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Sleep-disordered breathing in heart failure

Sleep-disordered breathing in heart failure
Authors:
Atul Malhotra, MD
James C Fang, MD
Section Editor:
M Safwan Badr, MD
Deputy Editor:
April F Eichler, MD, MPH
Literature review current through: Nov 2022. | This topic last updated: Jul 15, 2021.

INTRODUCTION — Sleep-disordered breathing (SDB) is common and under-diagnosed in patients with heart failure across a range of ejection fractions and New York Heart Association (NYHA) classes. The most common forms of SDB in heart failure patients are obstructive sleep apnea and central sleep apnea with Cheyne-Stokes breathing. SDB is important to recognize because it is associated with adverse cardiovascular outcomes and mortality, and because accumulating evidence suggests that treatment of SDB can improve heart failure-related outcomes and quality of life.

In this review, the prevalence, risk factors, pathogenesis, clinical manifestations, diagnosis, and treatment of SDB in patients with heart failure are discussed. In addition, the impact of treatment on heart failure-related outcomes is reviewed. The treatment of SDB in more general populations is discussed separately. (See "Management of obstructive sleep apnea in adults" and "Central sleep apnea: Treatment".)

OBSTRUCTIVE VERSUS CENTRAL SLEEP APNEA — Two types of sleep-disordered breathing (SDB) are common among patients with heart failure: obstructive sleep apnea (OSA) and central sleep apnea with Cheyne-Stokes breathing (CSA-CSB):

OSA is characterized by reductions or cessations of airflow during sleep, despite ongoing respiratory effort. It is due to upper airway obstruction. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)

CSB is characterized by cyclic crescendo-decrescendo respiratory effort and airflow during wakefulness or sleep, without upper airway obstruction. When the decrescendo effort is accompanied by apnea during sleep, it is considered a type of central sleep apnea syndrome. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Cheyne-Stokes respiration' and "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Diagnostic criteria'.)

We refer to OSA and CSA-CSB collectively as sleep-disordered breathing (SDB) in this review. They frequently coexist and can be clinically difficult to distinguish from one another because there is overlap in pathophysiology and clinical manifestations.

PATHOGENESIS — The pathogenesis of obstructive sleep apnea (OSA) and central sleep apnea with Cheyne-Stokes breathing (CSA-CSB) are best conceptualized as distinct processes, although they share common pathophysiologic principles and adverse sleep consequences [1].

The pathogenesis of OSA involves abnormalities in pharyngeal anatomy, pharyngeal function, and ventilatory control. In patients with heart failure, edema of the upper airway is an additional factor that may contribute to pharyngeal airway narrowing [2]. The pathogenesis of OSA is discussed in detail separately. (See "Pathophysiology of upper airway obstruction in obstructive sleep apnea in adults".)

The pathogenesis of CSA-CSB is uncertain, but the favored hypothesis is based on the observation that patients who have heart failure and CSA-CSB tend to have lower arterial carbon dioxide tensions (PaCO2) than patients who have heart failure without CSA-CSB [3,4]. It is best conceptualized as a sequence of events:

In an effort to correct the hypocapnia, a hypersensitive respiratory control center initiates an apnea. This occurs when the PaCO2 is below the "apneic threshold." The PaCO2 then begins to rise.

The duration from the beginning of the apnea until the respiratory control center detects the increasing PaCO2 is prolonged due to the increased circulatory time caused by the heart failure. Although some circulatory delay is required for CSA-CSB to occur, its importance as a contributor to CSA-CSB is debated [5].

Hypercapnia exists by the time the respiratory control center terminates the apnea.

The hypercapnia then stimulates robust hyperpnea, which yields marked hypocapnia and allows the cycle of events to repeat.

The net effect is oscillation of ventilation between apnea and hyperpnea. Elimination of the hypocapnia with inhaled CO2, continuous positive airway pressure (CPAP), or oxygen can markedly attenuate CSA-CSB [6-9].

Both OSA and CSA-CSB can impair systolic and diastolic cardiac function by a variety of mechanisms. First, intermittent hypoxemia and arousals induce adrenergic surges that may lead to heart disease progression. Second, the extremely negative intrapleural pressures increase ventricular transmural wall stress and afterload [10]. More specifically, transmural pressure of the left ventricle is the pressure inside the left ventricle minus the pressure outside the left ventricle (ie, approximately the intrathoracic or pleural pressure). During spontaneous inspiration, the intrathoracic pressure becomes more negative, which increases the transmural pressure. The increase in transmural pressure contributes to left ventricular wall stress during left ventricular ejection (ie, afterload). This effect is greater in patients with heart failure who must generate more negative intrathoracic pressures to overcome low lung compliance caused by pulmonary congestion [11].

