INTRODUCTION:Nocturnal hypertension (NH) is a high-risk, underdiagnosed blood pressure (BP) phenotype strongly associated with cardiovascular morbidity. Obstructive sleep apnea (OSA), which is common in patients with NH, promotes vascular injury through sympathetic activation, inflammation, and endothelial dysfunction; however, the molecular mechanisms underlying this association in patients with NH remain poorly defined. This study explored these mechanisms using targeted proteomics and endothelial cell models. METHODS:Adults undergoing polysomnography (PSG) with NH, defined as nighttime BP ≥120/70mmHg at the time of 24-hour ambulatory BP monitoring, were included. Fasting blood samples were collected after PSG. Participants were classified as controls, defined as an apnea-hypopnea index (AHI) <15eventsh-1, or severe OSA, defined as AHI ≥30eventsh-1; patients with moderate OSA, defined as AHI between 15 and 30eventsh-1, were excluded to maximize contrast between groups. Participants were matched for age, sex, BMI, and nocturnal mean arterial pressure. The Olink® platform was used to quantify proteins. Differential abundance was assessed using linear models, and sparse partial least squares discriminant analysis was used to identify OSA-associated protein signatures. Endothelial integrity was assessed in cells exposed to extracellular vesicles derived from a subset of participants (n=8 controls; n=8 severe OSA). RESULTS:A total of 58 matched participants were included, with 29 participants per group. Overall, 70.7% were men, the median age was 48 years, and the median BMI was 29.5kg/m2. Twenty-one proteins were differentially abundant and were enriched in pathways related to cell adhesion maintenance and extracellular vesicle composition. A 13-protein signature associated with OSA showed interconnectivity and enrichment for endothelial regulatory pathways. Extracellular vesicles from patients with OSA showed a trend toward increased endothelial barrier disruption compared with controls. CONCLUSIONS:In patients with NH, severe OSA appears to be associated with molecular alterations indicative of endothelial dysfunction, providing preliminary mechanistic insight into elevated cardiovascular risk that may help refine risk stratification.

A substantial proportion of critical illness survivors experience circadian disruptions following intensive care unit (ICU) discharge. However, the long-term circadian function in these patients remains poorly understood. This study aimed to characterize the circadian health of ICU survivors over a 24 month follow-up. Patients admitted to the ICU due to SARS-CoV-2 infection were recruited, and rest–activity rhythms (7-day actigraphy), mental health (Hospital Anxiety and Depression Scale), quality of life (12-item Short Form Survey), and respiratory function (spirometry) were assessed at short-term follow-up and at 24 months. The main analysis included 52 patients (65.4% male) with a mean (SD) age of 59.2 (8.27) years. The cohort showed a mean (95% CI) increase in circadian function index (CFI) of 0.06 (0.03–0.09). Participants were categorized into two groups: those without and those with a clinically meaningful improvement, defined as a ≥ 10% increase in CFI. Improvements in CFI correlated with changes in DLCO (rrm = 0.31; 0.04–0.54) and FEV1 (0.43; 0.17–0.63). Longer duration of invasive mechanical ventilation was associated with lower CFI at 24 months (effect size = –0.338; –0.637 to –0.038). These findings indicate that while some survivors show circadian recovery over 24 months, others exhibit persistent alterations, supporting circadian-focused strategies in post-ICU rehabilitation.

BACKGROUND:Some evidence suggests that OSA may attenuate myocardial injury and reduce infarct severity during acute coronary syndromes (ACSs), potentially through stimulation of coronary collateral circulation (CCC). However, the relationship between OSA and collateral development, and their combined impact on ACS event severity, remains unclear. RESEARCH QUESTION:What is the relationship between OSA and coronary collateral development and what is their combined impact on ACS severity? STUDY DESIGN AND METHODS:Post hoc analysis of the Impact of Sleep Apnea in the Evolution of Acute Coronary Syndrome: Effect on Intervention With CPAP (ISAACC) trial, including patients with first-time ACS with CCC assessment using the Cohen-Rentrop scale (CRS), where a score of ≥ 2 (CRS grade 2 or 3) indicated well-developed collaterals. OSA was diagnosed via respiratory polygraphy performed within 24 to 72 hours of hospitalization. Associations between OSA and CRS grade 2 or 3 were evaluated using adjusted logistic regression. Peak creatine kinase (CK), peak cardiac troponin I (cTnI), and left ventricular ejection fraction (LVEF) were analyzed as ACS severity markers. RESULTS:Of 185 participants included, 79.5% had OSA. Participants were mainly middle-aged male individuals and demonstrated a high comorbidity burden. OSA was associated with greater odds of well-developed collaterals with an adjusted OR of 2.84 (95% CI, 1.24-7.19; P = .019), with a dose-response increase across OSA severity categories. Among patients with OSA, the presence of robust collaterals was associated with significantly lower peak CK and cTnI levels during the ACS episode, but not with improved LVEF. INTERPRETATION:Our research shows that in patients with first-time ACS, OSA was associated with a higher prevalence of well-developed coronary collaterals. Among patients with OSA, robust collateralization was associated with less myocardial injury during ACS, supporting the hypothesis that OSA may promote adaptive vascular remodeling, which warrants further mechanistic investigation. CLINICAL TRIAL REGISTRATION:ClinicalTrials.gov; No.: NCT01335087; URL: www. CLINICALTRIALS:gov.

