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The American Heart Association considers sleep health an essential component of cardiovascular health, and sleep is generally a time of cardiovascular quiescence, such that any deviation from normal sleep may be associated with adverse cardiovascular consequences. Many studies have shown that both impaired quantity and quality of sleep, particularly with obstructive sleep apnea (OSA) and comorbid sleep disorders, are associated with incident cardiometabolic consequences. OSA is associated with repetitive episodes of altered blood gases, arousals, large negative swings in intrathoracic pressures, and increased sympathetic activity. Recent studies show that OSA is also associated with altered gut microbiota, which could contribute to increased risk of cardiovascular disease. OSA has been associated with hypertension, atrial fibrillation, heart failure, coronary artery disease, stroke, and excess cardiovascular mortality. Association of OSA with chronic obstructive lung disease (overlap syndrome) and morbid obesity (obesity hypoventilation syndrome) increases the odds of mortality., Competing Interests: Funding Support and Author Disclosures No funding was received for this study. Dr Shahrokh Javaheri is funded by the National Institutes of Health (NIH) for an oxygen trial; has received income related to medical education from Jazz and Idorsia Pharmaceutical; and has served as a consultant to ZOLL Respicardia. Dr Sogol Javaheri has received grant funding from Zoll, the Massachusetts Technology Collaborative, and an internal health equity grant from Harvard Medical School. Dr Somers is funded by the National Heart, Lung, and Blood Institute (HL65176 and HL160619); has served as a consultant for Bayer, Jazz Pharmaceuticals, Huxley, Apnimed, ResMed, Lilly, Wesper, and ZOLL; and is on the Sleep Number Scientific Advisory Board. Dr Gozal is funded by the NIH for research on sleep apnea, mineralocorticoid receptors, and Alzheimer disease, University of Missouri grants, and the Leda J. Sears Foundation. Dr Mehra is supported by American Academy of Sleep Medicine and American Heart Association grants; has received honorarium from the American Academy of Sleep Medicine for speaking; and has received royalties from UpToDate. Dr Zee is funded by the NIH; has served as a consultant to Eisai, Idorsia, Jazz, Harmony, and Sanofi; and reports grants to Northwestern University from Vanda. Dr Cistulli has an appointment to an endowed academic Chair at the University of Sydney that was established from ResMed funding; has received research support from ResMed and SomnoMed; is a consultant to ResMed, SomnoMed, Signifier Medical Technologies, Bayer, and Sunrise Medical; and has a pecuniary interest in SomnoMed related to a role in research and development (2004). Dr Malhotra is funded by the NIH; has received income related to medical education from Jazz, LivaNova, Eli Lilly, and Zoll; and ResMed provided a philanthropic donation to UC San Diego. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Many studies have shown an association of obstructive sleep apnea (OSA) with incident cardiovascular diseases, particularly when comorbid with insomnia, excessive sleepiness, obesity hypoventilation syndrome, and chronic obstructive pulmonary disease. Randomized controlled trials (RCTs) have demonstrated that treatment of OSA with positive airway pressure devices (CPAP) improves systemic hypertension, particularly in those with resistant hypertension who are adherent to CPAP. However, large RCTs have not shown long-term benefits of CPAP on hard cardiovascular outcomes, but post hoc analyses of these RCTs have demonstrated improved hard outcomes in those who use CPAP adequately. In theory, low CPAP adherence and patient selection may have contributed to neutral results in intention-to-treat analyses. Only by further research into clinical, translational, and basic underlying mechanisms is major progress likely to continue. This review highlights the various treatment approaches for sleep disorders, particularly OSA comorbid with various other disorders, the potential reasons for null results of RCTs treating OSA with CPAP, and suggested approaches for future trials., Competing Interests: Funding Support and Author Disclosures ResMed provided a philanthropic donation to UC San Diego. Dr Shahrokh Javaheri has received income related to medical education from Res Med, Jazz, Idorsia, Eli Lilly, and Avadel Pharmaceutical; and is a consultant to Zoll-Respicardia. Dr Sogol Javaheri has received grant funding from Zoll and the Massachusetts Technology Collaborative; and is supported by an internal health equity grant from Harvard Medical School. Dr Mehra has received an honorarium from the American Academy of Sleep Medicine; has received funds for service on the American Board of Internal Medicine writing group; has received NIH funding; and has received royalties from Up to Date. Dr Somers is supported by National Institutes of Health (NIH) grant HL65176; has served as a consultant for Bayer, Jazz Pharmaceuticals, Huxley, Apnimed, ResMed, Lilly, and Respicardia; and is on the Sleep Number Scientific Advisory Board. Dr Zee is a consultant to Eisai, Idorsia, Jazz, and Harmony; and has received institutional grants from Vanda and Sleep Number. Dr Cistulli has an appointment to an endowed academic Chair at the University of Sydney that was established from ResMed funding; has received research support from ResMed and SomnoMed; is a consultant to ResMed, SomnoMed, Signifier Medical Technologies, Bayer, and Sunrise Medical; and has a pecuniary interest in SomnoMed related to a role in research and development (2004). Dr Malhotra is funded by the NIH; and has received income related to medical education from Powell Mansfield, Livanova, Eli Lilly, and Zoll. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Medication-induced central sleep apnea (CSA) is one of the eight categories of causes of CSA but in the absence of awareness and careful history may be misclassified as primary CSA. While opioids are a well-known cause of respiratory depression and CSA, non-opioid medications including sodium oxybate, baclofen, valproic acid, gabapentin, and ticagrelor are less well-recognized. Opioids-induced respiratory depression and CSA are mediated primarily by µ-opioid receptors, which are abundant in the pontomedullary centers involved in breathing. The non-opioid medications, sodium oxybate, baclofen, valproic acid, and gabapentin, act upon brainstem gamma-aminobutyric acid (GABA) receptors, which co-colonize with µ-opioid receptors and mediate CSA. The pattern of ataxic breathing associated with these medications is like that induced by opioids on polysomnogram. Finally, ticagrelor also causes periodic breathing and CSA by increasing central chemosensitivity and ventilatory response to carbon dioxide. Given the potential consequences of CSA and the association between some of these medications with mortality, it is critical to recognize these adverse drug reactions, particularly because discontinuation of the offending agents has been shown to eliminate CSA., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

