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STUDY OBJECTIVES: Excessive daytime sleepiness (EDS) is a treatment target for many patients with obstructive sleep apnea (OSA). We aimed to understand the prevalence, risk factors, and quality of life associated with EDS in a nonclinical, “real world” sample of patients with OSA. METHODS: Cross-sectional survey of patients with OSA participating in an online peer support community, assessing demographics, comorbidities, treatment, and quality of life. Differences in those with and without EDS (Epworth Sleepiness Scale > and ≤ 10) were assessed. RESULTS: The sample (n = 422) was 54.2% male, 65.9% were ≥ 55 years, and 43.3% reported sleeping ≤ 6 hours/night. EDS was identified among 31.0% of respondents and 51.7% reported sleepiness as a precipitating factor for seeking initial OSA treatment. EDS was more prevalent in individuals reporting asthma, insomnia symptoms, positive airway pressure (PAP) use less than 6 hours/night on ≥ 5 nights/week, or sleep duration < 6 hours/night. After adjusting for demographics and comorbidities, patients with EDS reported poorer mental and physical health and well-being, lower disease-specific functional status, more activity and work impairment, and more driving impairment (P values < .05). In the subsample (n = 265) with high PAP adherence, 26.0% reported EDS, and similar associations between EDS and outcomes were observed. CONCLUSIONS: These “real world” data suggest that patients seeking online OSA support experience a high prevalence of EDS, which was associated with poorer quality of life and worse functional status. Associations persisted among respondents with high self-reported PAP-therapy adherence, potentially driving these individuals to seek online support for sleepiness-related symptoms. CITATION: Wanberg LJ, Rottapel RE, Reid ML, et al. Prevalence of sleepiness and associations with quality of life in patients with sleep apnea in an online cohort. J Clin Sleep Med. 2021;17(12):2363–2372.

This analysis determined ∼5-year incident hypertension rates using the 2017 American College of Cardiology/American Heart Association blood pressure (BP) guidelines in individuals with obstructive sleep apnea (OSA) with hypopneas defined by a ≥ 3% oxygen desaturation or arousal but not by a hypopnea criterion of ≥ 4% oxygen desaturation (4% only).Data were analyzed from participants in the Sleep Heart Health Study exam 2 (n = 1219) who were normotensive (BP ≤ 120/80 mm Hg) at exam 1. The AHI at exam 1 was classified into 4 categories of OSA severity:5, 5 ≤ 15, 15 ≤ 30, and ≥ 30 events/h using both the 3% oxygen desaturation or arousal and the 4% only definitions. Three definitions of hypertension-elevated BP (120/80 mm Hg), stage 1 (130/80 mm Hg), and stage 2 (140/90 mm Hg)-were used to determine incidence rates at exam 2.Five-year follow-up was available for 476 participants classified as having OSA by the 3% oxygen desaturation or arousal criterion but not by the 4% only standard at exam 1. Incident hypertension using American College of Cardiology/American Heart Association-defined BP categories in these discordantly classified individuals were 15% (elevated BP), 15% (stage 1), and 6% (stage 2). Hypertensive medications were used in 4% of participants who were normotensive. The overall incidence rate of at least an elevated BP was 40% (191/476) in those with OSA defined using the 3% oxygen desaturation or arousal criterion but not by the 4% only criterion.Use of the 4% only hypopnea definition resulted in the failure to identify a significant number of individuals with OSA who eventually developed hypertension and could have benefited from earlier diagnosis and treatment.

