Treatment of Obstructive Sleep Apnea in Patients With Cardiac Arrhythmias

OPINION STATEMENT: Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing that is prevalent in the population and frequently under diagnosed. Usually presenting with respiratory symptoms, the most significant consequences of OSA are cardiovascular, including arrhythmias. The pathophysiology of OSA through multiple mechanisms may promote bradyarrhythmias, atrial fibrillation, premature ventricular complexes, ventricular arrhythmias, and sudden death. These mechanisms may acutely trigger nocturnal arrhythmias and may chronically affect electrical and structural myocardial changes, causing arrhythmias. Numerous epidemiological data have identified an increased risk for atrial fibrillation, ventricular fibrillation and sudden death in subjects with OSA. Diagnosis of OSA should be considered in patients with arrhythmias. However, not all patients with arrhythmias need to undergo formal testing for sleep apnea. Patients who are observed to have nocturnal arrhythmias should be considered for evaluation for possible OSA. Also, if the arrhythmia is refractory to standard therapy and if other clinical indicators of OSA are also present, there should be a low threshold for pursuing the diagnosis of sleep apnea. The principal therapy for OSA is continuous positive airway pressure (CPAP). Currently, there are limited data to support the efficacy of CPAP for arrhythmia prevention or treatment. Randomized trials are necessary to determine the efficacy of OSA treatment on arrhythmia prevention.     

Sleep apnea: Implications for heart failure

It is likely sleep apnea is highly prevalent in patients with congestive heart failure (CHF). However, as awareness is low and consensus guidelines do not exist, sleep apnea is not routinely screened for or diagnosed in CHF practice. Untreated sleep apnea may promote fatigue as well as left ventricular dysfunction, disease progression, and increased mortality. Available screening tools lack sensitivity or specificity, and there are insufficient numbers of sleep laboratories to accommodate the potentially large number of patient referrals with CHF for definitive diagnosis. In CHF patients with obstructive sleep apnea and sleepiness, treatment includes continuous positive airway pressure which may improve left ventricular function; optimal treatment for the non-sleepy patient is not established. There is no consensus regarding treatment for central sleep apnea. Studies which evaluate cardiovascular endpoints will be necessary to define management strategies for patients with CHF and either obstructive or central sleep apnea.     

Sleep Apnea and Cardiovascular Disease

Cardiovascular disease is still the leading cause of death in North America. To improve outcomes, it will likely be necessary to identify new potentially treatable conditions. Sleep apnea affects approximately 50% of patients with cardiovascular disease and is associated with increased cardiovascular risk. Continuous positive airway pressure is currently the treatment of choice and has many short-term favorable effects. The long-term benefits, however, remain elusive. Further, it may not be the ideal treatment for central sleep apnea, and the benefits of alternatives such adaptive servo-ventilation are currently being tested. Randomized controlled trials are now needed to determine whether treating sleep apnea will improve survival and reduce cardiovascular disease risk. Until better evidence becomes available, testing for sleep apnea cannot be recommended as part of the routine cardiovascular disease risk assessment, nor can its treatment be recommended for the prevention or management of cardiovascular disease in asymptomatic patients.     

Schlafapnoesyndrom bei chronischer Niereninsuffizienz

The prevalence of sleep apnea is significantly increased in patients with all stages of chronic kidney disease. In end-stage renal disease the risk to suffer from obstructive sleep apnea is approximately 4 times higher compared to patients with the same risk factors but healthy kidneys. Renal patients often lack the typical constitution of sleep apnea patients. Furthermore, symptoms, such as daytime sleepiness, are often interpreted as consequences of anemia or uremia. This might explain why sleep apnea is currently underdiagnosed. Sleep apnea and chronic kidney disease potentiate the cardiovascular risk by targeting the same important systems, such as sympathetic nerve activity or the renin-angiotensin-aldosterone cascade. Continuous positive airway pressure therapy is the treatment of choice. There is a growing body of evidence that therapy of sleep apnea leads to a significant reduction of the cardiovascular risk in patients with normal kidney function. Looking at the pathomechanism it can be assumed that renal patients also benefit from therapy of sleep-related disorders. Therefore, validated out-patient screening devices should be used to identify renal patients at risk and initiate early treatment.     

Sleep-Disordered Breathing—Do We Have to Change Gears in Heart Failure?

