CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea.

BACKGROUND: Obstructive sleep apnea is associated with an increased risk of cardiovascular events; whether treatment with continuous positive airway pressure (CPAP) prevents major cardiovascular events is uncertain. METHODS: After a 1-week run-in period during which the participants used sham CPAP, we randomly assigned 2717 eligible adults between 45 and 75 years of age who had moderate-to-severe obstructive sleep apnea and coronary or cerebrovascular disease to receive CPAP treatment plus usual care (CPAP group) or usual care alone (usual-care group). The primary composite end point was death from cardiovascular causes, myocardial infarction, stroke, or hospitalization for unstable angina, heart failure, or transient ischemic attack. Secondary end points included other cardiovascular outcomes, health-related quality of life, snoring symptoms, daytime sleepiness, and mood. RESULTS: Most of the participants were men who had moderate-to-severe obstructive sleep apnea and minimal sleepiness. In the CPAP group, the mean duration of adherence to CPAP therapy was 3.3 hours per night, and the mean apnea-hypopnea index (the number of apnea or hypopnea events per hour of recording) decreased from 29.0 events per hour at baseline to 3.7 events per hour during follow-up. After a mean follow-up of 3.7 years, a primary end-point event had occurred in 229 participants in the CPAP group (17.0%) and in 207 participants in the usual-care group (15.4%) (hazard ratio with CPAP, 1.10; 95% confidence interval, 0.91 to 1.32; P=0.34). No significant effect on any individual or other composite cardiovascular end point was observed. CPAP significantly reduced snoring and daytime sleepiness and improved health-related quality of life and mood. CONCLUSIONS: Therapy with CPAP plus usual care, as compared with usual care alone, did not prevent cardiovascular events in patients with moderate-to-severe obstructive sleep apnea and established cardiovascular disease. (Funded by the National Health and Medical Research Council of Australia and others; SAVE ClinicalTrials.gov number, NCT00738179 ; Australian New Zealand Clinical Trials Registry number, ACTRN12608000409370 .).

Physician Decision Making and Clinical Outcomes With Laboratory Polysomnography or Limited-Channel Sleep Studies for Obstructive Sleep Apnea: A Randomized Trial.

BACKGROUND: The clinical utility of limited-channel sleep studies (which are increasingly conducted at home) versus laboratory polysomnography (PSG) for diagnosing obstructive sleep apnea (OSA) is unclear. OBJECTIVE: To compare patient outcomes after PSG versus limited-channel studies. DESIGN: Multicenter, randomized, noninferiority study. (Australian New Zealand Clinical Trials Registry: ACTRN12611000926932). SETTING: 7 academic sleep centers. PARTICIPANTS: Patients (n = 406) aged 25 to 80 years with suspected OSA. INTERVENTION: Sleep study information disclosed to sleep physicians comprised level 1 (L1) PSG data (n = 135); level 3 (L3), which included airflow, thoracoabdominal bands, body position, electrocardiography, and oxygen saturation (n = 136); or level 4 (L4), which included oxygen saturation and heart rate (n = 135). MEASUREMENTS: The primary outcome was change in Functional Outcomes of Sleep Questionnaire (FOSQ) score at 4 months. Secondary outcomes included the Epworth Sleepiness Scale (ESS), the Sleep Apnea Symptoms Questionnaire (SASQ), continuous positive airway pressure (CPAP) compliance, and physician decision making. RESULTS: Change in FOSQ score was not inferior for L3 (mean difference [MD], 0.01 [95% CI, -0.47 to 0.49; P = 0.96]) or L4 (MD, -0.46 [CI, -0.94 to 0.02; P = 0.058]) versus L1 (noninferiority margin [NIM], -1.0). Compared with L1, change in ESS score was not inferior for L3 (MD, 0.08 [CI, -0.98 to 1.13; P = 0.89]) but was inconclusive for L4 (MD, 1.30 [CI, 0.26 to 2.35; P = 0.015]) (NIM, 2.0). For L4 versus L1, there was less improvement in SASQ score (-17.8 vs. -24.7; P = 0.018), less CPAP use (4.5 vs. 5.3 hours per night; P = 0.04), and lower physician diagnostic confidence (P = 0.003). LIMITATION: Limited-channel studies were simulated by extracting laboratory PSG data and were not done in the home. CONCLUSION: The results support manually scored L3 testing in routine practice. Poorer outcomes with L4 testing may relate, in part, to reduced physician confidence. PRIMARY FUNDING SOURCE: National Health and Medical Research Council and Repat Foundation.

