Sleep and Breathing最新文献

Purpose: Patients with obstructive sleep apnea syndrome (OSAS) frequently experience cognitive dysfunction, which may be connected to chronic intermittent hypoxia (CIH). Insulin-like growth factor-1 (IGF-1) is thought to be closely associated with cognitive function, but its role in cognitive impairment caused by OSAS is unclear. The purpose of this study was to investigate the potential protective effect of IGF-1 on cognitive impairment in OSAS rats.

Methods: Healthy male SD rats (n = 40) were randomly assigned into four groups: control group, CIH group, NS + CIH group, and IGF-1 + CIH group. All experimental rats except for those in the control group were exposed to intermittent hypoxic (IH) environments for 8 h per day over 28 days. Prior to daily exposure to IH, rats in the IGF-1 + CIH group received subcutaneous injections of IGF-1. The Morris water maze test was conducted on all experimental rats. Brain tissue testing methods included Enzyme-Linked Immunosorbent Assay, Hematoxylin and eosin staining, Immunohistochemistry, and Western blotting.

Results: The rat model of OSAS was successfully established following exposure to CIH and exhibited significant cognitive impairment. However, daily subcutaneous injections of IGF-1 partially restored the impaired cognitive function in OSAS rats. Compared with the control group, there was a significant decrease in the expression levels of IGF-1, p-IGF-IR, and SYP in the CIH group; however, these expression levels increased significantly in the IGF-I + CIH group.

Conclusion: In OSAS rats, IGF-1 enhances learning memory; this effect may be linked to increased p-IGF-1R and SYP protein production in the hippocampus.

Purpose: Obstructive sleep apnea (OSA) is associated with metabolic, cardiovascular, and cerebrovascular comorbidities. Appropriate diagnosis and treatment of OSA might mitigate these comorbidities. This retrospective review sought to assess the impact of sex, age, race, ethnicity, and insurance status on polysomnography (PSG) referral rates.

Methods: An institutional STOP-Bang database of 299,320 patients was filtered for patients admitted to the hospital with an acute cardiac diagnosis between 2015-2020. A cohort of 4,735 patients were risk stratified by STOP-Bang (SB) score and correlations were made between PSG referrals and demographic and clinical variables (sex, age, race, ethnicity, and insurance status).

Results: Of the 25.3% of the cohort with high SB scores (5-8) only 21.3% were referred for PSG. Age and female sex were negatively associated with sleep study referrals (p < 0.001). No correlation was found between sleep study referral rates and race or ethnicity. No correlation was found between sleep study referrals and insurance provider. Admitting cardiac diagnosis significantly influenced sleep study referrals with diagnoses of arrhythmias and myocardial infarction being associated with an increased rate of PSG referrals compared to heart failure patients (p < 0.002).

Conclusions: Our study found no significant correlation between PSG referral rates and race, ethnicity, or insurance provider. However, we found low overall rates of PSG referral, with negative correlations between older age and female sex and a high-risk cardiac population. This represents a substantial missed opportunity to identify patients at risk for OSA, obtain a diagnosis, and provider adequate treatment.

Purpose: Hypoxia and sleep fragmentations that develop during sleep cause central nervous system damage in patients with obstructive sleep apnea (OSA). This study investigates the relationship between OSA severity and glial fibrillary acidic protein (GFAP) and c-Fos, which are considered indicators of neuronal damage.

Methods: The study included 84 participants (70 patients with OSA and 14 healthy individuals). All participants were evaluated with the Epworth Sleepiness Scale (ESS) before polysomnography (PSG), and serum GFAP and c-Fos values were measured after PSG. All participants were grouped according to the apnea-hypopnea index (AHI) score (control: AHI < 5, Mild OSA: 5 ≤ AHI < 15; moderate OSA: 15 ≤ AHI < 30; severe OSA: AHI ≥ 30).

Results: The average age of the participants was 48.5 ± 11.4 years. According to AHI scoring, 14 healthy individuals (16.7%) were in the control group, and 70 patients (83.3%) were in OSA groups. The serum GFAP levels and c-Fos levels were increased in the OSA groups (7.1 ± 5.7 ng/mL and 7.9 ± 7.5 pg/mL respectively) compared to the control group (1.3 ± 0.4 ng/mL and 2.7 ± 1.4 pg/mL p < 0.001 and p < 0.01, respectively). There was a significant positive correlation between AHI and oxygen desaturation index (ODI) values, which indicate disease severity, and serum c-Fos (r: 0.381 and r:0.931, p < 0.01, respectively) and GFAP (r: 0.793 and r:0.745, p < 0.01, respectively) values.

Conclusion: Serum GFAP and c-Fos values, which are considered indicators of neuronal damage, can be used as a serum marker to determine disease severity in OSA.

Purpose: This study aimed to evaluate polysomnographic (PSG) outcomes of tonsillectomy and adenoidectomy (T&A) in children with Down Syndrome (DS) and OSA, and the difference in PSG outcomes of T&A between children with DS and age- and gender-matched normally developing (non-DS) children.

