Effectiveness of adaptive servo-ventilation

Adaptive servo-ventilation (ASV) has been developed as a specific treatment for sleep-disordered breathing, in particular Cheyne-Stokes respiration with central sleep apnea (CSA). Heart failure patients often have sleep-disordered breathing, which consists of either obstructive sleep apnea (OSA) or CSA. Other medical conditions, such as stroke, acromegaly, renal failure, and opioid use may be associated with CSA. Continuous positive airway pressure (CPAP) therapy is widely used for patients with OSA, but some of these patients develop CSA on CPAP, which is called treatment-emergent CSA. CPAP can be useful as a treatment for these various forms of CSA, but it is insufficient to eliminate respiratory events in approximately half of patients with CSA. As compared to CPAP, ASV may be a better option to treat CSA, with sufficient alleviation of respiratory events as well as improvement of cardiac function in heart failure patients. In patients without heart failure, ASV can also alleviate CSA and relieve their symptom. Recently, ASV has been widely used for patients with various forms of CSA. ASV may be also used in the setting without CSA, but it should be assessed more carefully. Clinicians should have a better understanding of the indications for ASV in each setting.     

Treatment of Cheyne-Stokes respiration-central sleep apnea in patients with heart failure

Sleep disordered breathing including obstructive sleep apnea (OSA) and central sleep apnea (CSA) with Cheyne-Stokes respiration (CSR) is often accompanied by heart failure. Treatment of OSA centered on continuous positive airway pressure (CPAP) is established. However, treatment of CSR-CSA is still controversial. Since CSR-CSA occurs as a consequence of heart failure, optimization of heart failure is essential to treat CSR-CSA. For treatment directed at CSR-CSA itself, a variety of treatment approaches including night oxygen therapy and noninvasive positive pressure ventilation have been applied. Among them, night oxygen therapy improves patients' symptoms, quality of life (QOL), and left ventricular function, but had yet been shown to improve clinical outcome. For CPAP, there are responders and non-responders and for responders CPAP can also improve survival. Adaptive servo-ventilation (ASV), which most effectively treats CSR-CSA, improves exercise capacity, QOL, and cardiac function. Recent reports suggested ASV may also prevent cardiac events in patients with heart failure. However, further studies are needed to conclude that this treatment improves patient survival.     

Reliability and accuracy of sleep apnea scans in novel cardiac resynchronization therapy devices: an independent report of two cases

Pacemaker apnea scan algorithms are able to screen for sleep apnea. We investigated whether these systems were able to accurately detect sleep-disordered breathing (SDB) in two patients from an outpatient clinic. The first patient suffered from ischemic heart failure and severe central sleep apnea (CSA) and underwent adaptive servoventilation therapy (ASV). The second patient suffered from dilated cardiomyopathy and moderate obstructive sleep apnea (OSA). Pacemaker read-outs did not match polysomnography (PSG) recordings well and overestimated the apnea–hypopnea index. However, ASV therapy-induced SDB improvements were adequately recognized by the apnea scan of the Boston Scientific INVIVE® cardiac resynchronization therapy pacemaker. Detection of obstructive respiratory events using impedance-based technology may underestimate the number of events, as frustrane breathing efforts induce impedance changes without significant airflow. By contrast, in the second case, apnea scan overestimated the number of total events and of obstructive events, perhaps owing to a very sensitive but less specific hypopnea definition and detection within the diagnostic algorithm of the device. These two cases show that a pacemaker apnea scan is able to reflect SDB, but PSG precision is not met by far. The device scan revealed the decline of SDB through ASV therapy for CSA in one patient, but not for OSA in the second case. To achieve reliable monitoring of SDB, further technical developments and clinical studies are necessary.     

Sleep-disordered breathing in acute decompensated heart failure

Sleep-disordered breathing (SDB), including obstructive sleep apnea (OSA) and central sleep apnea (CSA), is highly prevalent and frequently unrecognized in patients with chronic heart failure (HF). Untreated SDB may worsen acute decompensation of HF and delay recovery by increasing vascular inflammation and oxidative stress, impeding control of the blood pressure, and promoting arrhythmias. Untreated OSA doubles the risk for developing HF, and patients with HF who develop OSA are thought to have a worse prognosis than patients with HF alone. Similar to the findings in the general population, treatment of OSA appears to reduce cardiovascular morbidity and mortality in HF. The presence of CSA is associated with increased mortality in HF patients. Efficacious suppression of central sleep apnea with continuous positive airway pressure therapy may reduce mortality in HF.     