Objective Self-reported "sleep quality" often is assessed in epidemiologic studies. However, the bases for variation in sleep quality is not fully understood. We quantified the extent to which subjective sleep quality was related to sleep disorders and sleep characteristics among 795 African American adults. Method Between 2012 and 2016, participants underwent home sleep apnea testing and 1-week actigraphy (estimating sleep duration, efficiency, fragmentation, latency). Sleep quality, insomnia and restless legs syndrome symptoms, sleepiness, and physician diagnosis of sleep disorders were self-reported. We fit linear regression models to determine the extent to which subjective and objective sleep measures as well as depressive symptoms and anxiety were related to subjective sleep quality. Results After adjustment for covariates, worse sleep quality scores were associated with insomnia and restless legs syndrome symptoms, sleep apnea, physician diagnosis of a sleep disorder, and actigraphy-based fragmented sleep, lower sleep efficiency, and shorter sleep duration. Insomnia symptoms explained the most variance in subjective sleep quality, 21%. Other sleep measures each explained 3% to 7% and psychosocial factors explained 8% to 9% of the variance in subjective sleep quality after adjustment for confounders. Conclusions The weak associations of sleep quality with sleep disorders and objectively measured sleep disturbances are consistent with concepts of "sleep health" as a multidimensional construct. Sleep quality is a patient-centered outcome that provides unique information over objective measurements of sleep disturbances.

International audience; No abstract available

Study Objectives:The association between obstructive sleep apnea (OSA) and hypertension in prior studies has been determined using a definition of hypopnea requiring a 4% O2 desaturation. However, ...

Objective The objective of this prospective pilot study was to examine the effects of a novel non-pharmacological device (BioBoosti) on insomnia symptoms in adults. Methods Subjects with chronic insomnia were instructed to hold the device in each hand for 8 mins for 6 cycles on a nightly basis for 2 weeks. Outcomes tested included standardized subjective sleep measures assessing sleep quality, insomnia symptoms, and daytime sleepiness. Sleep was objectively quantified using electroencephalogram (EEG) before and after 2 weeks of treatment with BioBoosti, and wrist actigraphy throughout the study. Results Twenty adults (mean age: 45.6±17.1 y/o; range 18-74 y/o) were enrolled in the study. No significant side effects were noted by any of the subjects. After 2 weeks of BioBoosti use, subjects reported improved sleep quality (Pittsburgh Sleep Quality Index: 12.6±3.3 versus 8.5±3.7, p=0.001) and reduced insomnia symptoms (Insomnia Severity Index: 18.2±5.2 versus 12.8±7.0, p

Obstructive sleep apnea (OSA) is highly prevalent among patients with asymptomatic left ventricular systolic and diastolic dysfunction and congestive heart failure, and if untreated may contribute to the clinical progression of heart failure (HF). Given the health and economic burden of HF, identifying potential modifiable risk factors such as OSA and whether appropriate treatment improves outcomes is of critical importance. Identifying the subgroups of patients with OSA and HF who would benefit most from OSA treatment is another important point. This focused review surveys current knowledge of OSA and HF in order to provide: (1) a better understanding of the pathophysiologic mechanisms that may increase morbidity among individuals with HF and comorbid OSA, (2) a summary of current observational data and small randomized trials, (3) an understanding of the limitations of current larger randomized controlled trials, and (4) future needs to more accurately determine the efficacy of OSA treatment among individuals with HF.

Introduction Post-COVID neuropsychiatric symptoms have a significant impact on morbidity following COVID-19 infection. We present three patients without a prior history of insomnia symptoms who developed new-onset and chronic insomnia following infection with COVID-19. Methods Retrospective chart review was performed on three patients who presented to an ambulatory sleep clinic with complaints of new onset insomnia following COVID-19 infection. Results Three patients without a history of prior insomnia developed difficulty initiating or maintaining sleep during or following COVID-19 infection. Patient 1 developed symptoms of insomnia 2 weeks after recovery from COVID-19 infection. Symptoms improved after 5 months with a combination of hydroxyzine and cognitive behavioral therapy for insomnia (CBTi). Patient 2 developed insomnia at the same time as COVID-19 infection and symptoms consisted of sleep onset and maintenance insomnia.Hydroxyzine and trazodone were ineffective. Symptoms improved with zolpidem and CBTi. Patient 3 had a more severe course of COVID-19 infection requiring management in the intensive care unit that coincided with onset of insomnia. He presented to sleep clinic with new insomnia complaints but was also found to have moderate obstructive sleep apnea and periodic limb movements on polysomnography and prior history of restless legs. The patient was treated with a combination of positive airway pressure therapy and a dopamine agonist with plans to follow up to reassess severity of insomnia at future visit. Conclusion Three patients without a prior history of insomnia developed insomnia following infection with COVID-19. Management included a combination of CBTi and pharmacotherapy as well as treatment of underlying sleep disorders (OSA, RLS) when applicable. Further work is needed to understand the prevalence of new onset insomnia in patients following COVID-19 infection and best therapeutic approaches in this unique population. Support (If Any)

