (β=-0.062, P=0.047), geographic area (β=0.268, P=0.035), occupation (β=0.254, P=0.047), and sampling strategy (β=-0.029, P=0.012) as key predictors of heterogeneity.

OSA prevalence in China has accelerated significantly. Standardized screening is urgently needed for aging populations, high-risk occupations (particularly drivers), and underserved regions. Policy priorities should address rural diagnostic inequities and integrate OSA surveillance into public health programs. Methodological harmonization is critical for tracking OSA's evolving burden.

Osteoarthritis (OA) is the most common joint disease, leading to pain and inflammation, two risk factors for sleep apnea (SA). We aimed to examine whether OA may increase the risk of incident SA, a common source of mortality and sudden death.

Using data from the IQVIA Medical Research Database, we conducted three cohort studies (i.e., knee, hip, and hand cohort) among individuals aged 50 years or older. For each patient with incident OA, up to five non-OA individuals were matched by age, sex, entry-time, and BMI. We calculated the incidence rate of SA for the OA and non-OA cohorts, respectively, and examined the relation of OA to the risk of incident SA using a Cox proportional hazard model adjusting for potential confounders.

During the follow-up, 869 SA cases occurred in 58,674 patients with knee OA and 2,186 in 235,850 non-OA individuals (2.29 vs. 1.41/1000 person-years). Compared with the non-OA cohort, the multivariable-adjusted hazard ratio (HR) of SA in the knee OA cohort was 1.45 (95% confidence interval [CI]: 1.34-1.56). A higher risk of SA was also observed among patients with incident hip OA (adjusted HR: 1.45, 95%CI: 1.28-1.66) and hand OA (adjusted HR: 1.50, 95%CI: 1.26-1.78) than the matched non-OA individuals.

This general population-based study provides the first evidence that patients with knee, hip, and hand OA may have an increased risk of incident SA. Strategies aimed at screening, prevention, and treatment of SA could be developed to reduce the disease burden in OA patients.

Attention deficit hyperactivity disorder (ADHD) and Obstructive sleep apnea (OSA) are highly clinically co-occurring, but the mechanisms behind this remain unclear, so this article analyzes the reasons for the co-morbidities from a genetic perspective.

We examined the genetic architecture of ADHD and OSA based on the large genome-wide association studies (GWAS). The global genetic relationship between OSA and ADHD was explored. Cross-trait analysis from single nucleotide polymorphism (SNP) and gene level was performed subsequently to detect the crucial genomic regions. Finally, we revealed the anatomical change on which genetic overlap relies and further explored whether genetic factors exert a causal effect.

After using both linkage disequilibrium score regression (LDSC) and High-definition likelihood inference (HDL) methods, we identified a significant genetic correlation between OSA and ADHD (PLDSC = 2.45E-28, PHDL = 1.09E-25), demonstrating a consistent direction. Furthermore, through the application of various cross-trait methods, we pinpointed 5 loci and 57 genes involved in regulating the co-occurrence of these disorders. These genetic regions were thought to be associated with the prefrontal lobes (P = 3.07E-06) and the nucleus accumbens basal ganglia (P = 2.85E-06). Lastly, utilizing Mendelian randomization (MR), we established a link indicating that individuals with ADHD were at an elevated risk of developing OSA (PIVM = 0.02, OR (95%CI):1.09 (1.01-1.17)).

This study reveals a strong genetic correlation between ADHD and OSA. It offers insights for future drug target development and sleep management in ADHD.

Despite mounting evidence linking circular RNAs (circRNAs) to various diseases, their specific role in liver damage triggered by obstructive sleep apnea (OSA) remains ambiguous. This study investigates alterations in circRNA expression patterns in a mouse model subjected to chronic intermittent hypoxia (CIH), aiming to elucidate the pathways that lead to liver damage associated with OSA. We established the CIH model and conducted circRNA microarray analysis on liver samples from both CIH and control groups. The findings were substantiated via qRT-PCR. Furthermore, a comprehensive circRNA-miRNA-mRNA (ceRNA) network was developed, followed by the analysis of GO and KEGG pathways to further elucidate the underlying biological processes. We identified 259 differentially expressed circRNAs, comprising 86 that were upregulated and 173 that were downregulated in CIH mice. The ceRNA analysis suggested that these circRNAs may modulate gene expression by sequestering miRNAs. Our findings highlight potential therapeutic targets for liver pathologies associated with OSA.