Predictors of obstructive sleep apnoea in patients admitted for acute coronary syndrome.

Identifying undiagnosed obstructive sleep apnoea (OSA) patients in cardiovascular clinics could improve their management. Aiming to build an OSA predictive model, a broad analysis of clinical variables was performed in a cohort of acute coronary syndrome (ACS) patients.Sociodemographic, anthropometric, life-style and pharmacological variables were recorded. Clinical measures included blood pressure, electrocardiography, echocardiography, blood count, troponin levels and a metabolic panel. OSA was diagnosed using respiratory polygraphy. Logistic regression models and classification and regression trees were used to create predictive models.A total of 978 patients were included (298 subjects with apnoea-hypopnoea index (AHI) <15 events·h-1 and 680 with AHI ≥15 events·h-1). Age, BMI, Epworth sleepiness scale, peak troponin levels and use of calcium antagonists were the main determinants of AHI ≥15 events·h-1 (C statistic 0.71; sensitivity 94%; specificity 24%). Age, BMI, blood triglycerides, peak troponin levels and Killip class ≥II were determinants of AHI ≥30 events·h-1 (C statistic of 0.67; sensitivity 31%; specificity 86%).Although a set of variables associated with OSA was identified, no model could successfully predict OSA in patients admitted for ACS. Given the high prevalence of OSA, the authors propose respiratory polygraphy as a to-be-explored strategy to identify OSA in ACS patients.

Association of daytime sleepiness with obstructive sleep apnoea and comorbidities varies by sleepiness definition in a population cohort of men.

BACKGROUND AND OBJECTIVE: To determine correlates of excessive daytime sleepiness (EDS) identified with the Epworth Sleepiness Scale (ESS) and a more broad definition, while accounting for obstructive sleep apnoea (OSA) in community dwelling men. METHODS: Participants of the Men Androgens Inflammation Lifestyle Environment and Stress (MAILES) Study (n = 837, ≥ 40 years) without a prior OSA diagnosis, underwent in-home full unattended polysomnography (PSG, Embletta X100), completed the ESS, STOP questionnaire and Pittsburgh Sleep Quality Index in 2010-2011. In 2007-2010, questionnaires and biomedical assessment (in South Australian public hospital-based clinics) identified medical conditions. An alternate EDS definition (EDSAlt ) consisted of ≥ 2 of 3 problems (feeling sleepy sitting quietly; feeling tired/fatigued/sleepy; trouble staying awake). RESULTS: EDSAlt (30.4%, n = 253), but not ESS ≥ 11 (EDSESS , 12.6%, n = 104), increased significantly across OSA severity and body mass index categories. In adjusted analyses, EDSESS was significantly associated with depression: odds ratio (OR), 95%CI: 2.2 (1.3-3.8) and nocturia: 2.0 (1.3-3.2). EDSAlt was associated with depression, financial stress, relationship, work-life balance problems and associations with nocturia and diabetes were borderline. After excluding men with EDSESS , EDSAlt was associated with oxygen desaturation index (3%) ≥ 16 and the highest arousal index quartile but not with comorbidities. CONCLUSION: Sleepiness not necessarily leading to dozing, but not ESS ≥ 11, was related to sleep disordered breathing. Clinicians should be alert to (1) differing perspectives of sleepiness for investigation and treatment of OSA, and (2) the presence of depression and nocturia in men presenting with significant Epworth sleepiness regardless of the presence of OSA.

Undiagnosed obstructive sleep apnea is independently associated with reductions in quality of life in middle-aged, but not elderly men of a population cohort.