PREVALENCE AND RISK FACTORS — While obstructive sleep apnea (OSA) is more common than central sleep apnea with Cheyne-Stokes breathing (CSA-CSB) in the general population, CSA-CSB may be more common than OSA in patients with heart failure, particularly among patients with reduced ejection fraction [1,12,13].

Single-center observational studies estimate that the prevalence of SDB may be as high as 50 percent among all patients with heart failure and as high as 70 percent among patients with heart failure who are referred to a sleep laboratory [12-15]. The prevalence may be even higher among patients with acute decompensated heart failure [16], as suggested by a study that detected an apnea-hypopnea index ≥10 events per hour of sleep in 22 out of 29 such patients (76 percent) [17].

Such prevalence estimates are limited by referral bias, variable definitions of SDB, variable severities of heart failure, and variable optimization of the medical management of the heart failure.

SDB appears to be common even among patients whose heart failure is optimally managed. A prospective cohort study followed 108 patients who visited a heart failure clinic with stable heart failure, which was defined as clinical stability without hospitalizations or medication changes within the past 30 days [18]. SDB was detected in 61 percent of patients and was independently associated with the presence of atrial fibrillation and a worse New York Heart Association (NYHA) functional class.

Risk factors for SDB in patients with heart failure vary according to the type of SDB. Risk factors for OSA include advanced age and an increasing body mass index (BMI). Risk factors for CSA-CSB in patients with heart failure include male sex, advanced age, atrial fibrillation, and hypocapnia (ie, transcutaneous carbon dioxide ≤38 mmHg) [15].

PROGNOSTIC IMPLICATIONS — Sleep-disordered breathing (SDB) in patients with heart failure is under-recognized but important because it may independently predict mortality due to heart failure and may contribute to disease progression.

Multiple observational studies have found that heart failure accompanied by SDB is associated with a worse prognosis than heart failure in the absence of SDB [19]. This is illustrated by the following observations:

With respect to obstructive sleep apnea (OSA), a prospective cohort study followed 164 patients who had heart failure and a left ventricular ejection fraction of 45 percent or less [20]. At a mean of three years, patients who had OSA (defined as an apnea-hypopnea index (AHI) of at least 15 events per hour) had a higher cardiac mortality than patients who did not have OSA (8.7 versus 4.2 deaths per 100 patient-years).

With respect to central sleep apnea with Cheyne-Stokes breathing (CSA-CSB), a prospective cohort study followed 62 patients with NYHA class II to III heart failure [21]. At a mean of 28 months, cardiac mortality was associated with an AHI greater than 30 events per hour. The AHI was a better predictor of cardiac mortality than demographic variables, Holter monitoring, exercise studies, echocardiography, or autonomic testing. CSB was found to predict mortality in numerous other studies of patients with heart failure [13,22-25].

These studies do not definitively indicate the mechanism by which SDB is associated with increased cardiac mortality. SDB could be a marker of more severe heart failure, a precipitant of worsening heart failure, or both. SDB may also carry prognostic implications for hospitalized patients [26].

CLINICAL FEATURES — Sleep-disordered breathing (SDB) can be asymptomatic or symptomatic in patients who have heart failure [27]. A sleep history should be sought from both the patient and the bed partner because, in many cases, it is only the bed partner who is aware of the abnormal ventilatory pattern.

When obstructive sleep apnea (OSA) is the predominant type of SDB, poor sleep quality and snoring are common. As a result, sleep disruption and easy fatigability often exist and may be out of proportion to the severity of the heart failure. However, sleepiness is relatively uncommon in patients with heart failure for reasons that remain unclear [28].

While not specific to OSA, additional signs and symptoms may include awakening with a sensation of gasping or choking, morning headaches, and poor concentration or memory impairment. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)

When central sleep apnea with Cheyne-Stokes breathing (CSA-CSB) is the predominant type of SDB, symptoms due to CSA-CSB may be indistinguishable from those due to the heart failure [12]. Symptoms of poor sleep quality (eg, excessive daytime sleepiness) are subtle and generally unreliable. Occasionally, patients with CSA-CSB report paroxysmal nocturnal dyspnea (due to the hyperpnea that follows an apnea) [29]. A bed partner may report episodic hyperpnea, hypopnea, and apneic periods. (See "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Clinical findings'.)

