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.     

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.     

Evaluation and Treatment of Central Sleep Apnea in Patients with Heart Failure

Sleep-disordered breathing (SDB) is a common comorbidity in patients with heart failure (HF). Prevalence of the most common subtypes of SDB, central sleep apnea (CSA) and obstructive sleep apnea (OSA), is increasing, which is concerning due to the association of SDB with increased mortality in patients with HF. Despite an increasing burden of CSA in HF, it is difficult to detect using current diagnostic tools and the treatment modalities are limited by variable efficacy and patient adherence. Though positive airway pressure therapies remain the cornerstone of OSA treatment, the management of CSA in the setting of HF continues to evolve. The association of the presence of CSA with worse prognosis in HF patients warrants the need for routine screening for signs and symptoms of CSA in this population. In this review, we examine the connection between CSA and HF, and highlight advancements in timely diagnostics, treatment modalities, and strategies to promote facilitation of compliance in this high-risk cohort.     

Temporal worsening of sleep-disordered breathing in the acute phase of myocardial infarction.

BACKGROUND: Sleep apnea is an important risk factor for cardiovascular diseases, but whether the severity of sleep-disordered breathing (SDB) changes in the acute phase of myocardial infarction (MI) has not been well determined, nor has it been determined what type of SDB, central or obstructive, (CSA or OSA) is exacerbated. METHODS AND RESULTS: Polysomnography was performed in patients with acute phase of MI during the acute (days 3-5) and chronic (day 14) phases. On the same day, the ventilatory equivalent (VE)/carbon dioxide production (VCO(2)) slope, urinary catecholamines secretion and arterial carbon dioxide tension were assessed before sleep. The apnea/hypopnea index was significantly decreased in the chronic phase (13.26+/-11.30 vs 6.97+/-5.67, p<0.05). The distribution of the types of SDB was unchanged, indicating both CSA and OSA can be exacerbated in the acute phase of MI. The VE/VCO(2) slope and arterial carbon dioxide tension before sleep were also unchanged. Urinary norepinephrine secretion was slightly decreased, although the difference was not significant. CONCLUSIONS: SDB is temporarily worsened in the acute phase of AMI and both CSA and OSA are worsened in AMI.     

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.     

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.     

Efficacy of adaptive servoventilation in treatment of complex and central sleep apnea syndromes

BACKGROUND: Complex sleep apnea syndrome (CompSAS) is recognized by the concurrence of mixed or obstructive events with central apneas, the latter predominating on exposure to continuous positive airway pressure (CPAP). Treatment of CompSAS or central sleep apnea (CSA) syndrome with adaptive servoventilation (ASV) is now an option, but no large series exist describing the application and effectiveness of ASV. METHODS: Retrospective chart review of the first 100 patients who underwent polysomnography using ASV at Mayo Clinic Sleep Center. RESULTS: ASV titration was performed for CompSAS (63%), CSA (22%), or CSA/Cheyne Stokes breathing patterns (15%). The median diagnostic sleep apnea hypopnea index (AHI) was 48 events per hour (range, 24 to 62). With CPAP, obstructive apneas decreased, but the appearance of central apneas maintained the AHI at 31 events per hour (range, 17 to 47) [p = 0.02]. With bilevel positive airway pressure (BPAP) in spontaneous mode, AHI trended toward worsening vs baseline, with a median of 75 events per hour (range, 46 to 111) [p = 0.055]. BPAP with a backup rate improved the AHI to 15 events per hour (range, 11 to 31) [p = 0.002]. Use of ASV dramatically improved the AHI to a mean of 5 events per hour (range, 1 to 11) vs baseline and vs CPAP (p < 0.0001). ASV also resulted in an increase in rapid eye movement sleep vs baseline and CPAP (18% vs 12% and 10%, respectively; p < 0.0001). Overall, 64 patients responded to the ASV treatment with a mean AHI < 10 events per hour. Of the 44 successful survey follow-up patients contacted, 32 patients reported some improvement in sleep quality. CONCLUSION: The ASV device appears to be an effective treatment of both CompSAS and CSA syndromes that are resistant to CPAP.     

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.     