PURPOSE: Obstructive sleep apnea (OSA) is now highly prevalent but largely undiagnosed. Quality of life is an indicator of both the impact of undiagnosed OSA and the need for strategies to increase OSA diagnosis. We determined age-related impacts of undiagnosed OSA on health-related quality of life (HRQL) and whether this was independent of sleepiness and comorbidities. METHODS: In 2010-2012, 837 participants from the Men Androgen Inflammation Lifestyle Environment and Stress Study (population cohort n = 1869, ≥40 years, Adelaide, Australia), without a prior OSA diagnosis underwent full in-home polysomnography (Embletta X100) and completed the Epworth Sleepiness Scale and SF-36 questionnaire. The effects of the apnea-hypopnea index (AHI) on SF-36 physical (PCS) and mental (MCS) component summary scores and standardized SF-36 scale z-scores were estimated using multiple linear regression adjusted for major comorbidities and sleepiness, stratified by age. RESULTS: Men ≤69 years demonstrated significant (p < 0.05) decrements/event increase in AHI in PCS score [unstandardized B coefficient (SE) = -0.068 (0.023)], physical functioning, role physical, general health, and vitality z-scores in fully adjusted models. Severe OSA (AHI ≥30) was associated with significant reductions in PCS [B = -4.1 (1.1)] and MCS score [B = -3.6 (1.2)] independent of sleepiness and comorbidities which were attenuated but persisted in men <69 years without depression. In men aged ≥70 years, statistically significant AHI-associated impairments were generally not seen. CONCLUSIONS: Undiagnosed OSA was a major independent contributor to HRQL impairments in men <69 years. Improved strategies to identify undiagnosed OSA are indicated that may require a reduced focus on daytime sleepiness.

Ambulatory management strategies for obstructive sleep apnea.

The prevalence of obstructive sleep apnea (OSA) has been steadily rising over recent decades and patient access to laboratory-based sleep services and specialist consultations have become increasingly limited, resulting in potential delays in treatment. As a result, there has been growing interest in the use of non-sleep laboratory methods for diagnosing and managing OSA, including the use of screening questionnaires, portable sleep monitoring devices, and home autotitrating continuous positive airway pressure. There is also evidence in support of a role for alternative health care professionals, such as sleep-trained nurses and primary care physicians in the diagnosis and treatment of OSA. In this review, we compare the different types of home monitoring devices, discuss the limitations of portable monitoring compared with full laboratory polysomnography, and summarize the results from published comparative effectiveness studies which have evaluated ambulatory models of care for the management of OSA. We also consider how future models of care that may be needed to deal with the burden of disease will evolve and some of the issues that prevent the translation of such models of care in many countries.

Comparative Effectiveness of Supine Avoidance versus Continuous Positive Airway Pressure for Treating Supine-isolated Sleep Apnea: A Clinical Trial.

Rationale: About 20-35% of patients with obstructive sleep apnea (OSA) have supine-isolated OSA, for which supine sleep avoidance could be an effective therapy. However, traditional supine discomfort-based methods show poor tolerance and compliance to treatment and so cannot be recommended. Supine alarm devices show promise, but evidence to support favorable adherence to treatment and effectiveness at reducing excessive daytime sleepiness compared with continuous positive airway pressure (CPAP) remains limited. Objectives: To establish if alarm-based supine-avoidance treatment in patients with supine-isolated OSA is noninferior to CPAP in reducing daytime sleepiness. Methods: After baseline questionnaire administration and in-home supine-time and polysomnography assessments, patients with supine-isolated OSA and Epworth Sleepiness Scale scores ⩾8 were randomized to ⩾6 weeks of supine-avoidance or CPAP treatment, followed by crossover to the remaining treatment with repeat assessments. Noninferiority was assessed from change in Epworth Sleepiness Scale with supine avoidance compared with CPAP using a prespecified noninferiority margin of 1.5. Average nightly treatment use over all nights and treatment efficacy and effectiveness at reducing respiratory disturbances were also compared between treatments. Results: The reduction in sleepiness score with supine avoidance (mean [95% confidence interval], -1.9 [-2.8 to -1.0]) was noninferior to that with CPAP (-2.4 [-3.3 to -1.4]) (supine avoidance-CPAP difference, -0.4 [-1.3 to 0.6]), and the lower confidence limit did not cross the noninferiority margin of 1.5 (P = 0.021). Average treatment use was higher with supine avoidance compared with CPAP (mean ± standard deviation, 5.7 ± 2.4 vs. 3.9 ± 2.7 h/night; P < 0.001). Conclusions: In patients with supine-isolated OSA, vibrotactile supine alarm device therapy is noninferior to CPAP for reducing sleepiness and shows superior treatment adherence. Clinical trial registered with www.anzctr.org.au (ACTRN 12613001242718).