Diagnosis and treatment of sleep apnea in heart disease

Opinion statement One of the most common yet unidentified conditions in heart disease is sleep-disordered breathing (SDB). Although it is most prevalent in patients with heart failure, it has been epidemiologically and pathophysiologically linked to ischemic heart disease, hypertension, sudden cardiac death, atrial fibrillation, and stroke. There are two primary SDB syndromes: obstructive sleep apnea (OSA) and central sleep apnea (CSA; also known as Cheyne-Stokes respiration). The pathophysiologic mechanisms that underlie these disorders appear to be distinct but both involve recurrent cycles of excessive sympathetic activation, hypoxemias and hypercapnias, and increases in ventricular wall stress. Signs and symptoms may include daytime somnolence, snoring, difficult-to-control hypertension, and refractory arrhythmias or angina. In heart failure, half of patients will have SDB and most patients will exhibit evidence of both OSA and CSA, although one or the other may predominate. The current standard diagnostic method is overnight laboratory polysomnography. Primary therapies for OSA include lifestyle changes, various facial and oral appliances, head and neck surgery, and continuous positive airway pressure (CPAP). CPAP is the most effective form of therapy for OSA, with few side effects, but is limited by compliance because of comfort-related issues. In patients with cardiovascular disease who predominantly suffer from OSA, treatment recommendations should be based on current guidelines for OSA. For patients with heart failure with predominant CSA, the current cornerstone of therapy is the optimization of medical therapy and resynchronization therapy when indicated. When SDB persists despite optimal medical management, referral to a sleep medicine consultant should be considered.     

Sleep-disordered breathing in patients with decompensated heart failure

Sleep-disordered breathing (SDB) has a higher prevalence in patients with heart failure than in the general middle-aged population. Obstructive sleep apnea (OSA), one of the forms of SBD, promotes poorly controlled hypertension, coronary events, and atrial fibrillation events that can lead to acutely decompensated heart failure (ADHF), and evidence suggests that untreated OSA increases mortality in patients with heart failure. Cheyne–Stokes respiration and central sleep apnea (CSA) have long been associated with heart failure and, in many patients, can coexist with OSA. In this article, we propose a systematic approach to diagnose and treat OSA in patients with ADHF based on current evidence.     

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.     

Respiratory sleep disorders in patients with congestive heart failure

Respiratory sleep disorders (RSD) occur in about 40-50% of patients with symptomatic congestive heart failure (CHF). Obstructive sleep apnea (OSA) is considered a cause of CHF, whereas central sleep apnea (CSA) is considered a response to heart failure, perhaps even compensatory. In the setting of heart failure, continuous positive airway pressure (CPAP) has a definite role in treating OSA with improvements in cardiac parameters expected. However in CSA, CPAP is an adjunctive therapy to other standard therapies directed towards the heart failure (pharmacological, device and surgical options). Whether adaptive servo controlled ventilatory support, a variant of CPAP, is beneficial is yet to be proven. Supplemental oxygen therapy should be used with caution in heart failure, in particular, by avoiding hyperoxia as indicated by SpO₂ values >95%.     

Sleep Apnea in Heart Failure

Purpose of review

In this review, we discuss the current treatment options for sleep-disordered breathing (SDB) in patients with heart failure (HF). We address the role of positive airway pressure (PAP) devices and other emerging therapies. The review includes discussion of recent trials that reported negative consequences for the PAP devices in patients with heart failure.

Recent findings

Optimal guideline-directed medical therapies of HF and PAP devices have been the mainstay treatments for HF patients with SDB. Recently, randomized controlled trials (RCTs) evaluated the effect of PAP on clinical outcomes in patients with cardiovascular (CV) disease and heart failure and found no benefit in decreasing fatal and non-fatal CV events. The Sleep Apnea Cardiovascular Endpoints (SAVE) trial evaluated continuous positive airway pressure (CPAP) ventilation in patients with CV disease and obstructive sleep apnea (OSA) and did not observe any improvement in CV effect. In patients with HF and central sleep apnea (CSA), adaptive servo-ventilation (ASV) was hypothesized to help HF outcomes, but the Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure (SERVE-HF) trial did not show any mortality benefit. Instead, the trial suggested an increase in all-cause and CV mortality in the treatment arm.

Summary

currently, studies have not shown the use of PAP therapy to improve any risks of CV outcomes or death in HF patients with sleep apnea, but some associations with improvements in symptoms from OSA have been observed.

     

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.     

Central sleep apnea treatment in patients with heart failure with reduced ejection fraction: a network meta-analysis

Sleep and Breathing - Adaptive servo-ventilation (ASV) is contraindicated for the treatment of central sleep apnea (CSA) in patients with heart failure with reduced ejection fraction (HFrEF),...     