Die Rolle der Schlafmedizin bei Herz-Kreislauf-Erkrankungen

Sleep-disordered breathing (SDB) is receiving more attention within the cardiology community. While obstructive sleep apnea (OSA) is thought to be an independent risk factor for the development for and prognosis of various cardiac and cardiovascular diseases, central sleep apnea (CSA) and Cheyne-Stokes respiration (CSR) in particular are thought to be comorbidities with an independent prognostic impact in patients with established cardiovascular diseases. Simplified screening tools enable the cardiologist to easily screen for or at least rule out significant SDB in their patients. Even the diagnosis of OSA or CSA seems to be feasible using multichannel cardiorespiratory polygraphy or polysomnography. In addition, apnea screening is becoming more and more integrated into various cardiac devices, e. g. Holter electrocardiogram (ECG) and implantable cardiac rhythm devices. Modern therapeutic devices using automatic adjustment of positive airway pressure facilitate treatment of patients with SDB and fully implantable respiratory devices using transvenous approaches, e. g. transvenous phrenic nerve stimulation to treat Cheyne-Stokes respiration, might open up a new field in cardiology. Once therapeutic interventions to treat SDB are proven to improve quality of life, cardiovascular function and prognostic outcome in patients with cardiovascular diseases, new pathways to diagnose and treat these patients need to be determined.     

Sleepiness and hypertension in obstructive sleep apnea.

In order to assess the complications of sleep apnea, we have reviewed a data base of 619 consecutive admissions to a university sleep disorders center. Although patients with obstructive sleep apnea (OSA) described more subjective sleepiness than patients with central sleep apnea (CSA) or primary snoring (PS), the multiple sleep latency test (MSLT) indicated similar levels of physiologic sleepiness in the two apneic groups, which was greater than among those with PS. There was no significant relationship between individual subjective estimates of habitual sleepiness and the MSLT values. Among the OSA patients the mean minimum arterial oxygen desaturation during REM sleep accounted for 65 percent of the variance of the mean sleep latency on the MSLT, with an additional, smaller, contribution of the disordered breathing rate per hour. Subjective reports of sleepiness were associated with sleep efficiency and the number of disordered breathing events in NREM sleep. Patients with OSA or CSA had similar diastolic blood pressures and frequencies of history of treatment for hypertension, which were significantly higher in OSA than in the PS group. In the OSA group the absolute minimum arterial oxygen desaturation during NREM sleep was the most significant contributor to waking diastolic blood pressure, with an additional small contribution by weight. A history of treatment for hypertension was most strongly associated with weight, without significant additional contributions by measures of disordered breathing events or oxygen desaturation; however, weight was highly intercorrelated with measures of the apnea/hypopnea index and minimum arterial oxygen desaturation. In summary, these data support recent findings which show a close relation of obesity to a history of hypertension in OSA, and extend to this group a previous observation that in regular heavy snorers, there may be a disparity between levels of physiologic and subjective sleepiness.     

Sleep-disordered breathing and inappropriate defibrillator shocks in chronic heart failure

Purpose

Supraventricular tachyarrhythmias are a major cause of inappropriate defibrillator shocks. Sleep-disordered breathing (SDB) is a known risk factor for atrial fibrillation (AF). We hypothesized that Cheyne–Stokes respiration (CSA) and obstructive sleep apnea (OSA) have an impact on inappropriate defibrillator discharges in patients witch chronic heart failure (CHF) and cardiac resynchronization therapy with defibrillator (CRT-D).

Methods

In this study, 172 patients with CHF (LVEF ≤?45?%, NYHA-class ≥?2) and CRT-D underwent overnight polygraphy; 54 had no SDB (apnea–hypopnea index Results In all, 17 patients had inappropriate defibrillator shocks (9.9?%; eight oversensing due to lead fractures, five caused by atrial fibrillation, four because of sinus tachycardia). Mean event-free survival time was 33.5?±?1.2 months in the CSA group, 35.2?±?0.7 months in the OSA group, and 32.1?±?1.5 months in the no SDB group, respectively (CSA vs. no SDB p?=?0.63; OSA vs. no SDB p?=?0.31; CSA vs. OSA p?=?0.45). Stepwise Cox proportional hazard regression analysis revealed an independent association for age (per year: hazard ratio 0.90, 95?% confidence interval 0.85–0.96, p?Conclusions SDB was not associated with inappropriate defibrillator shocks. We assume this is due to the low incidenceand low proportion of inappropriate therapies in response to AF.     

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.     