The majority of patients with heart failure have sleep-disordered breathing (SDB)—with central (rather than obstructive) sleep apnoea becoming the predominant form in those with more severe disease. Cyclical apnoeas and hypopnoeas are associated with sleep disturbance, hypoxaemia, haemodynamic changes, and sympathetic activation. Such patients have a worse prognosis than those without SDB. Mask-based therapies of positive airway pressure targeted at SDB can improve measures of sleep quality and partially normalise the sleep and respiratory physiology, but recent randomised trials of cardiovascular outcomes in central sleep apnoea have been neutral or suggested the possibility of harm, likely from increased sudden death. Further randomised outcome studies (with cardiovascular mortality and hospitalisation endpoints) are required to determine whether mask-based treatment for SDB is appropriate for patients with chronic systolic heart failure and obstructive sleep apnoea, for those with heart failure with preserved ejection fraction, and for those with decompensated heart failure. New therapies for sleep apnoea—such as implantable phrenic nerve stimulators—also require robust assessment. No longer can the surrogate endpoints of improvement in respiratory and sleep metrics be taken as adequate therapeutic outcome measures in patients with heart failure and sleep apnoea.     

Sleep apnea and heart failure

Sleep apnea is frequently observed in patients with heart failure (HF). In general, sleep apnea consists of two types: obstructive and central sleep apnea (OSA and CSA, respectively). OSA results from upper airway collapse, whereas CSA arises from reductions in central respiratory drive. In patients with OSA, blood pressure is frequently elevated as a result of sympathetic nervous system overactivation. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular (LV) afterload, reduces cardiac output, and may promote the progression of HF. Intermittent hypoxia and post-apneic reoxygenation cause vascular endothelial damage and possibly atherosclerosis and consequently coronary artery disease and ischemic cardiomyopathy. CSA is also characterized by apnea, hypoxia, and increased sympathetic nervous activity and, when present in HF, is associated with increased risk of death. In patients with HF, abolition of coexisting OSA by continuous positive airway pressure (CPAP) improves LV function and may contribute to the improvement of long-term outcomes. Although treatment options of CSA vary compared with OSA treatment, CPAP and other types of positive airway ventilation improve LV function and may be a promising adjunctive therapy for HF patients with CSA. Since HF remains one of the major causes of mortality in the industrialized countries, the significance of identifying and managing sleep apnea should be more emphasized to prevent the development or progression of HF.     

Prevalence and treatment of breathing disorders during sleep in patients with heart failure

Opinion statement Heart failure is a highly prevalent disorder, with significant economic impact, and is associated with excess morbidity and mortality. One factor that may contribute to the progressively declining course of heart failure is the occurrence of recurrent episodes of apnea and hypopnea. There are two major kinds of sleep-related breathing disorders: obstructive and central sleep apnea. In patients with heart failure, in contrast to the general population, central sleep apnea is the most common form of sleep-related breathing disorder. Episodes of apnea, hypopnea, and the subsequent hyperpnea cause sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure. These pathophysiologic consequences of sleep-related breathing disorders have deleterious effects on the cardiovascular system, and may be even more pronounced in the setting of established heart failure and coronary artery disease. Therefore, sleep apnea in heart failure should be treated. Central sleep apnea may be treated with nocturnal supplemental nasal oxygen, theophylline, or nasal-positive pressure devices, such as nasal continuous positive airway pressure (CPAP). The treatment of choice for obstructive sleep apnea is nasal CPAP. Although long-term controlled trials of the effect of treatment of sleep apnea on mortality in patients with heart failure are still pending, treatment of sleep apnea, both obstructive and central, does result in a decrease in sympathetic activity and an improvement in systolic function, which are known surrogates of mortality. Therefore, diagnosis and treatment of sleep-related breathing disorders may increase survival of patients with heart failure.     

Moderne Therapie der Schlafapnoe

There are different treatment options for obstructive sleep apnea, which are selectively used based on severity of sleep apnea, physical structure of the upper airway, and other medical aspects including co-morbidities. Weight loss as well as avoidance of alcohol and other CNS depressants is generally recommended. Positional training, oral appliances and surgery of the upper airways are used in selected cases. CPAP is the most effective method for treating obstructive sleep apnea irrespective of disease severity. In patients with central sleep apnea or Cheyne-Stokes respiration (CSA/CSR) diagnosis and treatment of the underlying cause is mandatory. Adaptive servo-ventilation appears to be an effective treatment modality for patients with complex sleep apnea and with CSA/CSR that is resistant to CPAP.     

