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.     

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.     

Treatment of sleep apnea in congestive heart failure with a dental device

The aim of the present study was to investigate the effect of a mandibular advancement device (MAD) for the treatment of sleep apnea (SA) on plasma brain natriuretic peptide (BNP), left ventricular ejection fraction (LVEF), and health-related qualify of life (HRQL) in patients with mild to moderate stable congestive heart failure (CHF). Seventeen male patients aged 68.4±5.5 with an apnea–hypopnea index (AHI) ≥10 were equipped with an individually fitted MAD. SA was evaluated using a portable respiratory multirecording system before and after the initiation of treatment. Eleven patients completed follow-up and were evaluated after 6 months of treatment. The AHI reduced from 25.4±10.3 to 16.5±10.0 (p=0.033) compared to baseline and mean plasma BNP levels decreased from 195.8±180.5 pg/ml to 148.1±139.9pg/ml (p=0.035). SA-related symptoms, e.g., excessive daytime sleepiness, were also reduced (p=0.003). LVEF and HRQL were unchanged. We conclude that SA treatment with a MAD on patients with mild to moderate stable CHF appears to result in the reduction of plasma BNP levels. Further studies to investigate if the observed reduction in BNP concentrations also result in improved prognosis are warranted.     

Associated factors for sleep apnea in heart failure

Objective

Genesis of sleep apnoea syndrome (SAS) in chronic heart failure (CHF) is not well known. The aim of our study was to find associated factors to SAS in heart failure (HF) and to look for differences between central sleep apnea (CSA) and obstructive sleep apnea (OSA).

Patients and methods

We realised a cross-sectional and retrospective study. Thirty patients with stable heart failure under medical optimal therapy were included. Polygraphy, echocardiography and cardiopulmonary exercise were systematically performed.

Results

Men were predominant (80%) in the group. Mean age, left ventricular ejection fraction (LVEF) were respectively 64.1 ± 13.8 years and 40 ± 9.8%. SAS was present in 60% of patients (33.3% were classified as central sleep apnoea [CSA] and 26.7% as obstructive sleep apnoea [OSA]). Body mass index, blood pressure and left ventricular pressures estimated by the E/Ea ratio were significantly higher in the group with SAS (P < 0.05) compared to the non SAS group. New York Heart Association class was significantly higher (P = 0.04) and the predicted peak VO₂ was significantly lower in CSA patients compared to OSA patients.

Conclusion

High left ventricular pressures estimated by the E/Ea are significantly associated with SAS in heart failure. CSA patients tend to have a worse functional state than OSA patients.     

Diuretics in obstructive sleep apnea with diastolic heart failure

BACKGROUND: Upper airway edema might contribute to pharyngeal collapsibility and account for the high prevalence of obstructive sleep apnea (OSA) in patients with heart disease. The aim of this study was to evaluate if intensive unloading with diuretics improves sleep-disordered breathing and increases pharyngeal caliber in patients with severe OSA and diastolic heart failure. METHODS: Fifteen patients with severe OSA, hypertension, and diastolic heart failure were hospitalized to receive IV furosemide, 20 mg, and spironolactone, 100 mg, bid for 3 days. Polysomnography was performed for assessment of apnea-hypopnea index (AHI), acoustic pharyngometry was performed for assessment of the oropharyngeal junction (OPJ) area, and forced midinspiratory flow (FIF(50)), forced midexpiratory flow (FEF(50))/FIF(50) percentage, and exhaled nitric oxide (FeNO) were measured before and after diuretic treatment. RESULTS: Diuretic treatment produced a significant decrease in body weight, BP, and AHI (from 74.89 +/- 6.95 to 57.17 +/- 5.40/h, p < 0.001), associated with an improvement in OPJ area (from 1.33 +/- 0.10 to 1.78 +/- 0.16 cm(2), p = 0.007), FIF(50) (from 3.16 +/- 0.4 to 3.94 +/- 0.4 L/s, p = 0.006), and FEF(50)/FIF(50) percentage (from 117.9 +/- 11.8 to 93.15 +/- 10.1%, p = 0.002). Weight loss was significantly related to the decrease of AHI (R = 0.602; p = 0.018), to the increase of FIF(50) (R = 0.68; p = 0.005), and to the decrease of FEF(50)/FIF(50) (R = 0.635; p = 0.011). CONCLUSIONS: These findings suggest that pharyngeal edema contributes to sleep-disordered breathing in obese patients with severe OSA, hypertension, and diastolic heart failure. Upper airway edema may contribute to the frequent occurrence of OSA in patients with heart disease.     

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。     

Central sleep apnea in patients with congestive heart failure

Central apnea during sleep represents a manifestation of breathing instability in many clinical conditions of varied etiologies. Central apnea is the result of transient cessation of ventilatory motor output, which represents that inhibitory influences favoring instability predominate over excitatory influence favoring stable breathing. This article will review the determinants of central apnea, the specific features of CHF-related central apnea, and outline a management approach     

Treatment of central sleep apnea in patients with heart failure: Now and future

Heart failure (HF) is known to be associated with sleep-disordered breathing (SDB). In addition to disturbing patients’ sleep, SDB is also associated with a deterioration in the cardiac function and an increased mortality and morbidity. Central sleep apnea (CSA), typically characterized by Cheyne-Stokes breathing (CSB), is increasingly found in patients with HF compared to the general population. An important pathogenetic factor of CSA seen in HF patients is an instability in the control of the respiratory system, characterized by both hypocapnia and increased chemosensitivity. Sympathetic overactivation, pulmonary congestion and increased chemosensitivity associated with HF stimulate the pulmonary vagal irritant receptor, resulting in chronic hyperventilation and hypocapnia. Additionally, the repetitive apnea and arousal cycles induce cyclic sympathetic activation, which may worsen the cardiac prognosis. Correcting CSB may improve both patient’s quality of life and HF syndrome itself. However, a treatment for HF in patients also experiencing CSA is yet to be found. In fact, conflicting results from numerous clinical studies investigating sleep apnea with HF guide to a troubling question, that is whether (or not) sleep apnea should be treated in patients with HF? This editorial attempts to both collect the current evidence about randomized control trials investigating CSA in patients with HF and highlight the effect of specific CSA treatments on cardiovascular endpoints.     