There is an extraordinary and increasing global burden of atrial fibrillation (AF) and obstructive sleep apnea (OSA), two conditions that frequently accompany one another and that share underlying risk factors. Whether a causal pathophysiologic relationship connects OSA to the development and/or progression of AF, or whether shared risk factors promote both conditions, is unproven. With increasing recognition of the importance of controlling AF-related risk factors, numerous observational studies now highlight the potential benefits of OSA treatment in AF-related outcomes. Physicians are regularly faced with caring for this important and increasing population of patients despite a paucity of clinical guidance on the topic. Here, we review the clinical epidemiology and pathophysiology of AF and OSA with a focus on key clinical studies and major outstanding questions that should be addressed in future studies., (Copyright © 2023 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice and is associated with significant morbidity, mortality, and financial burden. Obstructive sleep apnea (OSA) is more common in individuals with AF and may impair the efficacy of rhythm control strategies including catheter ablation. However, the prevalence of undiagnosed OSA in all-comers with AF is unknown., Design: This pragmatic, phase IV prospective cohort study will test 250-300 consecutive ambulatory AF patients with all patterns of atrial fibrillation (paroxysmal, persistent, and long-term persistent) and no prior sleep testing for OSA using the WatchPAT system, a disposable home sleep test (HST). The primary outcome of the study is the prevalence of undiagnosed OSA in all-comers with atrial fibrillation., Results: Preliminary results from the initial pilot enrollment of approximately 15% (N = 38) of the planned sample size demonstrate a 79.0% prevalence of at least mild (AHI≥5) OSA or greater in consecutively enrolled patient with all patterns of AF., Conclusions: We report the design, methodology, and preliminary results of our study to define the prevalence of OSA in AF patients. This study will help inform approaches to OSA screening in patients with AF for which there is currently little practical guidance., Clinical Trial Registration: NCT05155813., Competing Interests: Conflict of interest None reported., (Copyright © 2023 Elsevier Inc. All rights reserved.)