Respiratory-event-associated hypoxia is crucial in cardiovascular comorbidities of obstructive sleep apnea (OSA). Intermittent hypoxia is an independent risk factor for atrial fibrillation (AF). The sleep breathing impairment index (SBII) is a novel metric that quantifies respiratory events and hypoxia, showing exceptional efficacy in predicting cardiovascular diseases. This study aims to evaluate the association between SBII and AF in OSA patients and compare the predictive performance of various OSA severity indices in predicting incident AF.

This study included 1660 OSA patients without pre-existing AF from the Sleep Heart Health Study. Baseline SBII values were stratified into quartiles. Multivariate logistic regression analysis and restricted cubic spline analysis were conducted to explore the association between SBII and incident AF. Harrell's concordance statistic (C-statistic) was performed to compare the predictive value of SBII against other OSA severity indices.

During a mean follow-up of 5.3 years, 190 (11.5 %) OSA patients developed AF. SBII and hypoxic burden (HB) were associated with an increased risk of incident AF, with adjusted odds ratios of 1.87 (95 %CI: 1.14, 3.11; P = 0.015) and 2.01 (95 %CI: 1.20, 3.41; P = 0.009) for the third and fourth quartiles of SBII, respectively, and 1.70 (95 %CI: 1.04, 2.81; P = 0.038) for the fourth quartile of HB. Moreover, SBII had the largest C-statistic (0.75, 95 % CI: 0.709, 0.782) compared with HB, AHI, and ODI.

This study demonstrated that elevated SBII and HB levels increased the risk of incident AF in OSA patients, with SBII outperforming other OSA severity indices in predicting AF.

Continuous positive airway pressure (CPAP) is the treatment of choice for obstructive sleep apnea; however, some people have residual respiratory events or require significantly higher CPAP pressure while on therapy. Our objective was to develop predictive models for CPAP outcomes and assess whether the inclusion of physiological traits enhances prediction.

We constructed predictive models from baseline information for subsequent residual apnea-hypopnea index and optimal CPAP pressure. We compared models utilizing clinical variables with those incorporating both clinical and physiological factors. Furthermore, we assessed the performance of regression vs machine learning. All performances, including root mean square error, R-squared, accuracy, and area under the curve, were evaluated using a 5-fold cross validation with 10 repeats.

For predicting residual apnea-hypopnea index, random forest models outperformed regression models, and models that incorporated both clinical and physiological variables also outperformed models using only clinical variables across all performance metrics. Random forest using both clinical features and physiological traits achieved the best performance. In both regression and random forest models, central apnea index is found to be the most important feature in predicting residual apnea-hypopnea index. For predicting CPAP pressure, there was no additional predictive value of physiological traits or random forest modeling.

Our findings demonstrated that the combined use of clinical and physiological variables yields the most robust predictive models for residual apnea-hypopnea index, with random forest models performing best. These findings support the notion that prediction of obstructive sleep apnea therapy outcomes may be improved by more flexible models using machine learning, potentially in combination with physiology-based models.

Lo J-E, Schmickl CN, Vaida F, et al. The combination of physiology and machine learning for prediction of CPAP pressure and residual AHI in OSA. J Clin Sleep Med. 2025;21(5):775-782.

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.

Obesity is a major risk factor in Obstructive sleep apnea (OSA), which is a prevalent disease that leads to significant morbidity. Multi-level Sleep Surgery (MLS) is a method of treatment for patients who cannot tolerate continuous positive airway pressure. Obesity has previously been identified as a risk factor that may decrease the success rate of MLS. The purpose of our study is to assess the success rates of MLS in obese patients.

A retrospective cohort study in 109 adults that underwent MLS in our institution. All the participants completed pre-operative and post-operative level 1 polysomnography. They were divided into four groups as per their body mass index (BMI): Normal (BMI < 25), overweight (25-30), obese (30-35), morbid obese (> 35) and the variables were compared. We measured the surgical success as defined by Sher Criteria (AHI drop > 50% from preoperative baseline and AHI < 20) and cure rates (AHI < 5).