SDB may contribute to nocturnal angina in patients with heart failure, presumably due to hypoxemia and catecholamine release [29].

In addition, recurrent arrhythmias, such as atrial fibrillation or ventricular tachycardia, may be triggered or perpetuated by SDB [15,30-33]. SDB has also been identified as a risk factor for appropriate cardioverter-defibrillator therapies in heart failure patients with ICDs. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy", section on 'Clinical manifestations'.)

These arrhythmias often occur in the absence of any symptoms or signs of SDB. Thus, a high index of suspicion should be maintained and evaluation for SDB should be considered in heart failure patients with recurrent arrhythmias.

WHO SHOULD BE TESTED? — Patients with heart failure who report snoring, excessive daytime somnolence, and poor sleep quality should have their sleep patterns assessed formally by polysomnography in a sleep laboratory or out-of-center sleep testing. We also consider diagnostic testing for sleep-disordered breathing (SDB) in heart failure patients with the following symptoms and signs, since they have been associated with SDB in observational studies:

Nocturnal angina

Recurrent arrhythmias

Refractory heart failure symptoms

Witnessed abnormal respiratory pattern or apneas

Repetitive oxygen desaturations during sleep [16]

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines on the diagnosis and treatment of chronic heart failure indicate that clinical judgment should be used to screen for SDB in selected patients (eg, those with risk factors) [34].

It is not known whether screening questionnaires developed in the general OSA population (eg, STOP-Bang, sleep apnea clinical score [SACS], Berlin questionnaire) have any validity in heart failure patients to help identify which patients to refer for a diagnostic sleep study. In addition, with a pretest probability of 50 percent or greater in heart failure patients, it is unclear whether a screening questionnaire would add any additional benefit [35]. In a prospective study that included over 1500 patients with heart failure, a 7-item questionnaire assessing snoring, nocturnal sweating, nocturia, witnessed apneas, chronic fatigue, and frequent napping had low sensitivity and specificity for the diagnosis of SDB [36].

The use of screening questionnaires in the general population is reviewed in detail separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Screening questionnaires'.)

DIAGNOSIS — The diagnostic evaluation of suspected sleep-disordered breathing (SDB) is the same for patients with or without heart failure. An in-laboratory overnight polysomnogram is the gold standard diagnostic test.

Out-of-center sleep testing is also available and is now sometimes mandated by insurers for uncomplicated OSA. Although it has not been as well studied in patients with heart failure, who are at risk for more complicated SDB, emerging data suggest that unattended diagnostic sleep studies may be feasible and accurate in patients hospitalized with heart failure and allow for expedited diagnosis and treatment [37-40].

These tests are described separately, as are the diagnostic criteria for obstructive sleep apnea (OSA) and central sleep apnea syndromes. (See "Home sleep apnea testing for obstructive sleep apnea in adults" and "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "Central sleep apnea: Risk factors, clinical presentation, and diagnosis" and "Polysomnography in the evaluation of sleep-disordered breathing in adults".)

MANAGEMENT — Management of sleep-disordered breathing (SDB) in patients with heart failure should focus both on optimizing heart failure and treating the abnormal breathing pattern.

Heart failure therapy — Case series and observational studies suggest that the following interventions are associated with improved SDB in patients with heart failure:

Optimal medical management (eg, renin angiotensin system inhibitors, beta blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter 2 inhibitors for heart failure with reduced ejection fraction; angiotensin receptor-neprilysin inhibitors and spironolactone for heart failure with preserved ejection fraction) [2,20,41,42]

Cardiac transplantation [43-45]

Cardiac resynchronization (ie, biventricular pacing) [46-48]

Left ventricular assist device (LVAD) implantation [49]

For the most part, such interventions do not lead to complete resolution of the abnormal breathing pattern and should be considered complementary to positive airway pressure therapy.

Treatment of heart failure is discussed in detail separately. (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Management of refractory heart failure with reduced ejection fraction" and "Short-term mechanical circulatory assist devices".)

