Insomnia is the most prevalent sleep disorder, affecting up to one third of the adult population and is increasingly recognised as a potential contributor to cardiovascular disease (CVD), a leading cause of global morbidity and mortality. This narrative review examines the complex relationship between insomnia and CVD, integrating epidemiological, genetic and mechanistic evidence to assess whether insomnia represents a causal cardiovascular risk factor. Large prospective cohort studies and meta-analyses consistently show that insomnia symptoms and clinically diagnosed insomnia are associated with increased risks of hypertension, myocardial infarction, stroke, heart failure and cardiovascular mortality, with stronger associations observed in individuals with short sleep duration or persistent insomnia. Mendelian randomization studies involving millions of participants further support a likely causal link, suggesting that genetic liability to insomnia increases the risk of multiple cardiometabolic outcomes. Biological plausibility is supported by evidence of autonomic imbalance, hypothalamic-pituitary-adrenal axis activation, inflammation and adverse blood pressure profiles in individuals with insomnia. However, insomnia is a heterogeneous condition, frequently coexisting with other sleep disorders and influenced by psychosocial and circadian factors, which complicates causal inference. Importantly, evidence that treatment of insomnia reduces cardiovascular risk remains limited. While cognitive behavioural therapy for insomnia improves sleep outcomes and some cardiometabolic biomarkers, randomised trials have not demonstrated clear benefits on blood pressure or other cardiovascular endpoints and some pharmacological treatments may even be associated with harm. Overall, current evidence suggests that insomnia is a plausible and potentially causal risk factor for CVD, but definitive proof of reversibility through treatment is lacking. Well-powered, rigorously designed trials targeting patients with clinically defined insomnia are needed to determine whether effective insomnia treatment can meaningfully reduce cardiovascular risk and inform future prevention strategies.

Abstract Introduction Obstructive sleep apnea (OSA) is highly prevalent in symptomatic atrial fibrillation (AF) patients undergoing ablation and may reduce the efficacy of rhythm control strategies in patients with AF. However, consecutive sleep testing has not been confirmed in a larger general AF population and less is known regarding the prevalence of OSA by subtype of AF. Methods In this pragmatic, phase IV prospective cohort study, we performed first-time testing for sleep apnea on consecutively enrolled ambulatory AF patients from outpatient clinics using a home sleep test. The primary outcome of our study was the prevalence of undiagnosed mild or moderate/severe OSA in the AF cohort. Results We performed sleep testing in 180 AF patients (126 paroxysmal (70%) and 54 persistent or long standing persistent (30%)). Among enrolled patients, 40 (31.3%) had undergone AF catheter ablation, 35 (27.3%) had undergone a previous cardioversion, and 51 (40.0%) had undergone no prior AF related procedure. The prevalence of undiagnosed OSA was 83.3% with 47.2% meeting moderate or severe criteria. Patients with persistent/longstanding persistent AF demonstrated the highest rates of OSA with 52 (96.3%) testing positive for OSA and with 35 (64.2%) demonstrating moderate/severe OSA. Conclusion Consecutive sleep testing in ambulatory AF patients enrolled from outpatient clinics, regardless of AF symptom status or AF treatment strategy, demonstrated a high prevalence of undiagnosed OSA with more severe OSA among those with persistent AF compared to non-paroxysmal AF. Our study demonstrates higher prevalence of OSA among those with persistent AF compared to paroxysmal AF as well. Widely used clinical prediction instruments cannot effectively be used to guide sleep testing decisions in AF patients and our results suggest routine sleep apnea testing should be strongly considered in the comprehensive evaluation of all AF patients, but particularly those with persistent AF. Support (if any) This study was sponsored by the Zoll Medical Corporation. The study was performed at the Brigham and Women’s Hospital AF Center of Excellence that is funded partly by the Brigham Research Institute Director’s Transformative Award #2019A018348.

OBJECTIVES:MassHealth Limited (MHL), a subset of Massachusetts' Medicaid program, covers sleep studies but not obstructive sleep apnea (OSA) treatment, including positive airway pressure (PAP) therapy. This study characterizes the demographics and OSA severity of patients receiving MHL and compares them to those with full MassHealth (MH) benefits to assess inequities in treatment access. PARTICIPANTS AND METHODS:We conducted a retrospective cohort study of 134 MHL and 402 MH patients who underwent a sleep study for OSA evaluation at the Brigham and Women's Faulkner Hospital (2019-2024). We analyzed age, BMI, OSA severity, SpO2 % nadir, and comorbidity burden across four patient groups based on insurance and self-reported ethnicity: MHL-Latinx, MH-Latinx, MH-Black, and MH-White, with men and women assessed separately. RESULTS:The MHL population was predominantly Latinx (90 %), with 82 % preferring Spanish, Haitian Creole, or Brazilian Portuguese as their primary language. Moderate-to-severe OSA was most prevalent in MHL-Latinx men (77.5 %) and MHL-Latinx women (53.0 %). On follow-up, about one-third of MHL-Latinx patients with moderate-to-severe OSA obtained PAP therapy through self-pay or insurance change. CONCLUSIONS:In this sample of MHL beneficiaries, a predominantly Latinx population, patients experience a high burden of moderate-to-severe OSA yet lack access to PAP therapy due to insurance limitations. Expanding MHL coverage to include OSA treatment is critical to addressing sleep health inequities.