Usefulness of home sleep apnea tests in heart failure patients

Sleep and Breathing -     

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近年来,睡眠呼吸暂停综合征(SAS)在慢性充血性心力衰竭(CHF)发生发展中的作用逐渐得到重视。研究表明,无论是阻塞性睡眠呼吸暂停综合征(OSAS)还是中枢性睡眠呼吸暂停综合征(CSAS)均与CHF密切相关。其中CSAS常见于严重CHF,并加重CHF病理生理进程;而OS-AS也是多种心血管疾病(包括     

Central sleep apnea: implications for congestive heart failure

Congestive heart failure (HF), an exceedingly common and costly disease, is frequently seen in association with central sleep apnea (CSA), which often manifests as a periodic breathing rhythm referred to as Cheyne-Stokes respiration. CSA has historically been considered to be a marker of heart disease, since improvement in cardiac status is often associated with the attenuation of CSA. However, this mirroring of HF and CSA may suggest bidirectional importance to their relationship. In fact, observational data suggest that CSA, associated with repetitive oxyhemoglobin desaturations and surges in sympathetic neural activity, may be of pathophysiologic significance in HF outcomes. In light of the disappointing results from the first large trial assessing therapy with continuous positive airway pressure in patients with CSA and HF, further large-scale interventional trials will be needed to assess the role, if any, of CSA treatment on the outcomes of patients with HF. This review will discuss epidemiologic, pathophysiologic, diagnostic, and therapeutic considerations of CSA in the setting of HF.     

Cycle length identifies obstructive sleep apnea and central sleep apnea in heart failure with reduced ejection fraction

Aim

To clarify whether unmasking of central sleep apnea during continuous positive airway pressure (CPAP) initiation can be identified from initial diagnostic polysomnography (PSG) in patients with heart failure with reduced ejection fraction (HFREF) and obstructive sleep apnea (OSA)

Materials and methods

Forty-three consecutive patients with obstructive sleep apnea and central sleep apnea (OSA/CSA) in HFREF were matched with 43 HFREF patients with OSA and successful CPAP initiation. Obstructive apneas during diagnostic PSG were then analyzed for cycle length (CL), ventilation length (VL), apnea length (AL), time to peak ventilation (TTPV), and circulatory delay (CD). We calculated duty ratio (DR) as the ratio of VL/CL and mathematic loop gain (LG).

Results

While AL was similar, CL, VL, TTPV, CD, and DR was significantly longer in patients with OSA/CSA compared to those with OSA, and LG was significantly higher. Receiver operator curves identified optimal cutoff values of 50.2 s for CL (area under the curve (AUC) 0.85, 29.2 s for VL (AUC 0.92), 11.5 s for TTPV (AUC 0.82), 26.4 s for CD (AUC 0.79), and 3.96 (AUC 0.78)) respectively for LG to identify OSA/CSA.

Conclusion

OSA/CSA in HFREF can be identified by longer CL, VL, TTPV, and CD from obstructive events in initial diagnostic PSG. The underlying mechanisms seem to be the presence of an increased LG.

     

The potential benefits of treatment of sleep apnea in heart failure

At least half of patients with heart failure (HF) suffer from sleep apnea. Growing evidence suggests that there may be a strong pathophysiological link between chronic HF and sleep apnea due to nocturnal oxygen desaturation and sympathetic activation. It seems that sleep apnea contributes to systolic and diastolic HF, reduced left and right ventricular function, and arrhythmia (e.g. atrial fibrillation, bradycardia, or ventricular ectopy). Therefore, treatment of sleep apnea might alleviate cardiac symptoms and improve cardiac function. Nevertheless, the exact role of long-term treatment of sleep apnea in HF patients remains to be elucidated, as important clinical endpoints (e.g mortality) have been assessed in only a few studies. Heart Fail Monit 2008;5(4):106-11.     

Prevalence and management of central sleep apnea in heart failure patients

There is increasing awareness of sleep-disordered breathing, which may manifest as obstructive sleep apnea, central sleep apnea (CSA), or a mixture of the two. Obstructive sleep apnea and CSA are strongly associated with heart failure (HF) and risk factors for developing HF. CSA may be considered a manifestation of the pathophysiology of HF; hence, approaches to optimize pharmacologic and nonpharmacologic treatment of HF should help to ameliorate CSA. However, if CSA also contributes to HF progression, CSA may represent a potential therapeutic target. There was hope that CSA prevalence would decline with better HF therapies. However, contemporary studies of HF patients on optimal medical therapy have shown that CSA prevalence remains 30% to 40%. Treating CSA poses significant challenges. Presently, the role of routine continuous positive airway pressure remains unclear, although newer ventilatory strategies may prove effective. Currently, CSA treatment involves standard optimal HF therapies, although growing evidence indicates that newer ventilation modes and cardiac resynchronization therapy may prove to be useful.