The Internet is a common source of sleep information but may be subject to commercial bias and misinformation. We compared the understandability, information quality, and presence of misinformation of popular YouTube videos on sleep to videos with credible experts. We identified the most popular YouTube videos on sleep/insomnia and 5 videos from experts. Videos were assessed for understanding and clarity using validated instruments. Misinformation and commercial bias were identified by consensus of sleep medicine experts. The most popular videos received, on average, 8.2 (± 2.2) million views; the expert-led videos received, on average, 0.3 (± 0.2) million views. Commercial bias was identified in 66.7% of popular videos and 0% of expert videos ( P < .012). The popular videos featured more misinformation than expert videos ( P < .001). The popular videos about sleep/insomnia on YouTube featured misinformation and commercial bias. Future research may explore methods for disseminating evidence-based sleep information., Citation: Robbins R, Epstein LJ, Iyer JM, et al. Examining understandability, information quality, and presence of misinformation in popular YouTube videos on sleep compared to expert-led videos. J Clin Sleep Med . 2023;19(5):991-994., (© 2023 American Academy of Sleep Medicine.)

The aim of this retrospective analysis is to determine the most frequently prescribed medications for the treatment of NREM parasomnias and evaluate reported outcomes. We performed a retrospective chart review of all patients with NREM parasomnia diagnosed within Brigham and Women's Hospital (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 follow-up visits. From 2012 to 2019, 110 patients (59 females, 51 male) at BWH clinics received a diagnosis of NREM parasomnia, including sleepwalking and night terrors. The mean age was 44. Comorbidities included obstructive sleep apnea (OSA) (46%), periodic limb movement syndrome (PLMS) (13%), insomnia (19%), Restless leg syndrome (RLS) (9%), epilepsy (4%), and REM behavior disorder (RBD) (9%). Initial treatment strategies include behavioral and safety counseling only (34%), pharmacological treatment (29%), treatment of any comorbidity (28%), and combined treatment of any of the above (9%). Improvement was reported with: treatment of OSA ( n = 23 52% reported improvement), melatonin ( n = 8, improvement reported by 88%.,benzodiazepine ( n = 7, improvement reported by 57%). Treating comorbid conditions is a frequent treatment strategy, often associated with symptom improvement. The pharmacologic treatment most commonly included melatonin and benzodiazepines. Comprehensive management should include behavioral and safety recommendations, assessment of comorbid conditions, and individually tailored pharmaceutical treatment.

Competing Interests: Conflict of interest: none declared.

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.

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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., (© 2021 American Academy of Sleep Medicine.)

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., (Copyright © 2020 by the American Thoracic Society.)

Study Objectives: 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)., Methods: 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., Results: 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., Conclusions: 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., (© 2020 American Academy of Sleep Medicine.)

OSA is a highly prevalent sleep disorder, and subjective excessive daytime sleepiness (EDS) is the cardinal symptom for which many individuals seek medical advice. Positive airway pressure (PAP) devices, first-line treatment for OSA, eliminates EDS in most patients. However, a subset of patients suffers from persistent EDS despite adherence to therapy. Multiple conditions, some reversible, could account for the residual sleepiness and need to be explored, requiring detailed history, review of PAP data from the smart card, and sometimes additional testing. When all known causes of EDS are excluded, in adequately treated subjects, the purported mechanisms could relate to long-term exposure to the OSA-related sleep fragmentation, sleep deprivation, and hypoxic injury to the arousal system, shifts in melatonin secretion, or altered microbiome. Independent of the mechanism, in well-treated OSA, pharmacological therapy with approved drugs can be considered. Modafinil is commonly prescribed to combat residual EDS, but more recently two drugs, solriamfetol, a dual dopamine-norepinephrine reuptake inhibitor, and pitolisant, a histamine H3 receptor inverse agonist, were approved for EDS. Solriamfetol has undergone randomized controlled trials for treatment of EDS associated with both OSA and narcolepsy, exhibiting robust efficacy. Solriamfetol is renally excreted, with no known drug interactions. Pitolisant, which is nonscheduled, has undergone multiple RCTs in narcolepsy, showing improvement in subjective and objective EDS and one OSA trial showing improvement in subjective EDS., (Copyright © 2020 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Objective : Observational data demonstrate increased risk of recurrent acute coronary syndrome in patients with comorbid insomnia. We conducted a pragmatic randomized controlled pilot study to address knowledge gaps and inform future large-scale randomized trials to test the impact of Web-based cognitive behavioral therapy for insomnia (wCBT-I) on coronary heart disease (CHD) outcomes. Participants : Thirty-five adults recruited from Brigham and Women's and Cleveland Clinic Hospitals with insomnia, defined by Insomnia Severity Index (ISI) score ≥ 10 and symptoms of at least 3 months, and comorbid CHD identified from medical records. Methods : We randomized 34 patients to either general sleep education coupled with wCBT-I or general sleep education alone followed by an opportunity for treatment after the study (a wait-list control) to evaluate feasibility and uptake of insomnia treatment in patients with heart disease. Participants completed the ISI at baseline and 6 weeks to assess insomnia severity. Results : Twenty-nine adults completed the trial, yielding an 85% retention rate, and adherence rate in the treatment arm was 80%. Mean age was 71.6 ± 9.5 years, 75% were male, and mean body mass index (BMI) was 29 ± 4.5 kg/m 2 . Baseline ISI scores were 15.6. There was a 6.2 ± 5.3 point reduction in ISI scores in the intervention arm and a 3.3 ± 5.1 reduction in the control arm ( p value 0.1). Conclusion : Web-based CBT-I intervention was feasible in an older sample with prevalent CHD and resulted in clinically meaningful improvement in insomnia severity, though statistical significance was limited by lack of power.

