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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adaptive servo-ventilation (ASV) is a novel method of ventilatory support designed for Cheyne-Stokes respiration (CSR) in heart failure. The aim of our study was to compare the effect of one night of ASV on sleep and breathing with the effect of other treatments. Fourteen subjects with stable cardiac failure and receiving optimal medical treatment were tested untreated and on four treatment nights in random order: nasal oxygen (2 L/min), continuous positive airway pressure (CPAP) (mean 9.25 cm H(2)O), bilevel (mean 13.5/5.2 cm H(2)O), or ASV largely at the default settings (mean pressure 7 to 9 cm H(2)O) during polysomnography. Thermistor apnea + hypopnea index (AHI) declined from 44.5 +/- 3.4/h (SEM) untreated to 28.2 +/- 3.4/h oxygen and 26.8 +/- 4.6/h CPAP (both p < 0.001 versus control), 14.8 +/- 2.3/h bilevel, and 6.3 +/- 0.9/h ASV (p < 0.001 versus bilevel). Effort band AHI behaved similarly. Arousal index decreased from 65.1 +/- 3.9/h untreated to 29.8 +/- 2.8/h oxygen and 29.9 +/- 3.2/h CPAP, to 16.0 +/- 1.3/h bilevel and 14.7 +/- 1.8/h ASV (p < 0.01 versus all except bilevel). There were large increases in slow-wave and rapid eye movement (REM) sleep with ASV but not with oxygen or CPAP. All subjects preferred ASV to CPAP. One night ASV suppresses central sleep apnea and/or CSR (CSA/CSR) in heart failure and improves sleep quality better than CPAP or 2 L/min oxygen.
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PMID:Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. 1152 Jul 25

Previous small-scale studies of the effect of sleep-disordered breathing (SDB) on prognosis in congestive heart failure (CHF) are either lacking or conflicting. The aim of this study was to assess the impact of the presence and type of SDB on mortality in a patient group with severe CHF referred to a specialised heart failure centre. Out of 78 patients ((mean +/- SD) 53 +/- 9 yrs, left ventricular ejection fraction 19.9 +/- 7.2% and pulmonary capillary wedge pressure 16.5 +/- 8.3 mmHg) followed-up over a median period of 52 months, 29% had no apnoea (CHF-N), 28% had obstructive sleep apnoea (CHF-OSA) and 42% had central sleep apnoea (CHF-CSA). At 52 months, their overall mortality was 40%, and combined mortality and transplantation was 72%. Mortality rates were similar between the three apnoea groups. Survivors had a similar prevalence of SDB (71%) as the nonsurvivors (70%). Although a significant increase in mortality was evident at 500 days in those patients with either CHF-SDB or CHF-CSA as compared with CHF-N, this was not significant at final follow-up (52 months) using Kaplan Meier analysis. Multivariate analysis identified transplantation but not SDB type or severity as a significant predictor of survival. In conclusion, sleep-disordered breathing impacts upon early (500 day), but not long-term (52 month), mortality in a specialised heart failure centre.
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PMID:Increased long-term mortality in heart failure due to sleep apnoea is not yet proven. 1517 74

A 57-year-old man was admitted with dyspnea. Clinical evaluation revealed atrial fibrillation and congestive heart failure (CHF). Standard medical therapy of CHF failed to completely improve the dyspnea and polysomnography revealed Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). He was equipped with noninvasive positive pressure ventilation (NPPV) with bilevel positive airway pressure (BiPAP). The combined therapy of medical treatment of the CHF and administration of NPPV with BiPAP reduced the CSR-CSA. This regimen resulted in marked improvement of cardiac function, evaluated by echocardiography, and reduction of plasma concentration of brain natriuretic peptide. After the patient recovered from CHF and was discharged from hospital, he continued to use NPPV with BiPAP at home. In patients with CHF, it is important to be aware of sleep-related breathing disorders because treatment will not only improve the hypoxemia, but also the cardiac dysfunction.
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PMID:Improvement of cheyne-stokes respiration, central sleep apnea and congestive heart failure by noninvasive bilevel positive pressure and medical treatment. 1532 13