Ambulatory models of care for obstructive sleep apnoea: Diagnosis and management.

The high prevalence of obstructive sleep apnoea (OSA) and increasing awareness of its potential health consequences has placed significant pressure on laboratory-based sleep services leading to growing waiting lists and delays in diagnosis and treatment. Consequently, there has been increasing interest in the use of simplified, ambulatory models of care involving clinical prediction tools, portable sleep monitoring and home autotitrating continuous positive airway pressure. Researchers are also exploring the potential role for a wider range of health-care providers, including trained nurses and general practitioners, in the primary management of OSA. Recent randomized, controlled studies evaluating the clinical effectiveness of ambulatory management strategies versus traditional laboratory-based care for patients with OSA have consistently demonstrated that comparable patient outcomes can be achieved. The cost-effectiveness of these strategies is currently being debated, and further research examining the long-term economic implications of ambulatory models of care is needed.

Obstructive sleep apnoea in adults.

Obstructive sleep apnoea (OSA) is characterised by repetitive closure of the upper airway, repetitive oxygen desaturations and sleep fragmentation. The prevalence of adult OSA is increasing because of a worldwide increase in obesity and the ageing of populations. OSA presents with a variety of symptoms the most prominent of which are snoring and daytime tiredness. Interestingly though, a significant proportion of OSA sufferers report little or no daytime symptoms. OSA has been associated with an increased risk of cardiovascular disease, cognitive abnormalities and mental health problems. Randomised controlled trial evidence is awaited to confirm a causal relationship between OSA and these various disorders. The gold standard diagnostic investigation for OSA is overnight laboratory-based polysomnography (sleep study), however, ambulatory models of care incorporating screening questionnaires and home sleep studies have been recently evaluated and are now being incorporated into routine clinical practice. Patients with OSA are very often obese and exhibit a range of comorbidities, such as hypertension, depression and diabetes. Management, therefore, needs to be based on a multidisciplinary and holistic approach which includes lifestyle modifications. Continuous positive airway pressure (CPAP) is the first-line therapy for severe OSA. Oral appliances should be considered in patients with mild or moderate disease, or in those unable to tolerate CPAP. New, minimally invasive surgical techniques are currently being developed to achieve better patient outcomes and reduce surgical morbidity. Successful long-term management of OSA requires careful patient education, enlistment of the family's support and the adoption of self-management and patient goal-setting principles.

Primary care vs specialist sleep center management of obstructive sleep apnea and daytime sleepiness and quality of life: a randomized trial.

IMPORTANCE: Due to increasing demand for sleep services, there has been growing interest in ambulatory models of care for patients with obstructive sleep apnea. With appropriate training and simplified management tools, primary care physicians are ideally positioned to take on a greater role in diagnosis and treatment. OBJECTIVE: To compare the clinical efficacy and within-trial costs of a simplified model of diagnosis and care in primary care relative to that in specialist sleep centers. DESIGN, SETTING, AND PATIENTS: A randomized, controlled, noninferiority study involving 155 patients with obstructive sleep apnea that was treated at primary care practices (n=81) in metropolitan Adelaide, 3 rural regions of South Australia or at a university hospital sleep medicine center in Adelaide, Australia (n = 74), between September 2008 and June 2010. INTERVENTIONS: Primary care management of obstructive sleep apnea vs usual care in a specialist sleep center; both plans included continuous positive airway pressure, mandibular advancement splints, or conservative measures only. MAIN OUTCOME AND MEASURES: The primary outcome was 6-month change in Epworth Sleepiness Scale (ESS) score, which ranges from 0 (no daytime sleepiness) to 24 points (high level of daytime sleepiness). The noninferiority margin was -2.0. Secondary outcomes included disease-specific and general quality of life measures, obstructive sleep apnea symptoms, adherence to using continuous positive airway pressure, patient satisfaction, and health care costs. RESULTS: There were significant improvements in ESS scores from baseline to 6 months in both groups. In the primary care group, the mean baseline score of 12.8 decreased to 7.0 at 6 months (P < .001), and in the specialist group, the score decreased from a mean of 12.5 to 7.0 (P < .001). Primary care management was noninferior to specialist management with a mean change in ESS score of 5.8 vs 5.4 (adjusted difference, -0.13; lower bound of 1-sided 95% CI, -1.5; P = .43). There were no differences in secondary outcome measures between groups. Seventeen patients (21%) withdrew from the study in the primary care group vs 6 patients (8%) in the specialist group. CONCLUSIONS AND RELEVANCE: Among patients with obstructive sleep apnea, treatment under a primary care model compared with a specialist model did not result in worse sleepiness scores, suggesting that the 2 treatment modes may be comparable. TRIAL REGISTRATION anzctr.org.au Identifier: ACTRN12608000514303.