Objective: We 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., Methods: We 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., Results: Of 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., Conclusions: PLMS 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., (© 2019 American Academy of Neurology.)

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., (© 2019 European Sleep Research Society.)

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.

Background: Studies 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., Methods: Data were analyzed from 6307 Sleep Heart Health Study participants who had polysomnography. Self-reported CVD included angina, heart attack, heart failure, stroke, 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., Results: For 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., Conclusion: OSA 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 <68 years (odds ratio, 1.47; 95% CI, 1.05-2.06) but not in older individuals (odds ratio, 0.95; 95% CI, 0.67-1.37; P interaction=0.078). Greater hypoxemia (sleep time <90% saturation) was associated with increasing carotid intima-media thickness in younger (0.028±0.014 mm) but not in older individuals (-0.001±0.013 mm; 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 <68 years of age. The mechanisms underlying the association between SA and carotid atherosclerosis may differ for carotid plaque and carotid intima-media thickness.

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, the American Academy of Sleep Medicine (AASM) recommends using a 3% O₂ desaturation or an arousal. This analysis assesses the relationship between OSA and hypertension utilizing the AASM recommended definition and the 2018 American College of Cardiology/American Heart Association hypertension guidelines., Methods: Data from 6113 participants from the Sleep Heart Health Study were analyzed. The AASM recommended apnea-hypopnea index (AHI) was classified into 4 categories of OSA severity: < 5, 5 to < 15, 15 to < 30 and ≥ 30 events/h. Three definitions of hypertension were used: elevated (> 120/< 80 or use of hypertension medications [meds]), stage 1/stage 2 (> 130/80 or meds), stage 2 (> 140/90 or meds). Data were analyzed using logistic regression controlling for demographics, smoking and body mass index. Multiple linear regression analysis assessed the relationship between natural log AHI, and systolic and diastolic blood pressure controlling for the same covariates., Results: For all definitions of blood pressure elevation, increasing OSA severity was associated with greater likelihood of an elevated or hypertensive status in fully adjusted models (odds ratio [95% confidence interval]): elevated 1.30 (1.09-1.54), 1.39 (1.13-1.70) 1.69 (1.29-2.13); stage 1/2: 1.25 (1.06-1.47), 1.32 (1.10-1.59), 1.53 (1.23-1.91); stage 2: 1.07 (0.91-1.25), 1.21 (1.01-1.44), 1.37 (1.11-1.69) for AHI 5 to < 15, 15 to < 30 and > 30 events/h (< 5 events/h reference). Linear regression found that AHI was associated with both systolic and diastolic blood pressure in fully adjusted models., Conclusions: Use of the AASM recommended definition of hypopnea as a component of the AHI is associated with the presence of hypertension., Citation: Budhiraja R, Javaheri S, Parthasarathy S, Berry RB, Quan SF. The association between obstructive sleep apnea characterized by a minimum 3 percent oxygen desaturation or arousal hypopnea definition and hypertension. J Clin Sleep Med. 2019;15(9):1261-1270., (© 2019 American Academy of Sleep Medicine.)