Positive airway pressure therapy — For patients who have heart failure complicated by obstructive sleep apnea (OSA) or central sleep apnea with Cheyne-Stokes breathing (CSA-CSB), continuous positive airway pressure (CPAP) therapy may improve cardiac function, blood pressure, exercise capacity, and quality of life [1,8,23,50-57]. Limited data also suggest that treatment can reduce the burden of arrhythmias. (See "Obstructive sleep apnea and cardiovascular disease in adults".)

A major limitation with this body of evidence is that most studies evaluated the impact of SDB therapy on surrogate outcomes (eg, blood pressure, catecholamine levels, cardiac function) and did not measure clinically important outcomes (eg, quality of life, hospitalizations, mortality, functional class).

Taken together, the evidence suggests that CPAP may improve heart failure-related outcomes in patients who have persistent SDB despite optimization of their heart failure. The 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines for the management of heart failure endorse treatment of SDB in patients with heart failure for the purposes of increasing left ventricular ejection fraction and improving functional status [34].

Alternatives to positive airway pressure therapy for patients with OSA, such as oral appliances, surgery, and hypoglossal nerve stimulation, have not been adequately studied in patients with heart failure.

For patients with predominantly central sleep apnea who fail or do not tolerate CPAP, increased caution is warranted when considering alternative modes of positive airway pressure therapy, such as adaptive servo-ventilation (ASV) or bilevel positive airway pressure (BPAP) with a backup rate. In these patients, options include optimization of heart failure therapy and nocturnal oxygen.

The treatment of SDB, including indications and the choice of therapy, are discussed separately. (See "Management of obstructive sleep apnea in adults" and "Central sleep apnea: Treatment".)

Heart failure outcomes

Continuous positive pressure — With respect to patients whose heart failure is complicated by OSA, several small randomized trials found that CPAP improved left ventricular ejection fraction compared with untreated controls [51,52,58], although this finding has not been universal [53]. A meta-analysis that included six randomized trials found that CPAP was associated with a 5 percent improvement in ejection fraction in patients with heart failure and OSA [59]. A randomized trial that directly compared CPAP to bilevel positive airway pressure (BPAP) found greater improvement in cardiac function among patients receiving BPAP [54].

With respect to patients whose heart failure is complicated by CSA-CSB, CPAP appears to improve exercise capacity, ejection fraction (by approximately 4 percent), and nocturnal oxygenation, while decreasing catecholamine levels [8,23,50,56,60].

The most robust data come from the Canadian Positive Airway Pressure (CANPAP) trial, in which 258 patients who had heart failure and central sleep apnea syndrome were randomly assigned to receive CPAP or no CPAP for two years [50]. The CPAP group had a greater reduction in the apnea-hypopnea index (AHI), as well as greater improvements in mean nocturnal arterial oxyhemoglobin saturation, left ventricular ejection fraction, and the six-minute walk distance than the control group. However, there were no differences in the number of hospitalizations, quality of life, or transplant-free survival. There was an early mortality hazard associated with CPAP use, which may have been related to decreases in cardiac output among patients who were particularly preload dependent (eg, hypovolemic patients, patients with atrial fibrillation). A major limitation of the study is that the CPAP level was not titrated to effect.

In a post hoc subgroup analysis from the CANPAP trial, patients whose AHI was reduced to less than 15 events per hour by CPAP therapy had significant improvement in ejection fraction and transplant-free survival compared to controls, although the latter barely reached statistical significance (figure 1) [56]. There are two potential interpretations of this result. First, therapies that effectively and consistently lower the AHI may improve outcomes. Alternatively, improvement of AHI may not be a result of the CPAP per se, but simply a marker of a good prognosis that is unrelated to CPAP therapy.

Adaptive servoventilation — Adaptive servo-ventilation (ASV), a modified method of delivering positive airway pressure, has also been studied as a treatment for CSA-CSB in patients with heart failure. In patients with stable heart failure, a meta-analysis of 14 randomized studies (n = 538) comparing ASV to a control condition (subtherapeutic ASV, CPAP, supplemental oxygen or no treatment) found that ASV significantly improved AHI, left ventricular ejection fraction, and exercise capacity [61].