Methods: This was a single center retrospective study that included children with DS and OSA who underwent T&A and had pre-operative and post-operative PSG. The baseline and the differences of pre- and post-operative PSG variables were compared with those of an age- and gender-matched group of non-DS children.

Results: Forty-eight children with DS were included in the study; the median age was 5 years (IQR 5.5), 58% were males, and the median BMI was 18.2 (IQR 3.3). There was statistically significant improvement noted between pre-operative and post-operative OAHI 17.9 ± 26.7 vs. 9.1 ± 13.6 (p = 0.022) and non-REM AHI 13.9 ± 19.7 vs. 6.9 ± 14.2 (p = 0.027). However, there were no significant changes in sleep architecture, oxygen desaturation nadir, or CO2 levels. 54.2% of the DS children continued to have moderate to severe OSA after T&A. Univariate logistic regression showed that for every 1% increase in oxygen desaturation nadir, the odds of having residual moderate or severe OSA decreased by 28% (p = 0.002) compared to the cured and mild OSA groups. There was no significant pre- and post-operative differences in PSG variables noted in 16 children with DS compared to age- and gender-matched non-DS children.

Conclusion: Despite the overall significant reduction of OAHI in children with DS and OSA who underwent T&A, there was a residual moderate to severe OSA in about half of the included children. Oxygen desaturation nadir was a predicting factor for persistent moderate to severe OSA. There were no significant pre- and post-operative PSG differences in between DS children compared to non-DS children.

Background: Numerous risk factors in paediatric narcolepsy may predispose them to obstructive sleep apnea (OSA). The concurrent presence of OSA in these patients might lead to underdiagnosing narcolepsy. This research investigates the prevalence and potential causality between OSA and paediatric narcolepsy.

Methods: A case-control study coupled with a two-sample Mendelian randomization (MR) analysis was employed to explore the prevalence and causal link between paediatric narcolepsy and OSA risk.

Results: The case-control study revealed that paediatric narcolepsy patients are at an increased risk of OSA, with an Odds ratio (OR) of 4.87 (95% CI: 2.20-10.71; P < 0.001). The inverse-variance weighted (IVW) model further suggests a potential causal link between narcolepsy and OSA (IVW OR: 4.671, 95% CI: 1.925-11.290; P < 0.001). Additionally, sensitivity analysis confirmed these findings' reliability.

Conclusion: The findings highlight an elevated prevalence and genetic susceptibility to OSA among paediatric narcolepsy patients, underscoring the necessity for clinical screening of OSA. Continued research is essential to clarify the pathogenic mechanisms and develop potential treatments.

Purpose: Clinical studies suggested associations between obstructive sleep apnea (OSA) and gastrointestinal tract disorders. This study aims to investigate the genetic causal relationship between OSA and gastrointestinal tract disorders, specifically gastroesophageal reflux disease (GERD) and inflammatory bowel disease (IBD).

Methods: In this study, we employed two-sample Mendelian Randomization (MR) analysis to investigate the potential relationships between OSA and GERD, and between OSA and IBD. More specifically, the primary analysis utilized inverse variance weighting (IVW). Weighted median, MR Egger, and MR PRESSO were applied to complicate potential violations of MR assumptions. Also, sensitivity analysis was evaluated and similar analysis was performed again after outliers were removed. Additionally, multivariable MR (MVMR) was conducted for associated pairs to adjust for obesity.

Results: Genetically predicted risk of GERD increased OSA risk by approximately 60% (OR_IVW = 1.62, 95%CI = [1.43,1.84]) which was also stable by other complicated approaches, and even with BMI adjusted by MVMR (OR_adjBMI[95%CI] = 1.26 [1.15,1.37]). Besides, OSA showed a mild causal effect on increased GERD risk after adjusting for obesity (OR_adjBMI[95%CI] = 1.05 [1.02,1.08]). Additionally, OSA increased the risks for IBD (OR_IVW[95%CI] = 1.36 [1.12,1.65]), including a higher risk of CD (OR_IVW[95%CI] = 1.41 [1.08,1.83]), and a trend for increasing UC risk (OR_IVW[95%CI] = 1.29 [0.99,1.67]).

Conclusion: GERD exerts a substantial causality on increasing the risk of OSA. Conversely, the potential for a causal relationship that OSA contributes to the development of GERD or IBD remains probable. These findings support the crosstalk between gastrointestinal tract disorders and OSA.

Purpose: Phrenic nerve stimulation (PNS) was approved by the Food and Drug Administration (FDA) to treat moderate to severe central sleep apnea. We report here, results of a retrospective study regarding our institutional outcomes at one year. In this study we evaluated the change in the apnea hypopnea index, epworth sleepiness score, and functional outcomes of sleep score at one year post implant.