A simplified model of screening questionnaire and home monitoring for obstructive sleep apnoea in primary care.

BACKGROUND: To address the growing burden of disease and long waiting lists for sleep services, a simplified two-stage model was developed and validated for identifying obstructive sleep apnoea (OSA) in primary care using a screening questionnaire followed by home sleep monitoring. METHODS: 157 patients aged 25-70 years attending their primary care physician for any reason at six primary care clinics in rural and metropolitan regions of South Australia participated. The first 79 patients formed the development group and the next 78 patients the validation group. A screening questionnaire was developed from factors identified from sleep surveys, demographic and anthropometric data to be predictive of moderate to severe OSA. Receiver operating characteristic (ROC) curve analysis was used to validate the two-channel ApneaLink device against full polysomnography. The diagnostic accuracy of the overall two-stage model was then evaluated. RESULTS: Snoring, waist circumference, witnessed apnoeas and age were predictive of OSA and incorporated into a screening questionnaire (ROC area under curve (AUC) 0.84, 95% CI 0.75 to 0.94, p<0.001). ApneaLink oximetry with a 3% dip rate was highly predictive of OSA (AUC 0.96, 95% CI 0.91 to 1.0, p<0.001). The two-stage diagnostic model showed a sensitivity of 0.97 (95% CI 0.81 to 1.00) and specificity of 0.87 (95% CI 0.74 to 0.95) in the development group, and a sensitivity of 0.88 (95% CI 0.60 to 0.98) and specificity of 0.82 (95% CI 0.70 to 0.90) in the validation group. CONCLUSION: A two-stage model of screening questionnaire followed by home oximetry can accurately identify patients with OSA in primary care and has the potential to expedite care for patients with this common sleep disorder.

Polysomnographic Predictors of Treatment Response to Cognitive Behavioral Therapy for Insomnia in Participants With Co-morbid Insomnia and Sleep Apnea: Secondary Analysis of a Randomized Controlled Trial.

OBJECTIVE: Co-morbid insomnia and sleep apnea (COMISA) is a common and debilitating condition that is more difficult to treat compared to insomnia or sleep apnea-alone. Emerging evidence suggests that cognitive behavioral therapy for insomnia (CBTi) is effective in patients with COMISA, however, those with more severe sleep apnea and evidence of greater objective sleep disturbance may be less responsive to CBTi. Polysomnographic sleep study data has been used to predict treatment response to CBTi in patients with insomnia-alone, but not in patients with COMISA. We used randomized controlled trial data to investigate polysomnographic predictors of insomnia improvement following CBTi, versus control in participants with COMISA. METHODS: One hundred and forty five participants with insomnia (ICSD-3) and sleep apnea [apnea-hypopnea index (AHI) ≥ 15] were randomized to CBTi (n = 72) or no-treatment control (n = 73). Mixed models were used to investigate the effect of pre-treatment AHI, sleep duration, and other traditional (AASM sleep macrostructure), and novel [quantitative electroencephalography (qEEG)] polysomnographic predictors of between-group changes in Insomnia Severity Index (ISI) scores from pre-treatment to post-treatment. RESULTS: Compared to control, CBTi was associated with greater ISI improvement among participants with; higher AHI (interaction p = 0.011), less wake after sleep onset (interaction p = 0.045), and less N3 sleep (interaction p = 0.005). No quantitative electroencephalographic, or other traditional polysomnographic variables predicted between-group ISI change (all p > 0.09). DISCUSSION: Among participants with COMISA, higher OSA severity predicted a greater treatment-response to CBTi, versus control. People with COMISA should be treated with CBTi, which is effective even in the presence of severe OSA and objective sleep disturbance.