The American Thoracic Society Core Curriculum updates clinicians annually in adult and pediatric pulmonary disease, medical critical care, and sleep medicine, in a 3-4-year recurring cycle of topics. These topics will be presented at the 2020 Virtual Conference. Below is the adult sleep medicine core that includes topics pertinent to sleep-disordered breathing and insomnia.

ObjectiveWe sought to assess the prevalence, correlates, and consequences of periodic limb movements of sleep (PLMS) in persons with obstructive sleep apnea (OSA) and the effect (worsening or improvement) of continuous positive airway pressure (CPAP) therapy on PLMS in a large prospective multicenter randomized controlled trial.MethodsWe performed retrospective analyses of data from the Apnea Positive Pressure Long-term Efficacy Study, a prospective multicenter randomized controlled trial. A total of 1,105 persons with OSA enrolled in this study underwent a polysomnographic investigation at baseline, another one for CPAP titration, and another study 6 months after randomization to either active CPAP or sham CPAP.ResultsOf all participants, 19.7% had PLM index (PLMI) ≥10/hour, 14.8% had PLMI ≥15/hour, 12.1% had PLMI ≥20/hour, 9.3% had PLMI ≥25/hour, and 7.5% had PLMI ≥30/hour. The odds of having a PLMI ≥10 were higher in older participants (odds ratio [OR] 1.03, p < 0.001), men (OR 1.63. p = 0.007), those using antidepressants (OR 1.48. p = 0.048), and those with higher caffeine use (OR 1.01, p = 0.04). After controlling for OSA and depression, PLMS were associated with increased sleep latency, reduced sleep efficiency, and reduced total sleep time. No significant relationships were noted between PLMS frequency and subjective sleepiness (Epworth Sleepiness Scale score) or objective sleepiness (Maintenance of Wakefulness Test). There was no differential effect of CPAP in comparison to sham CPAP on PLMS after 6 months of therapy.ConclusionsPLMS are common in patients with OSA and are associated with a significant reduction in sleep quality over and above that conferred by OSA. Treatment with CPAP does not affect the severity of PLMS.

Insomnia is the most prevalent sleep disorder in the United States and has high comorbidity with a number of cardiovascular diseases (CVDs). In the past decade, a number of observational studies have demonstrated an association between insomnia and incident cardiovascular disease (CVD) morbidity and mortality, including hypertension (HTN), coronary heart disease (CHD), and heart failure (HF). Despite some inconsistencies in the literature, likely due to variations in how insomnia is defined and measured, the existing data suggest that insomnia, especially when accompanied by short sleep duration, is associated with increased risk for HTN, CHD and recurrent acute coronary syndrome, and HF. Purported mechanisms likely relate to dysregulation of the hypothalamic-pituitary axis, increased sympathetic nervous system activity, and increased inflammation. This paper reviews the most recent studies of insomnia and CVD and the potential pathophysiological mechanisms underlying this relationship and highlights the need for randomized trials to further elucidate the nature of the relationship between insomnia and CVD.