Five adult patients with congestive heart failure (CHF) due to dilated cardiomyopathy complicated by Cheyne-Stokes respiration/central sleep apnea (CSR/CSA) were treated with continuous positive airway pressure (CPAP) with an initial pressure of 5 cm H2O. Four patients were followed up for 12 months with CPAP of 5 cm H2O. The rest, a 93-year-old patient, was followed up for 30 months, and the CPAP was reset at 8 cm H2O due to worsened cardiac function after 6 months and it was reset at 6 cm H2O due to dryness of the nose after 23 months. For all the patients with nightly CPAP use for 6.0+/-1.4 h per day for a year, frequency of CSR/CSA was significantly reduced after 3 and 12 months with CPAP (p<0.05). Moreover, their symptoms, cardiac function and sleep quality were significantly improved after 3 months (p<0.05), and were maintained above the pre-CPAP levels after 12 months, except for the oldest patient whose cardiac function tended to deteriorate. The results suggest that CSR/CSA in CHF can be treated with CPAP set at a lower pressure than the conventional method, and that CPAP at 5-8 cm H2O is often effective in eliminating CSR/CSA, improving sleep quality, and presumably maintaining cardiac function.
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PMID:Cheyne-Stokes respiration in congestive heart failure: continuous positive airway pressure of 5-8 cm H2O for 1 year in five cases. 1726 69

In subjects with sinus rhythm, respiration has a profound effect on heart rate variability (HRV) at high frequencies (HF). Because this HF respiratory arrhythmia is lost in atrial fibrillation (AF), it has been assumed that respiration does not influence the ventricular response. However, previous investigations have not considered the possibility that respiration might influence HRV at lower frequencies. We hypothesized that Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) would entrain HRV at very low frequency (VLF) in AF by modulating atrioventricular (AV) nodal refractory period and concealed conduction. Power spectral analysis of R-wave-to-R-wave (R-R) intervals and respiration during sleep were performed in 13 subjects with AF and CSR-CSA. As anticipated, no modulation of HRV was detected at HF during regular breathing. In contrast, VLF HRV was entrained by CSR-CSA [coherence between respiration and HRV of 0.69 (SD 0.22) at VLF during CSR-CSA vs. 0.20 (SD 0.19) at HF during regular breathing, P < 0.001]. Comparison of R-R intervals during CSR-CSA demonstrated a shorter AV node refractory period during hyperpnea than apnea [minimum R-R of 684 (SD 126) vs. 735 ms (SD 147), P < 0.001] and a lesser degree of concealed conduction [scatter of 178 (SD 56) vs. 246 ms (SD 72), P = 0.001]. We conclude that CSR-CSA entrains the ventricular response to AF, even in the absence of HF respiratory arrhythmia, by inducing rhythmic oscillations in AV node refractoriness and the degree of concealed conduction that may be a function of autonomic modulation of the AV node.
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PMID:Influence of Cheyne-Stokes respiration on ventricular response to atrial fibrillation in heart failure. 1599 46

In patients with obstructive sleep apnoea (OSA), the very low frequency power spectral density index (VLFI) derived from analysis of heart rate correlates with the severity of obstructive apnoeas. VLFI is also associated with Cheyne-Stokes respiration/central sleep apnoea (CSR/CSA) in congestive heart failure (CHF). The present authors have tested the hypothesis that per cent VLFI, derived from a standard Holter ECG recording, can be used to detect the presence of OSA and CSR/CSA in patients with mild-to-moderate CHF. In total, 60 CHF patients underwent polysomnography with monitoring of heart rate. Data from 33 patients were analysed for per cent VLFI. Of the 60 patients, 27 were excluded due to atrial fibrillation, extensive pacing or frequent ventricular extra systoles. Receiver operator characteristic curves were constructed to establish the per cent VLFI that would optimally identify the presence or absence of sleep-disordered breathing. Using an apnoea-hypopnoea index>20 events.h-1 and setting the per cent VLFI at 2.23% yielded a sensitivity of 85%, specificity of 65%, positive predictive value of 61% and a negative predictive value of 87%. The latter increased to 100% when using an apnoea-hypopnoea cut-off of 30 events.h-1. In conclusion, these results suggest that spectral analysis of heart rate may be useful as a "rule-out test" for sleep-disordered breathing in patients with mild-to-moderate congestive heart failure.
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PMID:Can heart rate variation rule out sleep-disordered breathing in heart failure? 1688 Mar 76