Effect of depression, anxiety, and stress symptoms on response to cognitive behavioral therapy for insomnia in patients with comorbid insomnia and sleep apnea: a randomized controlled trial.

STUDY OBJECTIVES: Patients with comorbid insomnia and sleep apnea (COMISA) report increased severity of depression, anxiety, and stress symptoms compared to patients with either insomnia or sleep apnea alone. Although cognitive behavioral therapy for insomnia (CBTi) is an effective treatment for COMISA, previous research suggests a reduced response to CBTi by patients with insomnia and depression, anxiety, and stress symptoms. Therefore, we used randomized controlled trial data to investigate the impact of depression, anxiety, and stress symptoms before treatment on changes in insomnia after CBTi vs control in patients with COMISA. METHODS: 145 patients with COMISA (insomnia as defined by the International Classification of Sleep Disorders, third edition and apnea-hypopnea index ≥ 15 events/h) were randomized to CBTi (n = 72) or no-treatment control (n = 73). One-week sleep diaries and standardized questionnaire measures of insomnia, sleepiness, fatigue, depression, anxiety, and stress were completed pretreatment and posttreatment. Mixed models were used to examine interactions between depression, anxiety, and stress symptoms before treatment, intervention-group (CBTi, control), and time (pretreatment, posttreatment) on insomnia symptoms. RESULTS: Approximately half of this COMISA sample reported at least mild symptoms of depression (57%), anxiety (53%), and stress (48%) before treatment. Patients reporting greater depression, anxiety, and stress symptoms before treatment also reported increased severity of insomnia, daytime fatigue, and sleepiness. Improvements in questionnaire and diary-measured insomnia symptoms improved during CBTi and were not moderated by severity of depression, anxiety, or stress symptoms before treatment (all interaction P ≥ .11). CONCLUSIONS: We found no evidence that symptoms of depression, anxiety, or stress impair the effectiveness of CBTi in improving insomnia symptoms in patients with COMISA. Patients with COMISA and comorbid symptoms of depression, anxiety, and stress should be referred for CBTi to treat insomnia and improve subsequent management of their obstructive sleep apnea. CLINICAL TRIAL REGISTRATION: Registry: Australian New Zealand Clinical Trials Registry; Name: Treating comorbid insomnia with obstructive sleep apnea (COMISA) study: A new treatment strategy for patients with combined insomnia and sleep apnea; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=365184; Identifier: ACTRN12613001178730.

Obstructive Sleep Apnoea: From pathogenesis to treatment: Current controversies and future directions.

Obstructive sleep apnoea (OSA) is a common disease, recognized as an independent risk factor for a range of clinical conditions, such as hypertension, stroke, depression and diabetes. Despite extensive research over the past two decades, the mechanistic links between OSA and other associated clinical conditions, including metabolic disorders and cardiovascular disease, remain unclear. Indeed, the pathogenesis of OSA itself remains incompletely understood. This review provides opinions from a number of leading experts on issues related to OSA and its pathogenesis, interaction with anaesthesia, metabolic consequences and comorbidities, cardiovascular disease, genetics, measurement and diagnosis, surgical treatment and pharmacotherapeutic targets.

A randomized controlled trial of nurse-led care for symptomatic moderate-severe obstructive sleep apnea.