We assessed whether the presence of central sleep apnea is associated with adverse left ventricular structural changes. We analysed 1412 participants from the Multi-Ethnic Study of Atherosclerosis who underwent both overnight polysomnography and cardiac magnetic resonance imaging. Subjects had been recruited 10 years earlier when free of cardiovascular disease. Our main exposure is the presence of central sleep apnea as defined by central apnea-hypopnea index = 5 or the presence of Cheyne-Stokes breathing. Outcome variables were left ventricular mass/height, left ventricular ejection fraction, and left ventricular mass/volume ratio. Multivariate linear regression models adjusted for age, gender, race, waist circumference, tobacco use, hypertension, and the obstructive apnea-hypopnea index were fit for the outcomes. Of the 1412 participants, 27 (2%) individuals had central sleep apnea. After adjusting for covariates, the presence of central sleep apnea was significantly associated with elevated left ventricular mass/volume ratio (β = 0.11 ± 0.04 g mL-1 , P = 0.0071), an adverse cardiac finding signifying concentric remodelling.

Sleep apnea is highly prevalent in patients with cardiovascular disease. These disordered breathing events are associated with a profile of perturbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction, all of which are critical mediators of cardiovascular disease. Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke. Several discoveries in the pathogenesis, along with developments in the treatment of sleep apnea, have accumulated in recent years. In this review, we discuss the mechanisms of sleep apnea, the evidence that addresses the links between sleep apnea and cardiovascular disease, and research that has addressed the effect of sleep apnea treatment on cardiovascular disease and clinical endpoints. Finally, we review the recent development in sleep apnea treatment options, with special consideration of treating patients with heart disease. Future directions for selective areas are suggested.

Introduction The impact of not treating OSA identified using AASM standards (hypopneas scored using a minimum 3% O2 desaturation or arousal), but misclassified by CMS standards (hypopneas scored only if minimum 4% O2 desaturation) remains unclear. This analysis determined the ~5 year incident hypertension rates using the new 2018 ACC/AHA blood pressure (BP) guidelines in these individuals. Methods Data were analyzed from all Sleep Heart Health Study exam 2 study participants (N=1219) who were normotensive (BP≤120/80) at exam 1. The apnea hypopnea index (AHI) at exam 1 was classified into 4 categories of OSA severity: 120/80), Stage 1 (>130/80) and Stage 2 (>140/90) to determine incidence rates at exam 2. Results Five year follow-up data were available for 476 participants classified as having OSA (AHI ≥5) by AASM criteria, but not by CMS standards at exam 1. Incident hypertension rates in these misclassified participants for ACC/AHA defined BP categories were 15% (Elevated BP), 15% (Stage 1) and 6% (Stage 2). 4% of normotensive participants used hypertensive medications. Overall incidence rate of at least an elevated BP was 40% (191/476) in those with OSA defined using AASM, but not by CMS criteria and 17% (191/1219) of the overall population at risk. In comparison to those with incident hypertension and OSA identified by CMS standards, BMI (27.7 vs 30.1 kg/m2, p Conclusion Use of the CMS hypopnea definition as a component of the AHI resulted in the failure to identify a significant number of individuals with OSA who eventually developed hypertension and could have benefited from earlier diagnosis and treatment. Support HL53938

CITATIONJavaheri S, Budhiraja R, Quan SF. Measurement of the severity of sleep-disordered breathing: a moving target. J Clin Sleep Med. 2020;16(2):337–338.