The average BMI was 30.9 pre-op and 30.4 post-op. The mean AHI was 29.8 pre-op and decreased to 10.1 (p < 0.001) and the Epworth Sleepiness Scale from 12.9 to 4.8 (p < 0.001). There were 13, 31, 43, and 22 patients in normal, overweight, obese and morbidly obese groups, respectively. The surgical success rate as defined by Sher's criteria was 84%, 84%, 72%, and 77% in the respective groups, with no statistical difference (p = 0.662). Moreover, the cure rate was 77%, 45%, 44%, and 45%, with no statistical difference (p = 0.192). The AHI reduction was 9.93, 19.73, 21.1 and 22.8 in the respective groups. A linear regression analysis revealed no significant difference in assessing the surgical success and cure rates as BMI increases.

Data regarding MLS success rates on obese patients is scarce. The current study demonstrates that MLS can offer positive outcomes for this population. However, further studies are warranted to investigate this relationship.

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.

Poor sleep health is associated with cardiometabolic disease and related risk factors, including heart disease, stroke, elevated blood pressure and lipid levels, inflammation, glucose intolerance, obesity, physical inactivity, poor diet, unhealthy substance use, poor mental health, and increased all-cause and cardiovascular mortality, and is associated with social determinants of cardiovascular health and health disparities. Therefore, sleep duration has been recognized by the American Heart Association as one of Life's Essential 8. Although chronic sleep duration is the sole metric used in Life's Essential 8, sleep health represents a multidimensional construct. This scientific statement outlines the concept of multidimensional sleep health (sleep duration, continuity, timing, regularity, sleep-related daytime functioning, architecture, and absence of sleep disorders) as it applies to cardiometabolic health. Considerations of how these dimensions are related to cardiometabolic health and patterned by sociodemographic status are explained, and knowledge gaps are highlighted. Additional data are needed to understand better how these various dimensions of sleep should be assessed and how interventions targeting sleep health in clinical and community settings can be leveraged to improve health.

The atherogenic index of plasma (AIP) has been demonstrated as a predictor for cardiovascular disease (CVD) in various populations. However, there are quite limited studies on the association between AIP and incident CVD among adults with obstructive sleep apnea (OSA).

Data were obtained from the Sleep Heart Health Study, including 2578 participants with OSA and without pre-existing CVD. AIP was calculated as lg (triglycerides/high-density lipoprotein-cholesterol). Baseline AIP was stratified into quartiles (Q1-Q4). Multivariate logistic regression and restricted cubic spline analyses were performed to examine the relationship between AIP and CVD.

After a median follow-up of 11.67 years, 580 (22.50 %) OSA patients developed CVD, including 184 (7.10 %) with myocardial infarction (MI), and 400 (15.50 %) with coronary artery disease (CHD [including MI]), and 127 (4.90 %) with stroke. The multivariate logistic regression and restricted cubic spline analyses demonstrated a significant association between AIP and incidence of CVD, CHD, and MI, but not stroke. Compared with Q1 group, the fully adjusted odds ratios from Q2 group to Q4 group were: 1.33 (0.98, 1.80), 1.41 (1.03, 1.92), and 1.54 (1.12, 2.14) for CVD; 1.71 (1.04, 2.86), 1.92 (1.17, 3.21), and 2.01 (1.19, 3.45) for MI; 1.48 (1.04, 2.11), 1.68 (1.18, 2.40), and 1.70 (1.18, 2.47) for CHD.

This study demonstrated that higher AIP level is associated with incident CVD, except stroke, independent of OSA severity and hypoxia among OSA patients. These findings suggest that monitoring AIP can facilitate the early identification of OSA patients at high risk of CVD.

Obstructive Sleep Apnea (OSA) affects up to 70 % of post-stroke patients, complicating recovery and rehabilitation. This study aimed to evaluate the utility of the Odds Ratio Product (ORP), a continuous EEG-derived metric of sleep depth, in predicting conventional respiratory and arousal measures in stroke patients. We hypothesized that ORP metrics will predict conventional measures in patients with a history of stroke or Transient ischemic attack (TIA).

A retrospective analysis was conducted on 113 stroke/TIA individuals who underwent in-laboratory polysomnography (PSG). ORP metrics, including ORPnrem, ORPrem, ORP9, and Wake Intrusion Indices (WIIs), were analyzed using multivariate linear regression models. Models were stratified by OSA status. Standardized coefficients were used to assess associations with the apnea-hypopnea index (AHI), respiratory disturbance index (RDI), and arousal indices.