Sleep apnea, delirium, depressed mood, cognition, and ADL ability after stroke

OBJECTIVES: The incidence of sleep apnea and stroke increases with age. The aim of this study was to investigate the presence of sleep apnea after stroke and its relationship to delirium, depressed mood, cognitive functioning, ability to perform activities of daily living (ADLs), and psychiatric and behavior symptoms. DESIGN: Cross-sectional study. SETTING: Geriatric stroke rehabilitation unit. PARTICIPANTS: 133 patients (78 women and 55 men, mean age 77.1 +/- 7.7 years) consecutively admitted to a geriatric stroke rehabilitation unit. MEASUREMENTS: All patients underwent overnight respiratory sleep recordings at 23 +/- 7 days (range 11 to 41 days) after suffering a stroke. The patients were assessed using the Organic Brain Syndrome Scale, Montgomery-Asberg-Depression-Rating Scale, Mini-Mental State Examination (MMSE), and Barthel-ADL Index. Sleep apnea was defined as an apnea-hypopnea index (AHI) of 10 or more. RESULTS: The median of the AHI for the studied sample (N = 133) was 13 (range 0-79; interquartile range 6-28). Fifty-nine percent fulfilled the criteria for sleep apnea; 52% with first-ever stroke had sleep apnea. More patients with sleep apnea than without were delirious, depressed, or more ADL-dependent. Sleep apnea patients also had a higher frequency of ischemic heart disease and had more often suffered from an earlier cerebral infarction. Multivariate analysis showed that obesity, low ADL scores, ischemic heart disease, and depressed mood were independently associated with sleep apnea. Low ADL scores, apnea-related hypoxemia, body mass index < or = 27, and impaired vision were independently associated with delirium. The presence of sleep apnea was not associated with any specific type of stroke or location of the brain lesion. CONCLUSIONS: Sleep apnea is common in stroke patients and is associated with delirium, depressed mood, latency in reaction and in response to verbal stimuli, and impaired ADL ability. We suggest a trial investigating whether delirium, depressed mood, and ADL ability improve with nasal continuous positive airway pressure treatment of sleep apnea in stroke patients.     

Das Schlafapnoe-Syndrom in der Rehabilitation

Sleep-related breathing disorders are a common finding in patients undergoing cardiological rehabilitation. Sleep apnoea is recognized as a major risk factor for cardiovascular disorders. The diagnosis of sleep-related breathing disorders begins with taking a thorough sleep medicine-related patient history and answering dedicated questionnaires. The second step involves portable monitoring to assess oxygen saturation, heart rate, respiratory flow and effort. Portable monitoring is able to detect the severity of the breathing disorder and forms the basis on which to refer the patient for further sleep laboratory diagnosis or, in the case of positive results, to initiate appropriate treatment. In order to exclude a sleep-related breathing disorder, to distinguish between obstructive and central sleep apnoea, or to diagnose other sleep disorders a cardiorespiratory polysomnography in a sleep laboratory is required. Polysomnography is also needed if comorbidities are present. Appropriate and prompt treatment of sleep-related breathing disorders can shorten cardiological rehabilitation and improve outcomes in this patient group.     

Treatment of obstructive sleep apnoea with nasal continuous positive airway pressure in stroke.

The prevalence of obstructive sleep apnoea (OSA) following stroke is high and OSA is associated with increased morbidity, mortality and poor functional outcome. Nasal continuous positive airway pressure (nCPAP) is the treatment of choice for OSA, but its effects in stroke patients are unknown. The effectiveness and acceptance of treatment with nCPAP in 105 stroke patients with OSA, admitted to rehabilitation was prospectively investigated. Subjective wellbeing was measured with a visual analogue scale in 41 patients and 24-h blood pressure was determined in 16 patients before and after 10 days of treatment. Differences were compared between patients who did and did not accept treatment. There was an 80% reduction of respiratory events with concomitant increase in oxygen saturation and improvement in sleep architecture. No serious side-effects were noticed. Seventy-four patients (70.5%) continued treatment at home. Nonacceptance was associated with a lower functional status, as measured by the Barthel Index, and the presence of aphasia. Ten days after initiation of nCPAP, compliant users showed a clear improvement in wellbeing (differences in visual analogue scale (deltaVAS) mean+/-SD 26+/-26 mm) versus noncompliant patients (deltaVAS 2+/-25 mm, p=0.021). Only the compliant group had a reduction in mean nocturnal blood pressure (deltaBP; -8+/-7.3 mmHg versus 0.8+/-8.4 mmHg, p=0.037). Stroke patients with obstructive sleep apnoea can be treated effectively with nasal continuous positive airway pressure and show a similar improvement and primary acceptance to obstructive sleep apnoea patients without stroke. Continuous positive airway pressure acceptance is associated with improved wellbeing and decreased nocturnal blood pressure.     