Methods: This is a retrospective analysis of patients ≥ 18 years of age who had PNS implanted for moderate to severe CSA at the Ohio State University Wexner Medical Center apnea between Feb 1, 2018 to July 1, 2021. Sleep disordered breathing parameters and objective sleepiness as measured by the Epworth Sleepiness Scale (ESS) scores, and Functional Outcomes of Sleep Questionnaire (FOSQ) scores were assessed at baseline and one-year post-implant.

Results: Twenty-two patients were implanted with PNS at OSU between February 1, 2018 and May, 31, 2022. The AHI showed a statistically significant decrease from a median of 40 events/hour at baseline to 18 at follow-up (p-value = 0.003). The CAI decreased from 16 events/hour to 2 events/hour (p-value of 0.001). The obstructive apnea index, mixed apnea index, and hypopnea index did not significantly change. The ESS scores had a statistically significant improvement from a median score of 12 to 9 (p-value = 0.028). While the FOSQ showed a trend to improvement from 15.0 to 17.8, it was not statistically significant (p-value of 0.086).

Conclusion: Our study found that PNS therapy for moderate to severe CSA improves overall AHI and CAI. Objective sleepiness as measured by the ESS also improved at one-year post implant.

Objective

To verify the relationship between sarcopenia and sleep in individuals with chronic obstructive pulmonary disease (COPD).

Methods

Individuals with COPD were cross-sectionally assessed for lung function (spirometry), sleep (both subjectively [Pittsburgh Sleep Quality Index, PSQI] and objectively [Actiwatch sleep monitor]) and the presence of sarcopenia (handgrip strength by dynamometry). All tests were carried out in accordance with international standards.

Results

Twenty-nine individuals with COPD were analyzed (16 women; 69 ± 7 years; BMI 27 ± 5 kg/m²; FEV₁ 59 ± 19% predicted). Upon division in groups according to the presence or absence of sarcopenia, individuals with sarcopenia (in comparison to those without sarcopenia) had shorter sleep time (81 [75–85] vs. 86 [81–90] %; p = 0.043), lower sleep efficiency (77 [69–83] vs. 85 [75–87] %; p = 0.038), longer time awake after sleep onset (92 [71–120] vs. 58 [47–83] minutes; p = 0.0012) and more marked sleep fragmentation, represented by a higher number of sleep blocks/night (46 [41–49] vs. 34 [26–48]; p = 0.018), higher number of awake blocks/night (45 [40–49] vs. 34 [26–48]; p = 0.018) and shorter duration of sleep blocks/night (9 [8–10] vs. 14 [8–58] minutes; p = 0.043). There was no statistical difference when comparing the PSQI variables between the groups. However, handgrip strength was negatively associated with PSQI components 2 [R= -0.51, p = 0.005] and 5 [R= -0.39, p = 0.037].

Conclusion

Individuals with COPD and sarcopenia (as measured by handgrip strength) have worse objectively measured sleep outcomes. This was not the case regarding a self-reported perception of worse sleep quality, although there was weak-to-moderate association between handgrip strength and subjective sleep.

Purpose

Obstructive sleep apnea (OSA) is a heterogeneous disorder requiring personalized diagnostic approaches. Restless sleep and excessive daytime sleepiness (EDS) frequently accompany OSA, and are mainly linked to sleep fragmentation secondary to apneas and/or hypopneas. In this study, we aimed to analyze the characteristics of LMMs in OSA and to evaluate interrelationship between LMMs and EDS.

Methods

Untreated-naïve adult OSA patients, with vs. without EDS were prospectively enrolled. Patients with comorbid neurological/psychiatric diagnosis, usage of drugs/substances known to affect sleep and positive airway pressure therapy were excluded. Routine evaluation of video-polysomnography was followed by LMM scoring. LMMs were compared between OSA with vs. without EDS, and correlations of LMMs with ESS scores and macrostructural sleep parameters were analyzed.

Results

Sixty patients were included (median age 43.5 [37.0] years, %78.3 men); 17 had EDS with Epworth Sleepiness Scale (ESS) ≥ 10 (28.3%). Total LMM index in total sleep time (TST) was 7.9 [20.6]. Total LMM index in TST (p = 0.048) and N1 (p = 0.020), and arousal-related LMM index in TST (p = 0.050) and N1 (p = 0.026) were higher in OSA with EDS than those without EDS. ESS scores were positively correlated with total (r = 0.332,p = 0.028) and arousal-related (r = 0.338,p = 0.025) LMM indexes in N1, and abnormal respiratory event-related LMM indexes in N1 (r = 0.440,p = 0.003) and N3 (r = 0.293,p = 0.050) after correction for age, sex, body-mass-index and apnea-hypopnea index.

Conclusion

Our study demonstrated that LMMs were more frequent in OSA with EDS than those without EDS. This may have broad implications for the mechanisms of motor restlessness and residual sleepiness in OSA and warrants larger-scale, long-term follow-up studies.

Clinical trial registration

No clinical trial registration due to the observational design of the study.

Purpose

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

Methods

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

Results

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

Conclusions

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