Rationale: Obstructive sleep apnea (OSA) is a frequent condition in patients with resistant hypertension (RH) and its treatment with continuous positive airway pressure (CPAP) has been associated with decrease in blood pressure. Objectives: We aimed to evaluate in real-life the long-term effect of OSA diagnosis and treatment with CPAP on the risk of cardiovascular events in patients with RH. Methods: The prospective and observational SARAH study was conducted in a cohort of 497 patients with RH recruited from hospital hypertension units. Patients underwent a sleep study and 24-hour ambulatory blood pressure (BP) monitoring at baseline. An annual visit was conducted during each year of the follow-up period. The primary outcome was the prevalence of a composite of cardiovascular endpoints. The effects of OSA severity and CPAP treatment on the time-to-first event of the primary endpoint were analyzed with univariate and multivariable Cox proportional hazard regression models. Measurements and Main Results: A total of 423 patients (85.1%) had an apnea-hypopnea index (AHI)≥5 events/hour, and 195 were treated with CPAP. The median [IQR] follow-up period was 42 [31.9;59.2] months. During the follow-up period 94 (28.9%) patients developed the primary endpoint (fatal and non-fatal CV events plus hypertensive crises). Patients with OSA had an increase in the risk of developing the primary endpoint with an adjusted hazard ratio (HR) of 2.00 [(0.94 to 4.25), p=0.07] and with a HR of 2.56 [(1.05 to 6.21), p=0.03] in severe OSA (AHI ≥ 30 events/hour).CPAP treatment was associated with a decrease in the risk of developing the primary endpoint, with an adjusted HR of 0.58 [(0.32 to 1.03), p=0.06](Table). Conclusions: Among patients with RH, the presence of severe OSA is associated with an increased long-term risk of developing a cardiovascular event. Additionally, CPAP treatment is associated with a near-significant decrease in this risk. Clincialtrials.gov: SARAH trial (NCT03002558).

Abstract Background Survivors of critical illness endure long-lasting physical and mental challenges. Despite the persistence of poor sleep quality in a considerable proportion of patients at the 12-month follow-up, studies with assessments exceeding this period are limited. We aimed to investigate the trajectory of sleep over the 24 months following critical illness. Methods Observational, prospective study. Patients diagnosed with SARS-CoV-2 infection were recruited during the intensive care unit stay. Evaluations of sleep (Pittsburgh Sleep Quality Index [PSQI]), mental health (Hospital Anxiety and Depression Scale [HADS]), quality of life (12-item Short Form Survey [SF-12]), and other factors were performed in the short-term, and at 12 and 24 months after hospital discharge. Good sleep quality was defined as a PSQI score of ≤ 5. Minimal clinically important improvement (MCII) was defined as a decrease of ≥ 4 points in the PSQI score between the short-term assessment and the 24-month follow-up. Results The cohort included 196 patients (69.9% males), with a median [p25;p75] age of 62.0 [53.0;67.2] years. The global population showed a mean (95% CI) change of − 0.91 ( − 1.50 to − 0.31) points in the PSQI score from the short-term assessment to the 24-month follow-up. Based on PSQI score trajectories, three distinct groups of patients were identified: (i) the healthy group, consisting of patients with good sleep quality in the short-term that was maintained throughout the follow-up period; (ii) the MCII group, consisting of patients with poor sleep quality in the short-term, but with improvement over time, ultimately reaching levels comparable to the healthy group; (iii) the non-MCII group, consisting of those with consistently poor sleep quality across the entire follow-up. Further analyses revealed that PSQI score trajectories were closely aligned with those of the HADS and SF-12 mental scores. Conclusions Our findings reveal that a subset of critical illness survivors requires up to 24 months after the acute phase to fully restore their sleep quality, while a significant proportion does not experience a clinically significant improvement in sleep quality over this period. These distinct sleep trajectories are strongly correlated with mental health status, highlighting the importance of addressing sleep alongside mental health within the framework of post-intensive care syndrome.