ORP metrics demonstrated statistically significant associations with conventional respiratory and arousal measures, with varying predictive strength across models. Specifically, ORPnrem and WIIs exhibited strong predictive effects across all models. ORP9 significantly predicted respiratory and arousal measures in the overall sample and the OSA subgroup, but its predictive value diminished in the non-OSA subgroup. ORPrem was statistically significantly associated with respiratory and arousal measures; however, its associations with arousal measures were weaker in participants with OSA compared to those without OSA.

ORP metrics have the potential to refine OSA diagnoses and improve therapeutic strategies in post-stroke/TIA populations. Their integration into sleep assessments could facilitate early intervention and potentially optimize stroke recovery outcomes, addressing gaps in current evaluation methods.

Evaluate the performance of the SANSA device to simultaneously assess obstructive sleep apnea and cardiac arrhythmias.

Participants suspected or known to have obstructive sleep apnea underwent polysomnography while wearing SANSA. SANSA's algorithm was trained using 86 records and tested on 67 to evaluate training bias. SANSA performance was evaluated against ground truth polysomnography scored by the consensus of 3 technologists. Polysomnography scoring from individual testing sites was also evaluated against consensus. Diagnostic performance was evaluated using standard apnea-hypopnea index cutoffs. Apnea-hypopnea index and total sleep time agreement was analyzed using correlation and Bland-Altman plots. Electrocardiogram was reviewed for presence of significant arrhythmias (frequent premature atrial/ventricular complexes and atrial fibrillation).

SANSA's sensitivity and specificity to detect obstructive sleep apnea ranged from 91-97% and 78-97%, respectively, across all severity levels. SANSA total sleep time correlation with consensus polysomnography total sleep time was 0.83 with a mean difference of 3.8 minutes (limits of agreement: -91.1 to 98.7). Significant arrhythmias were detected in 32% of participants. These participants had a greater apnea-hypopnea index (27.5 vs 15.8 events/h, P = .003) and spent nearly twice as long at reduced oxygenation levels (47.5 vs 20.5 minutes under 88% oxygen saturation, P = .009).

SANSA is a promising tool for comprehensive obstructive sleep apnea evaluation, offering the unique advantage of concurrent arrhythmia detection. This dual functionality may improve patient outcomes through early diagnosis and management of both conditions.

Goldstein C, Ghanbari H, Sharma S, et al. Multidiagnostic chest-worn patch to detect obstructive sleep apnea and cardiac arrhythmias. J Clin Sleep Med. 2025;21(5):855-866.

α1-Antitrypsin deficiency is a disease characterized by increased neutrophil elastase activity leading to tissue getting less elastic and robust. It is known that if tissue in the pharynx becomes less elastic and robust, it could contribute to obstructive sleep apnea. This paper seeks to investigate whether patients with α1-antitrypsin deficiency have an increased risk of sleep apnea.

We tested this hypothesis by doing a nationwide cohort study of 2702 individuals diagnosed with α1-antitrypsin deficiency compared with 26,750 individuals without α1-antitrypsin deficiency matched on sex, age, and municipality. All individuals were followed from birth and were censored at the time of outcome, emigration, death, or end of follow-up 31st of December 2018, whichever came first.

Individuals with α1-antitrypsin deficiency had a higher risk of sleep apnea with an adjusted hazard ratio of 1.81 (95% CI 1.36-2.40) compared to controls without α1-antitrypsin deficiency. Similarly, the risk of obstructive sleep apnea was nominally higher in individuals with α1-antitrypsin deficiency compared to controls without the disease (1.47, 95% CI 0.95-2.28). In stratified analysis, the risk of sleep apnea was higher in individuals without chronic obstructive pulmonary disease (2.33, 95% CI 1.54-3.51) (P for interaction < 0.05). The increased risk of SA was unaffected when the analysis was stratified by ischemic heart disease, ischemic cerebrovascular disease, type 2 diabetes, hypertension, and liver cirrhosis.

Individuals with α1-antitrypsin deficiency have a higher risk of sleep apnea in the Danish population.

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.