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Brief Summary: Non-rapid eye movement (NREM) parasomnias are relatively common among children and can often persist into adulthood, where they can pose as a clinical challenge:, the behaviors can result in injury or have negative impacts on functioning and quality of life, thus necessitating treatment, but the choice of treatment is complicated by the lack of evidence—based guidelines, as well as potential side effects. The aim of this retrospective analysis is to examine the most frequently used treatment strategies and pharmaceuticals for NREM parasomnias and evaluate perceived outcomes based on the patient's subjective reports of the frequency and severity of symptoms. 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Sleep disorders like insomnia and obstructive sleep apnoea (OSA) impair sleep quality and increase the risk of cardiovascular disease (CVD) including hypertension, heart failure (HF), and atrial fibrillation. Why that obese patient with snoring has recurrent atrial fibrillation Obstructive sleep apnoea commonly occurs with atrial fibrillation (AF) with prevalence rates of 21-74%. Obstructive sleep apnoea should be suspected if a non-dipping pattern or nocturnal hypertension is observed, and treatment of OSA may improve BP management. [Extracted from the article]

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. [ABSTRACT FROM AUTHOR]

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/m2. 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. [ABSTRACT FROM AUTHOR]

Summary: 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]