Introduction: Understanding the diverse pathogenetic pathways in obstructive sleep apnea (OSA) is crucial for improving outcomes. microRNA (miRNA) profiling is a promising strategy for elucidating these mechanisms. Objective: To characterize the pathogenetic pathways linked to OSA through the integration of miRNA profiles, machine learning (ML) and bioinformatics. Methods: This multicenter study involved 525 patients with suspected OSA who underwent polysomnography. Plasma miRNAs were quantified via RNA sequencing in the discovery phase, with validation in two subsequent phases using RT-qPCR. Supervised ML feature selection methods and comprehensive bioinformatic analyses were employed. The associations among miRNA targets, OSA and OSA treatment were further explored using publicly available external datasets. Results: Following the discovery and technical validation phases in a subset of patients with and without confirmed OSA (n = 53), eleven miRNAs were identified as candidates for the subsequent feature selection process. These miRNAs were then quantified in the remaining population (n = 472). Feature selection methods revealed that the miRNAs let-7d-5p, miR-15a-5p and miR-107 were the most informative of OSA. The predominant mechanisms linked to these miRNAs were closely related to cellular events such as cell death, cell differentiation, extracellular remodeling, autophagy and metabolism. One target of let-7d-5p and miR-15a-5p, the TFDP2 gene, exhibited significant differences in gene expression between subjects with and without OSA across three independent databases. Conclusion: Our study identified three plasma miRNAs that, in conjunction with their target genes, provide new insights into OSA pathogenesis and reveal novel regulators and potential drug targets. (c) 2024 The Authors. Published by Elsevier Espana, S.L.U. on behalf of SEPAR. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

BACKGROUND:The effects of continuous positive airway pressure (CPAP) on blood pressure (BP) in normotensive subjects, particularly among those with a dipping BP pattern, remain uncertain, raising questions about its indication for this group of patients. We assessed the impact of CPAP on BP in normotensive subjects with a dipping BP pattern and severe obstructive sleep apnoea (OSA). METHODS:This was a randomised, parallel, prospective, controlled trial. Inclusion criteria were: age ≥18 years, apnoea-hypopnoea index ≥30 events·h-1, mean 24-h BP <130/80 mmHg and daytime to night-time BP reduction ≥10%. Patients were randomly assigned to receive either CPAP treatment or usual care for 12 weeks. The primary outcome was the change in ambulatory BP monitoring (ABPM) parameters from baseline to the 3-month follow-up. RESULTS:The 60 patients who completed the follow-up had a mean±sd age of 52.2±10.8 years and 40 (66.7%) were male. The intention-to-treat analysis showed no significant changes with CPAP, whereas the usual care group experienced increases in ABPM parameters. This resulted in a mean difference of -3.4 mmHg (95% CI -6.124- -0.676; p=0.015) in night-time diastolic BP between the groups. The per-protocol analysis indicated significant differences between the CPAP and usual care groups for all primary end-points, except for daytime systolic BP. For night-time systolic BP, the mean difference was -6.052 mmHg (95% CI -10.895- -1.208; p=0.016). CONCLUSION:These findings suggest a protective effect of CPAP, highlighting the importance of CPAP prescription for this population to control potential increases in BP and possibly prevent the onset of hypertension.

Introduction: Among 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. Methods: This 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. Results: In 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 -8.69 mL/min/1.73 m(2) (-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. Conclusions: OSA could contribute to worsening renal function in patients with RH. No compliance with CPAP was associated with lower values of eGFR. (c) 2024 SEPAR. Published by Elsevier Espana, S.L.U. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