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.     

Sleep apnea and cardiovascular risk

Sleep apnea is evident in approximately 10% of adults in the general population, but in certain cardiovascular diseases, and in particular those characterized by sodium and water retention, its prevalence can exceed 50%. Although sleep apnea is not as yet integrated into formal cardiovascular risk assessment algorithms, there is increasing awareness of its importance in the causation or promotion of hypertension, coronary artery disease, heart failure, atrial arrhythmias, and stroke, and thus, not surprisingly, as a predictor of premature cardiovascular death.Sleep apnea manifests as two principal phenotypes, both characterized by respiratory instability: obstructive (OSA), which arises when sleep-related withdrawal of respiratory drive to the upper airway dilator muscles is superimposed upon a narrow and highly compliant airway predisposed to collapse, and central (CSA), which occurs when the partial pressure of arterial carbon dioxide falls below the apnea threshold, resulting in withdrawal of central drive to respiratory muscles.The present objectives are to: (1) review the epidemiology and patho-physiology of OSA and CSA, with particular emphasis on the role of renal sodium retention in initiating and promoting these processes, and on population studies that reveal the long-term consequences of untreated OSA and CSA; (2) illustrate mechanical, autonomic, chemical, and inflammatory mechanisms by which OSA and CSA can increase cardiovascular risk and event rates by initiating or promoting hypertension, atherosclerosis, coronary artery disease, heart failure, arrhythmias, and stroke; (3) highlight insights from randomized trials in which treating sleep apnea was the specific target of therapy; (4) emphasize the present lack of evidence that treating sleep apnea reduces cardiovascular risk and the current clinical equipoise concerning treatment of asymptomatic patients with sleep apnea; and (5) consider clinical implications and future directions of clinical research and practice.     

First experience of using new adaptive servo-ventilation device for Cheyne-Stokes respiration with central sleep apnea among Japanese patients with congestive heart failure: report of 4 clinical cases.

BACKGROUND: Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in congestive heart failure (CHF) is generally considered a poor prognostic indicator, but treatment of CSR-CSA using an adaptive servo-ventilation (ASV) device has been developed. This is the first evaluation of its use in the management of CSR-CSA in Japanese CHF patients. METHODS AND RESULTS: Four CHF patients with CSR-CSA that was unresponsive to conventional positive airway pressure (CPAP) underwent 3 nights of polysomnography: baseline, CPAP or bi-level PAP, and on the ASV. The apnea - hypopnea index (AHI) and central-AHI (CAHI) were markedly improved on ASV (AHI 62.7+/-10.1 to 5.9+/-2.2 /h, p=0.0006, CAHI 54.5+/-6.7 to 5.6+/-2.3 /h, p=0.007). In addition, the sleep quality improved significantly on ASV, including arousal index (62.0+/-10.5 to 18.7 +/-6.2 /h, p=0.012), percentage of slow-wave sleep (2.6+/-2.6 to 19.4+/-4.8 %, p=0.042). CONCLUSIONS: ASV markedly improved CSR-CSA in patients with CHF. It is a promising treatment for Japanese patients with CHF.     

Detektion und Therapie respiratorischer Störungen durch implantierbare (kardiale) Devices

Sleep-disordered breathing (SDB) represents a common comorbidity in cardiac patients. The prevalence of obstructive sleep apnea (OSA) and central sleep apnea (CSA) is very high, particularly in patients with heart rhythm disorders and heart failure (HF). Patients with pacemakers (PM) and implantable defibrillators (ICD) including cardiac resynchronization therapy (CRT) show SDB prevalences up to 75%. However, some modern PM, ICD and CRT devices allow the detection of SDB via transthoracic impedance analysis with high sensitivity compared to polysomnographic (PSG) controls. Thus, this method could be of relevance in screening and monitoring SDB in patients with implantable cardiac devices. Preliminary studies demonstrated the possibility to treat OSA in selected patients by stimulation of the cranial nerves, especially the hypoglossal nerve. However, this requires extensive diagnostics and advanced surgical approaches including many medical disciplines and is not part of this review article. However, unilateral and transvenous stimulation of the phrenic nerve to treat central sleep apnea and Cheyne-Stokes respiration in HF patients in particular can be performed by cardiologists. This article summarizes preliminary data on the results of this promising therapy.     

睡眠呼吸暂停与心功能不全

呼吸系统和循环系统必须协同作用在细胞及其外循环间运送氧和二氧化碳.循环在呼吸时的变化和持续变化的肺泡通气在心血管系统中均发挥重要作用.这些作用在阻塞性睡眠呼吸暂停患者中表现的尤为明显.近期更多证据表明阻塞性睡眠呼吸暂停会引起和加速左心室肥大和左心功能不全.陈-施呼吸是中枢性睡眠呼吸暂停的一种形式,多见于充血性心力衰竭患...     