Sleep apnea: State of the art

Many patient with, or at risk of, cardiovascular disease have sleep disordered breathing (SDB), which can be either obstructive (with intermittent collapse of the upper airway) or central (episodic loss of respiratory drive). SDB is associated with sleep disturbance, hypoxemia, hemodynamic changes, and sympathetic activation. Such patients have a worse prognosis than those without SDB. Mask-based therapies of positive airway pressure targeted at SDB can improve measures of sleep quality and partially normalize the sleep and respiratory physiology, but recent randomized trials of cardiovascular outcomes in SDB have either been neutral (obstructive sleep apnea) or suggested the possibility of harm, likely from increased sudden death, in central sleep apnea. Alternative methods for the treatment of SDB are being explored, including implantable technologies, but these have not been studied in adequately powered randomized controlled studies. International guidelines recommend screening for SDB, which can be done easily in clinical practice, as there may be a role for the treatment of patients with obstructive sleep apnea and daytime sleepiness, or resistant hypertension, or atrial fibrillation. Further randomised outcome studies are required to determine whether mask-based treatment for SDB is appropriate for patients with chronic systolic heart failure and obstructive sleep apnea; for those with heart failure with preserved ejection fraction; and for those with decompensated heart failure. The case is made that no longer can the surrogate endpoints of improvement in respiratory and sleep metrics be taken as adequate therapeutic outcome measures in patients with sleep apnea and cardiovascular disease.     

High prevalence and persistence of sleep apnoea in patients referred for acute left ventricular failure and medically treated over 2 months.

AIMS: Cardiac failure patients were studied systematically using polysomnography 1 month after recovering from acute pulmonary oedema, and again after 2 months of optimal medical treatment for cardiac failure. METHODS AND RESULTS: This prospective study of consecutive patients was conducted in a cardiac care unit of a university hospital. V o(2)measurements and left ventricular ejection fraction were recorded. Thirty-four patients, initially recruited with pulmonary oedema, improved after 1 month of medical treatment to NYHA II or III. They were aged less than 75 years and had a left ventricular ejection fraction less than 45% at the time of inclusion. Age was 62 (9) years, body mass index= 27 (5) kg x m(-2)and an ejection fraction= 30 (10)%. Eighteen of the 34 patients (53%) had coronary artery disease. Twenty-eight of the 34 had sleep apnoea syndrome with an apnoea+hypopnoea index >15 x h(-1)of sleep. Thus, the prevalence of sleep apnoea in this population was 82%. Twenty-one of 28 (75%) patients had central sleep apnoea and seven of 28 (25%) had obstructive sleep apnoea. Patients with central sleep apnoea had a lower Pa co(2)than those with obstructive sleep apnoea (33 (5) vs 37 (5) mmHg, P<0.005). Significant correlations were found between apnoea+hypopnoea index and peak exercise oxygen consumption (r= -0.73, P<0.01), and apnoea+hypopnoea index and Pa co(2)(r= -0.42, P = 0.03). When only central sleep apnoea patients were considered, a correlation between apnoea+hypopnoea index and left ventricular ejection fraction was also demonstrated (r= -0.46, P<0.04). After 2 months of optimal medical treatment only two patients (both with central sleep apnoea) showed improvement (apnoea+hypopnoea index <15 x h(-1)). CONCLUSIONS: We have demonstrated a high prevalence of sleep apnoea, which persisted after 2 months of medical treatment, in patients referred for acute left ventricular failure. Central sleep apnoea can be considered a marker of the severity of congestive heart failure.     

Obstructive sleep apnea and heart failure

Obstructive sleep apnea (OSA) exerts several effects that may be particularly deleterious in patients with heart failure (HF). OSA should be considered especially in HF patients who are obese or have the metabolic syndrome, systemic hypertension, or pulmonary hypertension. HF patients in whom OSA is suspected should undergo a full evaluation by a sleep specialist, including a polysomnogram, to diagnose OSA and differentiate this disease from central sleep apnea. Those found to have OSA should then receive continuous positive airway pressure and/or other interventions, and standard disease management strategies should be used to maximize compliance. Those who cannot tolerate continuous positive airway pressure may be candidates for mandibular advancement devices or surgical therapies including tracheostomy. Standard HF medications should be used to treat HF, and optimization of fluid balance may help minimize OSA severity. However, it is still unknown whether treatment of OSA in HF patients will reduce hospitalizations or mortality.     