BackgroundStudies have established that OSA defined using a hypopnea definition requiring a ≥4% oxygen desaturation (AHI4%) is associated with cardiovascular (CVD) or coronary heart (CHD) disease. This study determined whether OSA defined using a hypopnea definition characterized by a ≥3% oxygen desaturation or an arousal (AHI3%A) is associated with CVD/CHD.MethodsData were analyzed from 6307 Sleep Heart Health Study participants who had polysomnography. Self-reported CVD included angina, heart attack, heart failure, stroke or previous coronary bypass surgery or angioplasty. Self-reported CHD included the aforementioned conditions but not stroke or heart failure. The association between OSA and CVD/CHD was examined using logistic regression models with stepwise inclusion of demographic, anthropometric, social/behavioral and co-morbid medical conditions. A parsimonious model in which diabetes and hypertension were excluded because of their potential to be on the causal pathway between OSA and CVD/CHD also was constructed.ResultsFor CVD, the odds ratios and 95% confidence intervals for AHI3%A ≥30/hour were 1.39 (1.03-1.87) and 1.45 (1.09-1.94) in the fully adjusted and parsimonious models. Results for CHD were 1.29 (0.96-1.74) and 1.36 (0.99-1.85). In participants without OSA according to more stringent AHI4% criteria but with OSA using the AHI3%A definition, similar findings were observed.ConclusionOSA defined using an AHI3%A is associated with both CVD and CHD. Use of a more restrictive AHI4% definition will misidentify a large number of individuals with OSA who have CVD or CHD. These individuals may be denied access to therapy, potentially worsening their underlying CVD or CHD.

Background and Purpose— Many health effects of sleep apnea (SA) may be mediated through accelerated atherosclerosis. We examined the associations of snoring and several measurements of SA with subclinical carotid atherosclerosis in a large multiethnic population sample. Methods— This analysis included 1615 participants (mean age, 68 years) from examination 5 (2010–2013) of the MESA study (Multi-Ethnic Study of Atherosclerosis). Sleep measures including SA (apnea-hypopnea index [4%], ≥15 events/hour) were derived from full in-home polysomnography. Carotid atherosclerosis was measured using high-resolution B-mode ultrasound. Multivariable linear and logistic regression models were used to evaluate the associations between sleep exposures with carotid intima-media thickness and the presence of carotid plaque, respectively. Effect modification by age, sex, and race/ethnicity was examined. Results— In multivariable analysis, SA was associated with an increased odds of carotid plaque presence in individuals aged P interaction=0.078). Greater hypoxemia (sleep time P interaction=0.106). Self-reported snoring was not associated with carotid atherosclerosis. In assessing race-specific outcomes, greater hypoxemia was associated with increased carotid intima-media thickness in blacks (0.049±0.017 mm; P interaction=0.033). Conclusions— In this large multiethnic population-based sample, sleep disturbances are associated with subclinical carotid atherosclerosis in both men and women, particularly in those

Obstructive sleep apnea is associated with hypertension, and short-term studies have demonstrated a modest reduction in blood pressure with continuous positive airway pressure therapy. We evaluated the effects of continuous positive airway pressure versus sham continuous positive airway pressure on blood pressure in 1,101 participants with obstructive sleep apnea from the Apnea Positive Pressure Long-term Efficacy Study, a randomized, sham-controlled double-blinded study designed to assess the impact of continuous positive airway pressure on neurocognition. Participants with apnea-hypopnea index ≥ 10 were randomly assigned to continuous positive airway pressure or sham continuous positive airway pressure. Blood pressures measured in the morning and evening at baseline, 2 months and 6 months were analysed post hoc using a mixed-model repeated-measures analysis of variance. The largest magnitude reduction was approximately 2.4 mmHg in morning systolic pressure that occurred at 2 months in the continuous positive airway pressure arm as compared with an approximate 0.5 mmHg reduction in the sham group (continuous positive airway pressure effect -1.9 mmHg, p = .008). At 6 months, the difference between groups was diminished and no longer statistically significant (continuous positive airway pressure effect -0.9 mmHg, p = .12). Sensitivity analysis with use of multiple imputation approaches to account for missing data did not change the results. Treatment with continuous positive airway pressure for obstructive sleep apnea reduces morning but not evening blood pressure in a population with well-controlled blood pressure. The effect was greater after 2 than after 6 months of treatment.

Citation:Javaheri S, Javaheri S. The impact of SARS-CoV-2 on sleep. J Clin Sleep Med. 2020;16(8):1413.