Variation in severity and type of sleep-disordered breathing throughout 4 nights in patients with heart failure

BACKGROUND: Over 50% of patients with chronic heart failure (CHF) have sleep-disordered breathing (SDB). Any variation in the type of SDB in CHF will have implications for patient management. Currently there is good evidence for treatment of obstructive sleep apnea (OSA) in CHF with continuous positive airway pressure; however, for central sleep apnea (CSA) the treatment is less clear. AIMS: The aim of this study was to investigate the variation in the severity and type of SDB (OSA vs. CSA) throughout 4 consecutive nights in CHF patients with SDB. METHODS: Nineteen male CHF patients (mean+/-sd: age 61+/-9 years; left ventricular ejection fraction: 34+/-10% and percent predicted peak VO2: 67+/-19%) underwent cardiorespiratory monitoring in their own home throughout 4 consecutive nights. RESULTS: There was minimal variation in apnea-hypopnea index (AHI) throughout 4 nights in CHF patients with SDB [intraclass correlation coefficient (95% confidence interval (CI)): 0.97 (95% CI 0.76 and 0.97)]. Eight patients [42% (95% CI 20% and 64%)] demonstrated a shift in the type of their SDB, from CSA to OSA or vice versa; these patients had significantly smaller neck circumference (group mean+/-sd) 42+/-2 vs. 44+/-2 cm; p=0.04), and had significant variation in the central AHI [intraclass correlation coefficient: 0.51 (95% CI 0.16 and 0.85)]. CONCLUSIONS: A single night of cardiorespiratory monitoring is representative of moderate-to-severe SDB in patients with CHF. However, a high proportion of patients shift their type of SDB over 4 nights. These findings may have implications for the management of SDB in CHF.     

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.     

Schlafbezogene Atmungsst?rungen und kardiale Resynchronisationstherapie

Patients with progressive heart failure often suffer from sleep-disordered breathing (SDB). Upon receiving cardiac resynchronization therapy (CRT), there is an improvement of cardiac function and central sleep apnea syndrome (CSA) with Cheyne-Stokes respiration; however, effects of CRT on obstructive sleep apnea syndrome seemed to be without clinical relevance. Likewise, additional atrial overdrive pacing did not improve CRT effects relevantly in CSA patients. During CRT, there is an improvement in sleep parameters, sleep quality by reduction of depressive syndromes, and in long-term survival. Therefore, all patients with chronic heart failure and indication for CRT should be monitored regarding SDB before and after CRT device implantation.     

The significance and outcome of continuous positive airway pressure-related central sleep apnea during split-night sleep studies

OBJECTIVE: To determine whether central sleep apnea (CSA) occurring during continuous positive airway pressure (CPAP) titration in patients with obstructive sleep apnea (OSA) reflects subclinical congestive heart failure (CHF), and whether these events will improve with CPAP therapy. DESIGN: Cross-sectional analysis of patients with suspected sleep-related breathing disorders referred for split-night polysomnography PATIENTS AND METHODS: Forty-two OSA patients with and without CPAP-related CSA were analyzed. All CSA patients (n = 21) and control subjects (n = 21) underwent echocardiography, pulmonary function testing, and arterial blood gas (ABG) analysis. Repeat polysomnography with CPAP was performed 2 to 3 months after adequate CPAP therapy in CSA group patients. RESULTS: Demographic, Epworth sleepiness scale, pulmonary function test, ABG, and baseline diagnostic polysomnography findings were similar in both groups. There was no difference in the prevalence of subclinical left ventricular systolic dysfunction in the CSA group vs the control group. CSA patients had decreased sleep efficiency (SE), increased sleep stage 1 percentage, sleep stages shift, wake time after sleep onset (WASO), and total arousals compared to control subjects. Twelve of 14 patients (92%) in the CSA group demonstrated complete or near-complete resolution of CSA events on follow-up polysomnography and showed improvement in SE, WASO, and total arousals compared to their baseline study. CONCLUSIONS: CSA events occurring during CPAP titration are transient and self-limited. They may be precipitated by the sleep fragmentation associated with initial CPAP titration and are not associated with an increased prevalence of occult CHF compared to OSA patients without CPAP-related CSA.     

Does Treating Sleep Apnea Reduce Heart Failure Risks?

Sleep-disordered breathing (SDB) is the most common comorbidity in heart failure (HF) patients. SDB, including both central sleep apnea (CSA) and obstructive sleep apnea (OSA), affects up to 70 % of all heart patients. Numerous studies have identified intermittent hypoxia, oxidative stress, and sympathetic activation as the main pathways through which SDB exerts its negative cardiovascular consequences. The etiological relation between SDB and HF is complex and multi-layered. On one level, SDB contributes to the progression of cardiovascular disease (CVD) into HF; on another level, SDB is a consequence of severe advanced HF. At all stages of CVD, SDB likely contributes to the acceleration of disease progression into end-stage process including advanced HF, stroke, and death. Figure 1 describes the role of OSA in the progression of CVD risk status, the role of CSA in end-stage CVD (including HF) and the reciprocal relationship between advanced CVD and SDB. Current evidence supports that SDB treatment improves several physiological parameters and disease markers in patients with CVD and likely decreases the progression into HF. In patients with established HF, available evidence supports that untreated SDB is independently associated with negative consequences in heart failure. However, there are insufficient studies in support of a conclusion that treatment of SDB changes important HF outcomes. In particular, there are no adequately powered randomized controlled trials demonstrating improvement in mortality, admissions, or cardiac function in HF patients with SDB therapy. However, treatment of SDB is largely safe, associated with critical functional benefits, and is increasingly better tolerated, allowing for decision-making processes that favor treatment.     