Timing of nocturnal ventricular ectopy in heart failure patients with sleep apnea

BACKGROUND: Ventricular ectopy is frequent in heart failure (HF) patients with sleep apnea. A previous report indicated that in HF patients, ventricular premature beats (VPB) occurred more frequently during episodes of recurrent central sleep apnea (CSA) than during normal breathing, and their frequency was greater during hyperpnea than during apnea. We hypothesized that, because respiratory stimuli that might provoke ventricular ectopy are stronger during obstructive apneas than during central apneas, in contrast to CSA, VPBs would be more frequent during apnea than hyperpnea in HF patients with obstructive sleep apnea (OSA). METHODS: HF patients in sinus rhythm who have OSA or CSA (apnea-hypopnea index, > or = 15 events per hour) and with > 30 VPBs per hour were matched for severity of cardiac dysfunction and sleep apnea. The frequency of VPBs was then assessed during stage 2 sleep during the apneic and the hyperpneic phases of recurrent obstructive or central apneas. RESULTS: VPBs occurred more frequently during the apneic phase than during the hyperpneic phase in patients with OSA. In contrast, VPBs occurred more frequently during the hyperpneic phase than the apneic phase in patients with CSA. There was no difference in the degree of apnea-related oxygen desaturation between central and obstructive apneas. CONCLUSIONS: In patients with HF, nocturnal ventricular ectopy oscillates in time with oscillations in ventilation, with VPBs occurring predominantly during apneas in patients with OSA, but during hyperpneas in patients with CSA. This difference in VPB timing between OSA and CSA may be attributable to the differences in timing of arrhythmic stresses in these patients.     

Treatment of sleep apnea in heart failure

Obstructive and central sleep apnea are common in heart failure, and may participate in its progression by exposing the heart to intermittent hypoxia, increased preload and afterload, sympathetic activation, and vascular endothelial dysfunction. Treatment of sleep apnea in patients with heart failure may reverse these detrimental effects, in addition to alleviating symptoms of sleep apnea. In patients with heart failure and obstructive sleep apnea, short-term randomized trials have demonstrated that continuous positive airway pressure (CPAP) improves cardiac function, and lowers sympathetic activity and blood pressure. However, there are no data on whether treating obstructive sleep apnea in patients with heart failure improves morbidity and mortality. Various treatments have been tested in heart failure patients with central sleep apnea, particularly oxygen and CPAP. Both reduce the frequency of central respiratory events, and lower sympathetic activity. In addition, CPAP improves cardiac function. However, the largest randomized trial did not demonstrate any beneficial effect of CPAP on the rate of mortality and cardiac transplantation (32 vs. 32 events in the control and treatment groups, respectively; p=0.54), but ultimately lacked power to conclude with certainty whether CPAP has an effect on morbidity and mortality in such patients. Thus, although there are data to indicate that treating both obstructive and central sleep apnea in patients with heart failure improves cardiovascular function, larger randomized trials involving interventions such as oxygen, CPAP, or other forms of positive airway pressure will be required to determine whether treating these sleep-related breathing disorders reduces clinically important outcomes such as morbidity and mortality.     

中枢性睡眠呼吸暂停与心力衰竭研究新进展

心力衰竭(HF)患者常合并睡眠呼吸紊乱。目前有研究认为阻塞性睡眠呼吸暂停可促进HF的发生、发展,OSA引起的心功能恶化继而导致OSA向中枢性睡眠呼吸暂停(CSA)转变。并且,CSA也可认为是心功能加重到一定程度的代偿表现,然而这种代偿只在短期内有效,长期来看可能是有害的。目前CSA与HF的发病机制不明,但近些年来相关研究有了许多新的进展。本文就CSA与HF发病率、临床特点、分型、病理机制及治疗方面进行综述。     

Sleep apnea in the elderly

Obstructive sleep apnea (OSA) is a common clinical condition associated with obesity. A high prevalence of sleep apnea exists in the elderly, presumably because of changes in oropharyngeal collapsibility. Elderly patients may be less likely to seek medical attention for this condition, because they are less likely to be symptomatic. Excessive daytime somnolence is a known consequence of untreated OSA, but adverse cardiovascular consequences, such as hypertension, arrhythmias, and congestive heart failure, are more serious in older patients. Continuous positive airway pressure therapy is the most effective treatment of OSA, although compliance remains an issue.