BackgroundThere is a close relationship between obstructive sleep apnoea (OSA) and resistant hypertension (RH). However, studies assessing the long-term effect of diagnosing and treating OSA on blood pressure (BP) control in these patients are lacking.MethodsTo address this gap, we recruited 478 RH patients from hypertension units and followed them prospectively after they were screened for OSA through a sleep study. By performing 24-h ambulatory BP monitoring (ABPM) annually, the effect of OSA management was assessed.ResultsThe patients had a median (interquartile range (IQR)) age of 64.0 (57.2–69.0) years, 67% were males and most were nonsleepy, with a median (IQR) apnoea–hypopnoea index (AHI) of 15.8 (7.9–30.7) events·h−1. The median (IQR) follow-up time was 3.01 (2.93–3.12) years. At baseline, severe OSA was associated with uncontrolled BP, nocturnal hypertension and a nondipper circadian BP pattern. Moreover, these patients had higher BP values during follow-up than did patients in the other groups. However, among patients with moderate and severe OSA, the management of sleep disordered breathing, including the implementation of continuous positive airway pressure treatment, was associated with a reduction in 24-h ABPM parameters, especially night-time BP values, at the 1-year follow-up. These benefits were attenuated over time and only subjects with severe OSA maintained an ABPM night-time reduction at 3 years. Furthermore, clinical variables such as uncontrolled BP, sex and age showed a predictive value for the BP response at 1 year of follow-up.ConclusionA favourable long-term decrease in BP was detected by diagnosing and treating OSA in a cohort of RH patients from hypertension units, but over time this decrease was only partially maintained in severe OSA patients.

IntroductionAlzheimer's disease (AD) is a progressive neurodegenerative disorder. Current core cerebrospinal fluid (CSF) AD biomarkers, widely employed for diagnosis, require a lumbar puncture to be performed, making them impractical as screening tools. Considering the role of sleep disturbances in AD, recent research suggests quantitative sleep electroencephalography features as potential non-invasive biomarkers of AD pathology. However, quantitative analysis of comprehensive polysomnography (PSG) signals remains relatively understudied. PSG is a non-invasive test enabling qualitative and quantitative analysis of a wide range of parameters, offering additional insights alongside other biomarkers. Machine Learning (ML) gained interest for its ability to discern intricate patterns within complex datasets, offering promise in AD neuropathology detection. Therefore, this study aims to evaluate the effectiveness of a multimodal ML approach in predicting core AD CSF biomarkers.MethodsMild-moderate AD patients were prospectively recruited for PSG, followed by testing of CSF and blood samples for biomarkers. PSG signals underwent preprocessing to extract non-linear, time domain and frequency domain statistics quantitative features. Multiple ML algorithms were trained using four subsets of input features: clinical variables (CLINVAR), conventional PSG parameters (SLEEPVAR), quantitative PSG signal features (PSGVAR) and a combination of all subsets (ALL). Cross-validation techniques were employed to evaluate model performance and ensure generalizability. Regression models were developed to determine the most effective variable combinations for explaining variance in the biomarkers.ResultsOn 49 subjects, Gradient Boosting Regressors achieved the best results in estimating biomarkers levels, using different loss functions for each biomarker: least absolute deviation (LAD) for the Aβ42, least squares (LS) for p-tau and Huber for t-tau. The ALL subset demonstrated the lowest training errors for all three biomarkers, albeit with varying test performance. Specifically, the SLEEPVAR subset yielded the best test performance in predicting Aβ42, while the ALL subset most accurately predicted p-tau and t-tau due to the lowest test errors.ConclusionsMultimodal ML can help predict the outcome of CSF biomarkers in early AD by utilizing non-invasive and economically feasible variables. The integration of computational models into medical practice offers a promising tool for the screening of patients at risk of AD, potentially guiding clinical decisions.

OBJECTIVES:To investigate the sleep and circadian health of critical survivors 12 months after hospital discharge and to evaluate a possible effect of the severity of the disease within this context. DESIGN:Observational, prospective study. SETTING:Single-center study. PATIENTS:Two hundred sixty patients admitted to the ICU due to severe acute respiratory syndrome coronavirus 2 infection. INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:The cohort was composed of 260 patients (69.2% males), with a median (quartile 1-quartile 3) age of 61.5 years (52.0-67.0 yr). The median length of ICU stay was 11.0 days (6.00-21.8 d), where 56.2% of the patients required invasive mechanical ventilation (IMV). The Pittsburgh Sleep Quality Index (PSQI) revealed that 43.1% of the cohort presented poor sleep quality 12 months after hospital discharge. Actigraphy data indicated an influence of the disease severity on the fragmentation of the circadian rest-activity rhythm at the 3- and 6-month follow-ups, which was no longer significant in the long term. Still, the length of the ICU stay and the duration of IMV predicted a higher fragmentation of the rhythm at the 12-month follow-up with effect sizes (95% CI) of 0.248 (0.078-0.418) and 0.182 (0.005-0.359), respectively. Relevant associations between the PSQI and the Hospital Anxiety and Depression Scale (rho = 0.55, anxiety; rho = 0.5, depression) as well as between the fragmentation of the rhythm and the diffusing lung capacity for carbon monoxide (rho = -0.35) were observed at this time point. CONCLUSIONS:Our findings reveal a great prevalence of critical survivors presenting poor sleep quality 12 months after hospital discharge. Actigraphy data indicated the persistence of circadian alterations and a possible impact of the disease severity on the fragmentation of the circadian rest-activity rhythm, which was attenuated at the 12-month follow-up. This altogether highlights the relevance of considering the sleep and circadian health of critical survivors in the long term.