RATIONALE: Obstructive sleep apnea (OSA) is a prevalent disease. Often limited clinical resources result in long patient waiting lists. Simpler validated methods of care are needed. OBJECTIVES: To demonstrate that a nurse-led model of care can produce health outcomes in symptomatic moderate-severe OSA not inferior to physician-led care. METHODS: A randomized controlled multicenter noninferiority clinical trial was performed. Of 1,427 potentially eligible patients at 3 centers, 882 consented to the trial. Of these, 263 were excluded on the basis of clinical criteria. Of the remaining 619, 195 met home oximetry criteria for high-probability moderate-severe OSA and were randomized to 2 models of care: model A, the simplified model, using home autoadjusting positive airway pressure to set therapeutic continuous positive airway pressure (CPAP), with all care supervised by an experienced nurse; and model B, involving two laboratory polysomnograms to diagnose and treat OSA, with clinical care supervised by a sleep physician. The primary end point was change in Epworth Sleepiness Scale (ESS) score after 3 months of CPAP. Other outcome measures were collected. MEASUREMENTS AND MAIN RESULTS: For the primary outcome change in ESS score, nurse-led management was no worse than physician-led management (4.02 vs. 4.15; difference, -0.13; 95% confidence interval: -1.52, 1.25) given a prespecified noninferiority margin of -2 for the lower 95% confidence interval. There were also no differences between both groups in CPAP adherence at 3 months or other outcome measures. Within-trial costs were significantly less in model A. CONCLUSIONS: A simplified nurse-led model of care has demonstrated noninferior results to physician-directed care in the management of symptomatic moderate-severe OSA, while being less costly. Clinical trial registered with http://www.anzctr.org.au (ACTRN012605000064606).

Effects of alcohol and sleep restriction on simulated driving performance in untreated patients with obstructive sleep apnea.

BACKGROUND: Because of previous sleep disturbance and sleep hypoxia, patients with obstructive sleep apnea (OSA) might be more vulnerable to the effects of alcohol and sleep restriction than healthy persons. OBJECTIVE: To compare the effects of sleep restriction and alcohol on driving simulator performance in patients with OSA and age-matched control participants. DESIGN: Driving simulator assessments in 2 groups under 3 different conditions presented in random order. SETTING: Adelaide Institute for Sleep Health, Sleep Laboratory, Adelaide, Australia. PARTICIPANTS: 38 untreated patients with OSA and 20 control participants. MEASUREMENTS: Steering deviation, crashes, and braking reaction time. INTERVENTION: Unrestricted sleep, sleep restricted to a maximum of 4 hours, and ingestion of an amount of 40% vodka calculated to achieve a blood alcohol level of 0.05 g/dL. RESULTS: Patients with OSA demonstrated increased steering deviation compared with control participants (mean, 50.5 cm [95% CI, 46.1 to 54.9 cm] in the OSA group and 38.4 cm [CI, 32.4 to 44.4 cm] in the control group; P < 0.01) and significantly greater steering deterioration over time (group by time interaction, P = 0.02). The increase in steering deviation after sleep restriction and alcohol was approximately 40% greater in patients with OSA than in control participants (group by condition interaction, P = 0.04). Patients with OSA crashed more frequently than control participants (1 vs. 24 participants; odds ratio [OR], 25.4; P = 0.03) and crashed more frequently after sleep restriction (OR, 4.0; P < 0.01) and alcohol consumption (OR, 2.3; P = 0.02) than after normal sleep. In patients with OSA, prolonged eye closure (>2 seconds) and microsleeps (> 2 seconds of theta activity on electroencephalography) were significant crash predictors (OR, 19.2 and 7.2, respectively; P < 0.01). Braking reaction time was slower after sleep restriction than after normal sleep (mean, 1.39 [SD, 0.06] seconds vs. 1.22 [SD, 0.04] seconds; P < 0.01) but not after alcohol consumption. No group differences were found. LIMITATION: Simulated driving was assessed rather than on-road driving. CONCLUSION: Patients with OSA are more vulnerable than healthy persons to the effects of alcohol consumption and sleep restriction on various driving performance variables. PRIMARY FUNDING SOURCE: Australian National Health and Medical Research Council.

The effect of cognitive and behavioral therapy for insomnia on week-to-week changes in sleepiness and sleep parameters in patients with comorbid insomnia and sleep apnea: a randomized controlled trial.