However, results of a large randomized trial (SERVE-HF) of ASV in patients with symptomatic heart failure (New York Heart Association [NYHA] class II to IV) and a low ejection fraction (EF ≤45 percent) have raised concern that ASV may be harmful in this population [62]. With a median follow-up of 31 months, patients treated with ASV had an increased risk of both cardiovascular mortality (30 versus 24 percent; HR 1.34, 95% CI 1.09-1.65) and all-cause mortality (35 versus 29 percent; hazard ratio [HR] 1.28, 95% CI 1.06-1.55) compared with the control arm. Based on these results, ASV should not be initiated in patients with CSA-CSB due to symptomatic heart failure and a low EF [63]. Decisions about continuing or stopping therapy in patients already being treated with ASV should be individualized after disclosure of the available data from the SERVE-HF study and re-evaluation of the balance of risks and benefits [64,65]. The ongoing ADVENT-HF trial may help to further inform the role of ASV in this patient population [66]. (See "Central sleep apnea: Treatment", section on 'Patients with ejection fraction ≤45 percent'.)

The use of ASV to treat CSA in hospitalized patients with heart failure has also been attempted. A trial of 126 hospitalized patients (CAT-HF) with heart failure and moderate-to-severe sleep apnea (AHI >15, predominantly CSA) failed to show a difference in a combined endpoint of death, cardiovascular hospitalizations, and timed walk distance in patients randomly assigned to ASV plus optimized medical therapy compared with optimized medical therapy alone (HR 1.06, 95% CI 0.75-1.51) [67]. The trial was stopped early, in part due to the SERVE-HF trial results, which limits the interpretation of these results. A subgroup analysis found that patients with preserved ejection fraction derived benefit from ASV, but small numbers limit confidence in the finding, and further study is required in these patients.

Arrhythmias — Limited data suggest that treatment of SDB might reduce ventricular arrhythmia burden in heart failure patients with implantable cardioverter-defibrillators (ICDs). In an observational study that included 182 heart failure patients with an ICD and evidence of moderate to severe SDB on sleep polygraphy (AHI >15 events per hour), there was a significant prolongation in the time to first cardioverter-defibrillator therapy in patients who were treated with ASV compared with those who were not (35 versus 26 months) [68]. This effect remained significant in an adjusted analysis, although since therapy was non-randomized, results remain susceptible to confounding by unmeasured variables.

Overall survival — It is unknown whether positive airway pressure therapy improves heart failure-related mortality in patients with sleep apnea. As discussed above, published randomized trials of CPAP in patients with heart failure, such as the CANPAP trial, have failed to show a difference in overall survival [50].

In the subset of patients with CSA-CSB due to symptomatic heart failure and a low ejection fraction, there is now concern that one form of positive airway pressure, ASV, may actually increase the risk of cardiovascular mortality [62]. (See "Central sleep apnea: Treatment", section on 'Patients with ejection fraction ≤45 percent'.)

Weight loss and exercise — Obesity is the most important risk factor for OSA in the general adult population as well as those with heart failure. While weight loss alone rarely leads to complete remission of OSA, it has been shown to decrease the apnea-hypopnea index (AHI), improve quality of life, and probably decrease daytime sleepiness in unselected patients with OSA. Exercise can promote weight loss and may also be of benefit independent of weight loss. (See "Management of obstructive sleep apnea in adults", section on 'Weight loss and exercise'.)

In heart failure patients specifically, exercise programs have shown mixed results in small studies. In one study, a six-month aerobic exercise program reduced the number of central but not obstructive apneas [69]. In other studies, exercise training with or without CPAP improved the AHI, minimum oxyhemoglobin saturation, and sleep quality in patients with OSA [70,71].

Other therapies — Positive airway pressure therapy is the mainstay of treatment for SDB in patients with and without heart failure. Limited data also suggest that nocturnal oxygen is beneficial in heart failure patients with CSB who have hypoxemia during sleep. Theophylline has also been explored in patients with heart failure, but more data are needed before it can be suggested for use in this setting. Surgical therapy may also be an option in selected patients.

Nocturnal oxygen — Supplemental oxygen during sleep, typically used along with positive airway pressure, is suggested for patients with CSA-CSB who have hypoxemia during sleep [72]. It is also suggested in patients who do not tolerate positive airway pressure therapy. (See "Central sleep apnea: Treatment", section on 'Supplemental oxygen during sleep'.)