A non-dipping blood pressure (BP) pattern, which is frequently present in patients with obstructive sleep apnea (OSA), confers high cardiovascular risk. The mechanisms connecting these two conditions remain unclear. In the present study we performed a comprehensive analysis of the blood metabolipidome that aims to provide new insights into the molecular link between OSA and the dysregulation of circadian BP rhythmicity. This was an observational prospective longitudinal study involving adults with suspected OSA who were subjected to full polysomnography (PSG). Patients with an apnea–hypopnea index ≥ 5 events/h were included. Fasting plasma samples were obtained the morning after PSG. Based on the dipping ratio (DR; ratio of night/day BP values) measured via 24 h ambulatory BP monitoring, two groups were established: dippers (DR ≤ 0.9) and non-dippers (DR > 0.9). Treatment recommendations for OSA followed the clinical guidelines. Untargeted metabolomic and lipidomic analyses were performed in plasma samples via liquid chromatography–tandem mass spectrometry. Non-dipper patients represented 53.7% of the cohort (88/164 patients). A set of 31 metabolic species and 13 lipidic species were differentially detected between OSA patients who present a physiologic nocturnal BP decrease and those with abnormal BP dipping. Among the 44 differentially abundant plasma compounds, 25 were putatively identified, notably glycerophospholipids, glycolipids, sterols, and fatty acid derivates. Multivariate analysis defined a specific metabotype of non-dipping BP, which showed a significant dose-response relationship with PSG parameters of OSA severity, and with BP dipping changes after 6 months of OSA treatment with continuous positive airway pressure (CPAP). Bioinformatic analyses revealed that the identified metabolipidomic profile was found to be implicated in multiple systemic biological pathways, with potential physiopathologic implications for the circadian control of BP among individuals with OSA.

Additional file 3: Table S3. Pathological markers of Alzheimer’s disease according to the breathing cessation events in each sleep stage.

Abstract Background Previous studies challenge the impact of obstructive sleep apnea (OSA) once patients are diagnosed with Alzheimer’s disease (AD). Nevertheless, OSA recognizably disrupts sleep, and relevant associations between sleep, AD pathological markers, and cognition have been demonstrated. We aimed to further explore this, evaluating the associations between each breathing cessation event that compose the apnea–hypopnea index (AHI) and the sleep structure to finally investigate whether this was related to increased levels of AD markers and higher cognitive decline. Methods Observational, prospective study, including consecutive patients diagnosed with mild-moderate AD. The participants were submitted to overnight polysomnography followed by a cerebrospinal fluid collection for AD pathological markers levels determination. Neuropsychological assessment was performed at baseline and after 12 months of follow-up. Results The cohort was composed of 116 patients (55.2% females) with a median [p25;p75] age of 76.0 [72.0;80.0] years and an AHI of 25.9 [15.1;48.5], which was mainly defined by the presence of hypopneas and obstructive apneas. These were distinctively associated with the sleep structure, with obstructive apneas being related to arousals and sleep lightening and hypopneas being related to an increased number of arousals only. Despite having a lower frequency, mixed and central apneas also presented associations with the sleep structure, particularly increasing the time spent in the lighter sleep stages. In relation to AD pathological markers, obstructive and mixed apneas were related to an augment in neurofilament light levels while hypopneas were associated with a higher phosphorylated-tau/amyloid-beta protein ratio. Hypopneas were the most important event for an increased cognitive decline at the 12-month follow-up. Conclusions Our findings highlight the importance of a patient-centered approach, with a comprehensive and detailed analysis of the AHI to effectively predict the different outcomes and tailor the appropriate therapeutic strategies.