STUDY OBJECTIVES: While cognitive and behavioral therapy for insomnia (CBTi) is an effective treatment in patients with comorbid moderate and severe obstructive sleep apnea (OSA), there is concern that the bedtime restriction component of CBTi might dangerously exacerbate daytime sleepiness in such patients. We examined randomized controlled trial data to investigate the effect of OSA severity, and pretreatment daytime sleepiness on week-to-week changes in daytime sleepiness and sleep parameters during CBTi and no-treatment control. METHODS: One hundred and forty-five patients with untreated physician-diagnosed OSA (apnea-hypopnea index ≥15) and psychologist-diagnosed insomnia (ICSD-3) were randomized to a 4-week CBTi program (n = 72) or no-treatment control (n = 73). The Epworth sleepiness scale (ESS) and sleep diaries were completed during pretreatment, weekly CBTi sessions, and posttreatment. Effects of OSA severity, pretreatment daytime sleepiness, and intervention group on weekly changes in daytime sleepiness and sleep parameters were investigated. RESULTS: The CBTi group reported a 15% increase in ESS scores following the first week of bedtime restriction (M change = 1.3 points, 95% CI = 0.1-2.5, p = 0.031, Cohen's d = 0.27) which immediately returned to pretreatment levels for all subsequent weeks, while sleep parameters gradually improved throughout CBTi. There were no differences in changes in daytime sleepiness during treatment between CBTi and control groups or OSA-severity groups. Higher pretreatment ESS scores were associated with a greater ESS reduction during CBTi. CONCLUSIONS: CBTi appears to be a safe and effective treatment in the presence of comorbid moderate and severe OSA. Nevertheless, patients living with comorbid insomnia and sleep apnea and treated with CBTi should be monitored closely for increased daytime sleepiness during the initial weeks of bedtime restriction therapy. CLINICAL TRIAL REGISTRATION: Treating comorbid insomnia with obstructive sleep apnoea (COMISA) study: A new treatment strategy for patients with combined insomnia and sleep apnoea, https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id = 365184 Australian New Zealand Clinical Trials Registry: ACTRN12613001178730. Universal Trial Number: U1111-1149-4230.

Cognitive behavioural therapy for insomnia reduces sleep apnoea severity: a randomised controlled trial.

Insomnia and obstructive sleep apnoea (OSA) frequently co-occur and may be causally related through sleep fragmentation and/or hyperarousal mechanisms. Previous studies suggest that OSA treatment can improve insomnia severity. However, the effect of insomnia treatment on OSA severity has not been investigated. We performed a randomised controlled trial to investigate the effect of cognitive behavioural therapy for insomnia (CBTi) on OSA severity, controlling for potential sleep-stage and posture effects. 145 patients with comorbid insomnia (International Classification of Sleep Disorders, 3rd Edn) and untreated OSA (apnoea-hypopnoea index (AHI) ≥15 events·h-1 sleep) were randomised to a four-session CBTi programme or to a no-treatment control. Overnight sleep studies were completed pre- and post-treatment to measure AHI, arousal index and sleep architecture, to investigate the effect of intervention group, time, sleep stage (N1-3 or REM) and posture (supine or nonsupine) on OSA severity. The CBTi group showed a 7.5 event·h-1 greater AHI difference (mean (95% CI) decrease 5.5 (1.3-9.7) events·h-1, Cohen's d=0.2, from 36.4 events·h-1 pre-treatment) across sleep-stages and postures, compared to control (mean increase 2.0 (-2.0-6.1) events·h-1, d=0.01, from 37.5 events·h-1 at pre-treatment; interaction p=0.012). Compared to control, the CBTi group also had a greater reduction in total number (mean difference 5.6 (0.6-10.6) greater overall reduction; p=0.029) and duration of nocturnal awakenings (mean difference 21.1 (2.0-40.3) min greater reduction; p=0.031) but showed no difference in the arousal index, or sleep architecture. CBTi consolidates sleep periods and promotes a 15% decrease in OSA severity in patients with comorbid insomnia and OSA. This suggests that insomnia disorder may exacerbate OSA and provides further support for treating insomnia in the presence of comorbid OSA.