Introduction NREM parasomnias are relatively common among children and sometimes persist in adulthood. These behaviors may result in injury or have negative impacts on functioning and quality of life thus necessitating treatment. The treatment is challenging given the lack of evidence for frequently used medications such as benzodiazepines (BDZ) or tricyclic antidepressants (TCA). The aim of this retrospective analysis is to determine the most frequently prescribed medications for treatment of NREM parasomnias and evaluate reported outcomes. Methods We performed a retrospective chart review of all patients with NREM parasomnia diagnosed within BWH clinics examining the date of diagnosis, date of starting therapy, comorbidities, type of medication prescribed, and the reported change in symptoms or side effects at the individual’s follow-up visits. Results From 2012 to 2019, 123 patients (64 females, 59 male) at BWH clinics received the diagnosis of NREM parasomnia, including sleepwalking and night terrors. Mean age was 44. Comorbidities included depression=16, anxiety=32, seizures=6, RLS=9, epilepsy=5, insomnia=29, and OSA=57. Initial treatment included safety counseling (72), BDZ (7), TCA (4), and treatment of comorbidity (23). Treatment of OSA only (n=15) was effective in 66% (n=10) and 33% were lost to follow up. Of those with OSA treatment plus BDZ (n=6), treatment was effective in 50% (n=3). Of those receiving BDZ only (n=7), treatment was effective in 43%. Of those receiving Melatonin (8),treatment was effective among 62.5% (n=5). TCAS (n=4) were effective in 3 patients (75%). Treatment of comorbid conditions without pharmacotherapy (23) was effective in 35% (n=8) while the remaining 65% (n=15) were lost to follow up. Conclusion Treating comorbid conditions such as OSA, insomnia, RLS, depression, and anxiety is a frequent treatment strategy. Additional pharmacologic treatment most commonly includes melatonin, BDZs, and TCAs. Support None

We sought to quantify the association between slow-wave (stage N3) sleep and hypertension in a large cohort of middle-aged men and women. Data from 1850 participants free of baseline hypertension from the Sleep Heart Health Study were analyzed. The primary exposure was percentage of N3 sleep on baseline in-home polysomnography and the primary outcome was incident hypertension, defined as systolic blood pressure ≥ 140 mm Hg, diastolic blood pressure ≥ 90 mm Hg, and/or use of any blood pressure lowering medications at follow-up. Multivariable logistic regression models were adjusted for study site, age, sex, race, waist circumference, tobacco use, alcohol use, apnea–hypopnea index, nocturnal oxygen desaturation, sleep duration, sleep efficiency, and arousal index. Mean age was 59.4 ± 10.1 years and 55.5% were female. The mean baseline systolic and diastolic blood pressure was 118.8 and 70.6 mm Hg, respectively. Approximately 30% of the sample developed hypertension during a mean follow-up of 5.3 years. In the multi-adjusted model, participants in quartiles 1 (

The directionality of the relationship between sleep-disordered breathing and heart failure is controversial.We assessed whether elevations in the obstructive or central sleep apnea index or the presence of Cheyne-Stokes breathing are associated with decompensated and/or incident heart failure.We conducted a prospective, longitudinal study of 2,865 participants derived from the Osteoporotic Fractures in Men Study, a prospective multicenter observational study of community-dwelling older men. Participants underwent baseline polysomnography and were followed for a mean 7.3 years for development of incident or decompensated heart failure. Our main exposures were the obstructive apnea-hypopnea index (AHI), central apnea index (CAI ≥ 5), and Cheyne-Stokes breathing. Covariates included age, race, clinic site, comorbidities, physical activity, and alcohol and tobacco use.CAI greater than or equal to five and presence of Cheyne-Stokes breathing but not obstructive AHI were significant predictors of incident heart failure (adjusted hazard ratio [HR], 1.79; 95% confidence interval [CI], 1.16-2.77 for CAI ≥ 5) (HR, 2.23; 95% CI, 1.45-3.43 for Cheyne-Stokes breathing). After excluding those with baseline heart failure, the incident risk of heart failure was attenuated for those with CAI greater than or equal to five (HR, 1.57; 95% CI, 0.92-2.66) but remained significantly elevated for those with Cheyne-Stokes breathing (HR, 1.90; 95% CI, 1.10-3.30).An elevated CAI/Cheyne-Stokes breathing, but not an elevated obstructive AHI, is significantly associated with increased risk of decompensated heart failure and/or development of clinical heart failure in a community-based cohort of older men.