Washout Rate of Cardiac Iodine-123 Metaiodobenzylguanidine is High in Chronic Heart Failure Patients With Central Sleep Apnea

BackgroundThe association between sleep-disordered breathing (SDB) assessed by polysomnography and cardiac sympathetic nerve activity (SNA) assessed by cardiac iodine-123 metaiodobenzylguanidine (123I-MIBG) imaging has not been investigated in patients with chronic heart failure (CHF).Methods and ResultsWe performed cardiac 123I-MIBG scintigraphy and overnight polysomnography in 59 patients with stable CHF. The patients were classified into the 3 groups: 19 with no or mild SDB (NM-SDB, apnea-hypopnea index <15); 21 with central sleep apnea (CSA), and 19 with obstructive sleep apnea (OSA). The cardiac washout rate (WR) of 123I-MIBG was obtained from initial and delayed planar 123I-MIBG images. The WR was higher in patients with CSA (54.2 ± 11.6%) than in those with OSA (37.9 ± 8.6%, P < .05) or NM-SDB (40.8 ± 8.8%, P < .05). The WR correlated positively with central apnea index (ρ = 0.40, P = .002). A stepwise multiple regression analysis selected CSA and plasma brain natriuretic peptide levels as independent variables associated with the WR.ConclusionsThe WR was higher in CHF patients with CSA than in those with OSA or NM-SDB, and CSA was independently associated with the WR, suggesting a link of CSA to increased cardiac SNA in CHF.     

Sleep Disordered Breathing in Patients with Heart Failure: Pathophysiology and Management

Sleep disordered breathing (SDB) is common in heart failure patients across the range of ejection fractions and is associated with adverse prognosis. Although effective pharmacologic and device-based treatment of heart failure may reduce the frequency or severity of SDB, heart failure treatment alone may not be adequate to restore normal breathing during sleep. Continuous positive airway pressure (CPAP) is the major treatment for SDB in heart failure, especially if obstructive rather than central sleep apnea (CSA) predominates. Adequate suppression of CSA by PAP is associated with a heart transplant-free survival benefit, although randomized trials are ongoing. Bilevel PAP (BPAP) may be as effective as CPAP in treating SDB and may be preferable over CPAP in patients who experience expiratory pressure discomfort. Adaptive (or auto) servo-ventilation (ASV), which adjusts the PAP depending on the patient’s airflow or tidal volume, may be useful in congestive heart failure patients if CPAP is ineffective. Other therapies that have been proposed for SDB in congestive heart failure include nocturnal oxygen, CO₂ administration (by adding dead space), theophylline, and acetazolamide; most of which have not been systematically studied in outcome-based prospective randomized trials.     

Sleep‐disordered breathing in heart failure

Sleep‐disordered breathing—comprising obstructive sleep apnoea (OSA), central sleep apnoea (CSA), or a combination of the two—is found in over half of heart failure (HF) patients and may have harmful effects on cardiac function, with swings in intrathoracic pressure (and therefore preload and afterload), blood pressure, sympathetic activity, and repetitive hypoxaemia. It is associated with reduced health‐related quality of life, higher healthcare utilization, and a poor prognosis. Whilst continuous positive airway pressure (CPAP) is the treatment of choice for patients with daytime sleepiness due to OSA, the optimal management of CSA remains uncertain. There is much circumstantial evidence that the treatment of OSA in HF patients with CPAP can improve symptoms, cardiac function, biomarkers of cardiovascular disease, and quality of life, but the quality of evidence for an improvement in mortality is weak. For systolic HF patients with CSA, the CANPAP trial did not demonstrate an overall survival or hospitalization advantage for CPAP. A minute ventilation‐targeted positive airway therapy, adaptive servoventilation (ASV), can control CSA and improves several surrogate markers of cardiovascular outcome, but in the recently published SERVE‐HF randomized trial, ASV was associated with significantly increased mortality and no improvement in HF hospitalization or quality of life. Further research is needed to clarify the therapeutic rationale for the treatment of CSA in HF. Cardiologists should have a high index of suspicion for sleep‐disordered breathing in those with HF, and work closely with sleep physicians to optimize patient management.