An international expert group (European Sleep Foundation Think Tank) convened in 2022 to discuss the state of the evidence in the domain of hypersomnolence. The expert group considered the current state of knowledge based on the most relevant recent publications, discussed the current challenges in the field and identified future priorities. The purpose of this white paper is to summarize the definition, diagnosis, and pathophysiology of hypersomnolence, the epidemiology, phenotype, and management of hypersomnolence in obstructive sleep apnea and in neurological and psychiatric disorders, and the impact of hypersomnolence on daily activities, workability and health-related quality of life. The key results of the discussion were that: a) hypersomnolence is both prevalent and heterogeneous in its manifestations in a wide variety of pathological conditions encompassing obstructive sleep apnea and neurological and psychiatric disorders; and b) while multiple pathophysiological pathways are potentially involved in hypersomnolence, knowledge of the specific causal factors in individual patients remains undefined, and the specific factors responsible for excessive daytime sleepiness vs. excessive need for sleep remain largely unclear. The clinical implications of these results are the occurrence of important limitations to the development of personalized approaches to diagnosis, prognosis, and management of hypersomnolence, which is essential considering the high societal and personal costs of hypersomnolence, and its substantial adverse impact on quality of life. Research priorities should address these limitations with improved quantification of hypersomnolence and with an evidence base on the costs and benefit of hypersomnolence management in patients with respiratory, neurologic, and psychiatric disorders.

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.

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.

Background: Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice and is associated with significant morbidity, mortality, and health system costs. Obstructive sleep apnea (OSA) is a highly prevalent condition affecting more than one third of the global adult population and, among patients with comorbid AF, contributes to poor AF related quality of life. However, the prevalence of undiagnosed OSA in the general AF population is unknown. Methods: In this pragmatic, phase IV prospective cohort study, we performed sleep testing on consecutively enrolled ambulatory AF patients for OSA using a cloud-based disposable home sleep test (the WatchPAT system). The primary outcome of our study was the prevalence of undiagnosed mild (5≤AHI<15) or moderate/severe (AHI≥15) OSA in the general AF population. A prespecified power analysis supports 80% power to detect a <5% difference in OSA prevalence compared to the general population (defined by AHI cut-offs of ≥5 or ≥15). Results: We performed sleep testing in 180 AF patients. Enrollment concluded early after a prespecified interim power analysis showed a larger than predicted difference of OSA prevalence between AF patients and the general population. Among the patients tested, 126 (70.4%) had paroxysmal AF, and 53 (29.6%) had persistent/long standing persistent AF. None had previous sleep testing. Our results show that the prevalence of OSA was 83.3% by AHI≥5 and 47.2% had moderate/severe OSA (AHI≥15). Patients with persistent or long standing persistent AF demonstrated even higher rates of OSA with 51 (96.3%) testing positive for OSA (AHI≥5) and 35 (64.2%) with moderate/severe OSA (AHI≥15). Conversely, standardized OSA screening instruments (Stop-BANG questionnaire or Epworth Sleepiness Scale) were poorly predictive of OSA in AF patients (AUC 0.66 and AUC 0.44, respectively). Conclusions: Undiagnosed OSA is highly prevalent in the general AF population. Our results demonstrate that OSA prevalence in AF patients exceeds that in the general population with a high degree of confidence. Widely used clinical prediction instruments cannot effectively be used to guide sleep testing decisions in AF patients. Our results suggest routine OSA testing should be performed in the comprehensive evaluation of all AF patients.

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.

Central sleep apnea (CSA) is associated with increased mortality, particularly in heart failure. This review discusses current treatment options with a focus on different positive airway pressure (PAP) modalities, the clinical implication of continuous PAP (CPAP) failure, and key advancements in adaptive servo-ventilation (ASV). CPAP reduces CSA by about 50

The presentation of sleep disorders varies widely among women and men, and sleep disorders among women are frequently subject to under- and delayed diagnosis. Insomnia is a complex sleep disorder with a multifactorial etiology, and women face many sex-specific sleep health challenges that may contribute to and influence the presence of insomnia symptoms across their lifespan. These include sex differences in neurobiology, hormonal variation during menstruation, pregnancy and menopause, increased prevalence of mood disorders, increased vulnerability to adverse socioeconomic factors, and gender discrimination, among other psychosocial stressors, particularly among women of racial-ethnic minority. As the medical community continues to recognize the significance of sleep as a vital pillar of overall wellbeing, the integration of sex-specific considerations in research, diagnosis, and treatment strategies is essential to optimizing sleep health for women.

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.(Heart Rhythm 2023 (c) 2023 Heart Rhythm Society. All rights reserved.