Study objectives The presence and severity of obstructive sleep apnea (OSA) are associated with impaired left ventricular (LV) structure and function. Our goal was to quantify the associations between LV systolic function and mass with severity of OSA in an ethnically diverse cohort, assessing variations by age and sex. Methods We conducted a cross-sectional analysis of data from 1,412 racially/ethnically diverse participants across 6 US communities from the Multi-Ethnic Study of Atherosclerosis who underwent both overnight polysomnography and cardiac magnetic resonance imaging from 2010-2012. We evaluated the association between the obstructive apnea-hypopnea index (AHI) by clinical category ( 50) and secondary measures of sleep apnea with the outcomes left ventricular (LV) mass adjusted for height, LV mass/volume ratio, and LV ejection fraction. Results After adjusting for potential confounders and mediators, LV mass was significantly increased with increasing AHI category for subjects age 65 y or younger (β = 1.84 ± 0.47 g/m, P = 0.0001). The association between the AHI and LV mass appeared stronger in whites and Chinese compared to blacks and Hispanics, although interaction terms were not statistically significant. Additionally, while both LV mass and LV mass/volume ratio were significantly associated with hypoxia, ejection fraction was not associated with any OSA severity index. Comparable associations were observed in men and women. Conclusions Independent of confounders, higher levels of AHI are significantly associated with increased LV mass in both men and women younger than 65 y from a community-based cohort.

Objective To characterize the relationship between insulin sensitivity, assessed with the homeostasis model of insulin (HOMA), and objective measurements of sleep duration in adolescents. Study design We conducted a cross-sectional analysis from two examinations conducted in the Cleveland Children’s Sleep and Health Cohort (n = 387; 43% minorities). Biochemical and anthropometry measurements were made in a clinical research unit. Sleep duration was measured with actigraphy. Results Decreased sleep duration was associated with increased adiposity and minority race. Sleep duration had a quadratic “u-shape” association with HOMA. When adjusted for age, sex, race, preterm status, and activity, adolescents who slept 7.75 hours had the lowest predicted HOMA (1.96, 95% confidence interval [CI], 1.82-2.10), and adolescents who slept 5.0 hours or 10.5 hours had HOMA indices that were approximately 20% higher (2.36; 95% CI, 1.94-2.86; and 2.41; 95% CI, 1.93-3.01, respectively). After adjusting for adiposity, the association between shorter sleep and HOMA was appreciably attenuated, but the association with longer sleep persisted. Conclusions Shorter and longer sleep durations are associated with decreased insulin sensitivity in adolescents. Although the association between shorter sleep duration with insulin sensitivity likely is explained by the association between short sleep duration and obesity, the association between longer sleep and insulin sensitivity is independent of obesity.

Objectives: There is limited research on racial/ethnic variation in sleep disturbances. This study aimed to quantify the distributions of objectively measured sleep disordered breathing (SDB), short sleep duration, poor sleep quality, and self-reported sleep disturbances (e.g., insomnia) across racial/ethnic groups. Design: Cross-sectional study. Setting: Six US communities. Participants: Racially/ethnically diverse men and women aged 54–93 y in the Multi-Ethnic Study of Atherosclerosis Sleep Cohort (n = 2,230). Interventions: N/A. Measurements and Results: Information from polysomnography-measured SDB, actigraphy-measured sleep duration and quality, and selfreported daytime sleepiness were obtained between 2010 and 2013. Overall, 15.0% of individuals had severe SDB (apnea-hypopnea index [AHI] ≥ 30); 30.9% short sleep duration (< 6 h); 6.5% poor sleep quality (sleep efficiency