This practice is supported by several small randomized trials demonstrating that low flow nocturnal oxygen (2 to 3 L/min) reduces CSB and improves left ventricular function, heart failure functional class, sleep quality, and cognitive function [9,42,73-79]. However, this evidence is limited by small sample sizes and use of short-term and surrogate outcomes. In various studies, the relative reduction in AHI achieved by nocturnal oxygen ranged from 30 to 80 percent of baseline [73]; in the largest study (n = 36), the mean AHI decreased from 49 to 29 events per hour [80]. In two small studies that compared nocturnal oxygen with CPAP (19 total patients), both therapies were effective compared with baseline and the magnitude of the reduction in AHI was similar between groups [81,82].

Although data on clinically important outcomes remain limited, no harm has been demonstrated in these studies. Theoretical risks of hyperoxia have not been observed to date in small studies using oxygen supplementation to relieve hypoxemia.

Theophylline — The possible role of theophylline in patients with heart failure complicated by SDB was evaluated in a double-blind cross-over trial of 15 such patients who received either theophylline or placebo twice daily for five days [83]. Theophylline reduced the number of apneas plus hypopneas, as well as the percentage of sleep time during which the arterial oxyhemoglobin saturation was less than 90 percent. Clinical outcome data are required before routine use of theophylline can be recommended in this setting.

Phrenic nerve stimulation — An implantable device that causes diaphragmatic contraction via unilateral transvenous phrenic nerve stimulation is an approved therapy for CSA in symptomatic patients who have failed or do not tolerate CPAP. Regulatory approval was based on a trial of phrenic nerve stimulation in 151 patients with moderate to severe central sleep apnea (AHI >20 events per hour), 64 percent of whom had heart failure [84,85]. (See "Central sleep apnea: Treatment", section on 'Phrenic nerve stimulation'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults" and "Society guideline links: Sleep-related breathing disorders in adults".)

SUMMARY AND RECOMMENDATIONS

Two types of sleep-disordered breathing are common among patients with heart failure: obstructive sleep apnea (OSA) and central sleep apnea with Cheyne-Stokes breathing (CSA-CSB). They are referred to collectively as sleep-disordered breathing (SDB). (See 'Obstructive versus central sleep apnea' above.)

Patients who have heart failure and SDB can be asymptomatic or symptomatic. Symptoms typically include snoring and/or consequences of disrupted sleep (eg, excessive daytime sleepiness, fatigue). Nocturnal angina, paroxysmal nocturnal dyspnea, and recurrent refractory arrhythmias may occur with either type of SDB. (See 'Clinical features' above.)

The routine evaluation of patients with heart failure should include questions about potential SDB symptoms. Formal sleep testing via polysomnography in a sleep laboratory or out-of-center sleep testing is suggested in patients with heart failure who report snoring, excessive daytime somnolence, or poor sleep quality. Diagnostic sleep testing should also be considered in patients with nocturnal angina, recurrent arrhythmias, refractory heart failure symptoms, or repetitive oxygen desaturations during sleep. (See 'Who should be tested?' above and 'Diagnosis' above.)

Heart failure accompanied by SDB is associated with a worse prognosis than heart failure in the absence of SDB. (See 'Prognostic implications' above.)

Primary therapy for patients whose heart failure is complicated by SDB is optimization of the medical management of heart failure because it improves both heart failure-related and SDB-related outcomes. For patients who have persistent SDB despite the optimization of heart failure therapy, continuous positive airway pressure (CPAP) may also improve both heart failure-related and SDB-related outcomes. (See 'Management' above.)

Adaptive servo-ventilation (ASV), a modified method of positive airway pressure ventilation, appears to increase cardiovascular mortality in patients with CSA due to symptomatic heart failure and a reduced ejection fraction, based on results of the SERVE-HF trial. In these patients, we recommend not initiating ASV to treat CSA-CSB (Grade 1B).

Decisions about continuing or stopping therapy in heart failure patients already being treated with ASV must be individualized after disclosure of the available data from the SERVE-HF study and re-evaluation of the balance of risks and benefits. (See 'Heart failure outcomes' above.)

For heart failure patients with CSA-CSB and hypoxemia during sleep, we suggest supplemental oxygen during sleep (Grade 2C). (See 'Nocturnal oxygen' above.)

Treatment of SDB, including indications and the choice of therapy, is discussed separately. (See "Management of obstructive sleep apnea in adults" and "Central sleep apnea: Treatment".)

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Topic 7682 Version 42.0

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