In patients with heart failure, apnea type can shift overnight from mainly obstructive to mainly central in association with reductions in PCO(2) and increases in periodic breathing cycle length, indicative of a fall in cardiac output. We hypothesized that the predominant apnea type could also vary from one night to another in association with alterations in PCO(2) and cycle length. We studied 12 men with heart failure in whom the predominant apnea type changed from one night to the next over periods of at least 1 month, and two groups with either predominantly obstructive or central sleep apnea (OSA or CSA) in whom apnea type remained stable over time. In patients with unstable apnea type (n = 12, duration between sleep studies 9.0 +/- 4.4 months), PCO(2) was significantly lower (37.6 +/- 1.6 mmHg versus 41.7 +/- 1.9 mmHg, P < 0.01), and cycle length significantly longer (61.9 +/- 3.4 s versus 51.0 +/- 1.9 s, P < 0.001) during nights with predominantly central than nights with predominantly obstructive apnea. In contrast, in both the stable central (n = 8, duration between sleep studies 11.9 +/- 5.3 months) and the stable obstructive (n = 8, duration between studies 6.9 +/- 5.2 months) sleep apnea groups, neither PCO(2) nor cycle length changed significantly between the baseline and follow-up sleep studies. We conclude that in some patients with heart failure, OSA and CSA are part of a spectrum of periodic breathing that can shift over time in association with alterations in PCO(2), cycle length and probably cardiac function.
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PMID:Night-to-night alterations in sleep apnea type in patients with heart failure. 1691 Oct 35

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.
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PMID:Diagnosis and treatment of sleep apnea in heart disease. 1822 2

Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) is a form of periodic breathing, commonly observed in patients with heart failure (HF), in which central apneas alternate with hyperpneas that have a waxing-waning pattern of tidal volume. Uniform criteria by which to diagnose a clinically significant degree of CSR-CSA have yet to be established. CSR-CSA is caused by respiratory control system instability characterized by a tendency to hyperventilate. Central apnea occurs when Pa(CO(2)) falls below the threshold for apnea during sleep due to ventilatory overshoot. Patients with CSR-CSA are generally hypocapnic, with a Pa(CO(2)) closer than normal to the apneic threshold such that even slight augmentation in ventilation drives Pa(CO(2)) below threshold and triggers apnea. Factors contributing to hyperventilation in HF include stimulation of pulmonary irritant receptors by pulmonary congestion, increased chemoreceptor sensitivity, reduced cerebrovascular blood flow, and recurrent arousals from sleep. Controversy remains as to whether CSR-CSA is simply a reflection of HF severity, or whether it exerts unique adverse effects on prognosis. The main adverse influence of CSR-CSA on cardiovascular function appears to be excessive sympathetic nervous system activity due to apnea-related hypoxia and arousals from sleep. A number of studies have examined the potential relationship between CSR-CSA and mortality in HF. Most reported that CSR-CSA was associated with an increased risk for mortality, but these studies were small. Further research is therefore needed to elucidate mechanisms which contribute to the pathogenesis of CSR-CSA, and to determine whether its treatment can reduce morbidity and mortality in patients with HF.
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PMID:Central sleep apnea and Cheyne-Stokes respiration. 1825 Feb 16

There are three major types of sleep-disordered breathing (SDB) with respect to prevalence and health consequences, i.e. obstructive sleep apnoea syndrome (OSAS), Cheyne-Stokes respiration and central sleep apnoea (CSR-CSA) in chronic heart failure, and obesity hypoventilation syndrome (OHS). In all three conditions, hypoxia appears to affect body functioning in different ways. Most of the molecular and cellular mechanisms that occur in response to SDB-related hypoxia remain unknown. In OSAS, an inflammatory cascade mainly dependent upon intermittent hypoxia has been described. There is a strong interaction between haemodynamic and inflammatory changes in promoting vascular remodelling. Moreover, during OSAS, most organ, tissue or functional impairment is related to the severity of nocturnal hypoxia. CSR-CSA occurring during heart failure is primarily a consequence of cardiac impairment. CSR-CSA has deleterious consequences for cardiac prognosis and mortality since it favours sympathetic activation, ventricular ectopy and atrial fibrillation. Although correction of CSR-CSA seems to be critical, there is a need to establish therapy guidelines in large randomised controlled trials. Finally, OHS is a growing health concern, owing to the worldwide obesity epidemic and OHS morbidities. The pathophysiology of OHS remains largely unknown. However, resistance to leptin, obesity and severe nocturnal hypoxia lead to insulin resistance and endothelial dysfunction. In addition, several adipokines may be triggered by hypoxia and explain, at least in part, OHS morbidity and mortality. Overall, chronic intermittent hypoxia appears to have specific genomic effects that differ notably from continuous hypoxia. Further research is required to fully elucidate the molecular and cellular mechanisms.
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PMID:Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives. 1882 54


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