Objectives The objective of this study was to evaluate associations between obesity measures and sleep-disordered breathing severity among White, Black, Hispanic, and Chinese Americans. Methods The method used in this study was a community-based cross-sectional study of 2053 racially/ethnically diverse adults in the Multi-Ethnic Study of Atherosclerosis. Anthropometry and polysomnography were used to measure obesity and apnea–hypopnea index (AHI). Linear regression models were fitted to investigate associations of body mass index (BMI) and waist circumference with AHI (log transformed) with adjustment for sociodemographics, lifestyle factors, and comorbidities. Results The mean participant age was 68.4 (range: 54–93) years; 53.6% of participants were women. The median AHI was 9.1 events/h. There were significant associations of BMI and waist circumference with AHI in the overall cohort and within each racial/ethnic group. A significant interaction was observed between race/ethnicity and BMI ( P interaction = 0.017). Models predicted that for each unit increase in BMI (kg/m 2 ), the mean AHI increased by 19.7% for Chinese, 11.6% for Whites and Blacks, and 10.5% for Hispanics. Similarly, incremental changes in waist circumference were associated with larger increases in AHI among Chinese than among other groups. Conclusions Associations of BMI and waist circumference with AHI were stronger among Chinese than among other racial/ethnic groups. These findings highlight a potential emergence of elevated sleep-disordered breathing prevalence occurring in association with increasing obesity in Asian populations.

Despite the emergence of sleep apnea (SA) as a significant risk factor for heart failure (HF) mortality, data indicate that SA remains under-diagnosed and under-treated. Less well established, though perhaps more emphasized, is the role of sleep apnea in pulmonary hypertension (PH). SA occurs in approximately 50 % of HF patients, and its consequences include intermittent hypoxemia, arousal, and intra-thoracic pressure swings leading to neurohormonal stimulation, oxidative stress and inflammation. While SA is also considered a cause of PH, severe PH due solely to SA is rare. Combining the results of several studies using Swan-Ganz catheters for diagnosis of PH, approximately 10 % of patients with OSA have PH. Effective treatment of SA in HF is associated with improved survival, while treatment of SA in PH is typically associated with modest hemodynamic improvement.

Background— We assessed whether insufficient sleep is associated with prehypertension in healthy adolescents. Methods and Results— We undertook a cross-sectional analysis of 238 adolescents, all without sleep apnea or severe comorbidities. Participants underwent multiple-day wrist actigraphy at home to provide objective estimates of sleep patterns. In a clinical research facility, overnight polysomnography, anthropometry, and 9 blood pressure measurements over 2 days were made. Exposures were actigraphy-defined low weekday sleep efficiency, an objective measure of sleep quality (low sleep efficiency ≤85%), and short sleep duration (≤6.5 hours). The main outcome was prehypertension (≥90th percentile for age, sex, and height), with systolic and diastolic blood pressures as continuous measures as secondary outcomes. Prehypertension, low sleep efficiency, and short sleep duration occurred in 14%, 26%, and 11% of the sample, respectively. In unadjusted analyses, the odds of prehypertension increased 4.5-fold (95% CI, 2.1 to 9.7) in adolescents with low sleep efficiency and 2.8-fold (95% CI, 1.1 to 7.3) in those with short sleep. In analyses adjusted for sex, body mass index percentile, and socioeconomic status, the odds of prehypertension increased 3.5-fold (95% CI, 1.5. 8.0) for low sleep efficiency and 2.5-fold (95% CI, 0.9 to 6.9) for short sleep. Adjusted analyses showed that adolescents with low sleep efficiency had on average a 4.0±1.2-mm Hg higher systolic blood pressure than other children ( P Conclusions— Poor sleep quality is associated with prehypertension in healthy adolescents. Associations are not explained by socioeconomic status, obesity, sleep apnea, or known comorbidities, suggesting that inadequate sleep quality is associated with elevated blood pressure.