老年阻塞性睡眠呼吸暂停综合征与血栓性脑血管病

阻塞性睡眠呼吸暂停综合征是高血压、脑卒中等发病的独立危险因素，脑血管病患者中50％以上合并睡眠呼吸障碍，为老年人的高发病。观察血黏度、血小板聚集率、血小板膜糖蛋白阳性率、纤维蛋白原、内皮素、降钙素基因相关肽及低氧对脑血流的影响等多种相关因素，揭示其内在规律，为进一步治疗及预防提供依据。     

Heart failure and sleep apnoea: to sleep perchance to dream

Heart failure and sleep apnoea are major health problems with an increasingly recognized association; evidence suggests that sleep apnoea may play a role in the progression of heart failure. However, confounding factors such as obesity, hypertension and coronary heart disease make this relationship uncertain and an independent correlation remains unproven. Diagnosis of sleep apnoea is suboptimal, as it is often asymptomatic and polysomnography is expensive and time-consuming. A simple and reliable screening protocol is required. All heart failure patients should be considered to be at high risk of sleep apnoea, as this association might be linked to adverse outcome. Continuous positive airway pressure has shown some beneficial effects, but long-term outcome and improvement in survival remains to be demonstrated. Despite recent advances in the understanding of the complex relationship between heart failure and sleep apnoea, there are a number of areas requiring further investigation, which may have important implications for the management and prognosis of a significant number of patients.     

阻塞性睡眠呼吸暂停综合征与脑卒中

探讨阻塞性睡眠呼吸暂停综合征（OSAS）与脑卒中在流行病学与人体生物学之间的相关性及其发病机制。睡眠呼吸暂停是脑卒中的危险因素,独立相关于心血管危险因素,对卒中的预防有重大意义。     

Obstructive sleep apnea and cardiovascular disease - time to act!

Sleep related breathing disorders are common and their potential to disrupt sleep leading to daytime fatigue and hypersomnolence is widely acknowledged. In the future, obstructive sleep apnoea (OSA) may become even more important because obesity as a main risk factor is increasingly prevalent. Apart from disturbing sleep, OSA has also been recognised as a risk factor for hypertension, acute cardiovascular events and metabolic disturbance such as insulin resistance. Several randomised controlled trials demonstrated a positive effect of nasal continuous positive airway pressure (CPAP) treatment on arterial blood pressure, leading the "Joint National Council on High Blood Pressure" to list obstructive sleep apnoea as the first identifiable cause of arterial hypertension. Recently, a growing body of evidence demonstrated also a risk reduction of fatal and non-fatal cardiovascular events by treatment of obstructive sleep apnoea. A beneficial effect of treatment of OSA was also shown for patients with heart failure, or heart rhythm disturbance. Obstructive sleep apnoea may no longer be seen as a cause for daytime sleepiness and impaired quality of life only, but also as an independent risk factor, at least for the occurrence of hypertension but probably for any cardiovascular and cerebrovascular disease. While prospective controlled trials to document a reduction of cardiovascular morbidity and mortality are awaited, therapeutic nihilism seems no longer appropriate. With effective treatment available, subgroups that may profit best remain to be identified.     

阻塞性睡眠呼吸暂停心血管相关血清学标志物研究进展

阻塞性睡眠呼吸暂停（OSA）最常见的临床症状是夜间睡眠打鼾伴呼吸暂停,以慢性间歇性缺氧、高碳酸血症、反复微觉醒和睡眠结构紊乱为病理生理基础,是心血管疾病的源头疾病和危险因素。在临床实践中,多导睡眠监测仍是确诊OSA的金标准,但是受多导睡眠监测局限性、需专业的睡眠医师阅读报告等诸多因素的影响,导致多数患者诊治延迟。因此,目前研究热点是探寻一种简易、便捷的血清学标志物,从OSA患者中筛选心血管疾病高危患者,实现早期防治、精准治疗。     

Severe obstructive sleep apnea in a patient with spinal muscle atrophy

Patients with spinal muscle atrophy (SMA) who survive to adulthood experience a slow, continuous loss of motor function but typically have a normal life expectancy. These patients, however, require vigilance on the part of their health-care providers to reverse treatable disorders to maintain a satisfactory quality of life. We report on a patient with obstructive sleep apnea and type 3 SMA. The treatment of his sleep-disordered breathing resulted in the resolution of symptoms that were initially attributed to his neuromuscular disease.