Aims and objectives: To describe the longitudinal evolution of pulmonary function, radiological abnormalities, symptoms, quality of life and health care consumption among survivors throughout the 2 years after critical COVID-19 infection. Methods: Longitudinal cohort study among patients admitted to the ICUs of the University Hospitals Arnau de Vilanova and Santa Maria of Lleida (Spain) between March and December 2020. Eligible COVID-19 survivors were evaluated 3, 6, 12 and 24 months after hospital discharge. Results: A total of 109 patients were evaluated. Over 2 years, patients showed a progressive recovery of lung function and exercise capacity. However, there were still 45.7% and 53.9% with impairment in lung diffusing capacity and radiological abnormalities, respectively. This was pronounced among patients who required mechanical ventilation. At 24 months, patients presented quality of life, anxiety, depression and cognition levels similar to those of the general population. Nevertheless, 35%, 14%, 10.9%, and 7.9% had persistently abnormal scores for fatigue, cognition, anxiety and depression, respectively. A total of 54.3% presented post-COVID syndrome. The consumption of health resources remained high and was related to symptom burden. Most patients returned to work 2 years after hospital discharge. Conclusions: Critical COVID-19 showed longitudinal improvements in health outcomes and returned to work within 2 years. There was still a high proportion of patients with functional and radiological abnormalities, especially intubated patients. A high burden of symptoms and post-COVID syndrome was present in the long term, affecting quality of life and implying high levels of health care consumption.

BackgroundThe influence of body position in obstructive sleep apnoea patients is well known. A positional therapy device placed at the forehead has proven to be effective in reducing the severity of positional obstructive sleep apnoea (POSA) symptoms. The aim of the study was to evaluate patients' therapy compliance and satisfaction in the short term and mid-term. MethodsA post hoc analysis of a randomised controlled trial was conducted using an inactive device (ID) or an active device (AD) for 3 months. The primary outcomes were device usage and the percentage of patients with good compliance (defined as device use for more than 4 hours per night and more than 70% of nights per week). Secondary outcomes included time spent with head in the supine position, patient satisfaction and side effects. ResultsThe median duration of using the device was 6.9 hours in the ID group and 6.7 hours in the AD group (p=0.309), and the durations were similar throughout the follow-up period and from the first day of use. The percentage of patients with good compliance was similar and greater than 60% in both groups. The median time spent with head in the supine position was significantly lower in the AD group (2.9%) than in the ID group (12.4%) since the first day of treatment. Both groups showed satisfaction scores values above 8.5 (out of 10) in all items, while side effects were scarcely reported. ConclusionHigh device compliance was achieved in POSA patients, both in terms of device usage time and percentage of days used. Patients were highly satisfied, and the device effectively reduced the time spent with the head in the supine position from the first day of use.

Background: Assessments to evaluate whether the effects of intensive care unit (ICU) on sleep and circadian health persist in the long term are scarce. Objective: To evaluate the sleep and circadian health of critical survivors after a 12-month follow-up. Methods: Prospective, observational study. Critical patients due to SARS-CoV-2 infection were recruited during the ICU stay. Clinical evaluations including the Pittsburgh Sleep Quality Index (PSQI) and actigraphy (7 days) were performed 3, 6, and 12 months after hospital discharge. Results: The cohort was composed of 230 patients (29.6% females), with a median [p25; p75] age of 62.0 [52.0;67.0] years. The median length of ICU stay was 12.0 [7.00;23.0] days, where 58.7% of the patients required invasive mechanical ventilation (IMV). According to the PSQI, 41.7% of the cohort presented poor sleep quality at the 12-month follow-up, demonstrating an improvement of 18.8% in relation to the 3-month follow-up. The high fragmentation of the rest-activity rhythm observed was similar to the previous assessments. Additional analyses revealed that female sex was associated with a decreased sleep quality at the 12-month follow-up (effect size [SD]: 0.346 [0.143]), whereas ICU stay duration (0.227 [0.094]), use of IMV (0.387 [0.204]), and IMV duration (0.178 [0.095]) were associated with increased fragmentation of the rhythm. Conclusions: Our findings reveal an improvement in the sleep quality of critical survivors, whereas the fragmentation of the rest-activity rhythm persists in the long term. This highlights the importance of considering circadian health after hospital discharge and addresses possible predictors for such outcome.