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 <0.001). Sleepiness, as assessed by a visual analog scale, was significantly reduced after treatment (5.7±2.8 versus 4.0±3.3, p =0.03)., Conclusion: BioBoosti use yielded an improvement in insomnia symptoms. Larger placebo-controlled studies are needed to fully assess efficacy., Competing Interests: Research funding for the study included a grant from Biomobie, Inc., to the Brigham and Women’s hospital which included coverage of study cost (testing, subjects remuneration, fees), and partial salary support covering the time involved in the study for Dr Pavlova (principal investigator), Mr Puri (research coordinator), and Dr Latreille (data analysis). Dr Matthew has received non-monetary compensation related to a similar project. Dr Matthew also reports non-financial support from BioMobie, during the conduct of the study. Drs Batool, Javaheri, and Johnsen have no relevant financial relationships. Drs Pavlova and Latreille have received also funding from the Trustee Fund, unrelated to this study. Dr Pavlova has received funding also from Lundbeck, Inc. and Jazz Pharmaceuticals for research unrelated to this study. Dr Latreille has received funding by the Canadian Institute of Health, unrelated to this study. Dr Javaheri is a consultant for Jazz Pharmaceuticals on treatment of type 2 narcolepsy. The authors report no other conflicts of interest in this work., (© 2019 Pavlova et al.)

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 (<9.8%) and 2 (9.8%-17.7%) of N3 sleep had significantly greater odds of incident hypertension compared with those in quartile 3 (17.7%-25.2%) (OR 1.69, 95% CI 1.21-2.36, p = .002 and OR 1.45, 95% CI 1.04-2.00, p = .03, respectively). No significant effect modification by sex on the N3-hypertension association was observed. In conclusion, compared with intermediate levels of N3 sleep (overlapping the "normal" adult range), lower levels of percent N3 sleep are associated with increased odds of incident hypertension in both men and women, independent of potential confounders, including indices of sleep apnea and sleep fragmentation., (© Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.)

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., (© 2017 European Sleep Research Society.)

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., (Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

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., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

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., Competing Interests: All authors have no conflict of interest in relation to the work described., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Rationale: The directionality of the relationship between sleep-disordered breathing and heart failure is controversial., Objectives: 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., Methods: 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., Measurements and Main Results: 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)., Conclusions: 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 (< 5, 5-15, 15-30, 30-50, > 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., (© 2016 Associated Professional Sleep Societies, LLC.)

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 self-reported 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 < 85%); and 13.9% had daytime sleepiness. Compared with Whites, Blacks had higher odds of sleep apnea syndrome (AHI ≥ 5 plus sleepiness) (sex-, age-, and study site-adjusted odds ratio [OR] = 1.78, 95% confidence interval [CI]: 1.20, 2.63), short sleep (OR = 4.95, 95% CI: 3.56, 6.90), poor sleep quality (OR = 1.57, 95% CI: 1.00, 2.48), and daytime sleepiness (OR = 1.89, 95% CI: 1.38, 2.60). Hispanics and Chinese had higher odds of SDB and short sleep than Whites. Among non-obese individuals, Chinese had the highest odds of SDB compared to Whites. Only 7.4% to 16.2% of individuals with an AHI ≥ 15 reported a prior diagnosis of sleep apnea., Conclusions: Sleep disturbances are prevalent among middle-aged and older adults, and vary by race/ethnicity, sex, and obesity status. The high prevalence of sleep disturbances and undiagnosed sleep apnea among racial/ethnic minorities may contribute to health disparities., (© 2015 Associated Professional Sleep Societies, LLC.)

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.

There is increasing evidence that alterations in sleep continuity due to central nervous system arousal and/or reductions in deeper stages of sleep adversely affect blood pressure and contribute to hypertension. Disturbed sleep also blunts the normal nocturnal dip in blood pressure and may lead to sustained daytime hypertension as well. Nocturnal drops in blood pressure result from increased parasympathetic and reduced sympathetic activity during sleep. Slow-wave sleep, considered to be the most "restorative," is the specific sleep state associated with the largest decline in sympathetic activity. The time in slow-wave sleep declines with age as well as in association with other health problems. A reduction in the time in slow-wave sleep has recently been reported to predict increased incident hypertension. The mechanisms by which this occurs have not been well described but may include alterations in dipping patterns, sympathetic nervous system activity, corticotrophin pathways, and the renin-angiotensin system. This article reviews the overall association between sleep and hypertension, with a specific focus on slow-wave sleep, a possible novel target for future blood pressure interventions.

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., (Copyright © 2011 Mosby, Inc. All rights reserved.)

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 < or =85%), and short sleep duration (< or =6.5 hours). The main outcome was prehypertension (> or =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<0.01)., 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.