Sleep apnea in heart failure increases heart rate variability and sympathetic dominance

AIMS: Sleep disordered breathing (SDB) is common in heart failure and ventilation is known to influence heart rate. Our aims were to assess the influence of SDB on heart rate variability (HRV) and to determine whether central sleep apnea (CSA) and obstructive sleep apnea (OSA) produced different patterns of HRV. METHODS AND RESULTS: Overnight polysomnography was performed in 21 patients with heart failure and SDB. Two 10-minute segments each of SDB and stable breathing from each patient were visually identified and ECG signal exported for HRV analysis. SDB increased total power (TP) with very low frequency (VLF) power accounting for the greatest increase (1.89+/-0.54 vs 2.96+/-0.46 ms2, P <0.001); LF/HF ratio increased during SDB (1.2+/-1.0 vs 2.7+/-2.1, P <0.001). Compared to OSA, CSA was associated with lower absolute LF (2.10+/-0.47 vs 2.52+/-0.55 ms2, P = 0.049) and HF power (1.69+/-0.41 vs 2.34+/-0.58 ms2, P = 0.004), increased VLF% (78.9%+/-13.4% vs 60.9%+/-19.2%, P = 0.008), decreased HF% (6.9%+/-7.8% vs 16.0%+/-11.7%, P = 0.046) with a trend to higher LF/HF ratio. CONCLUSIONS: SDB increases HRV in the setting of increased sympathetic dominance. HRV in CSA and OSA have unique HRV patterns which are likely to reflect the different pathophysiological mechanisms involved.     

Sleep-disordered breathing and cardiovascular risk

Sleep-disordered breathing, broadly characterized by obstructive sleep apnea (OSA) and central sleep apnea (CSA), is an increasingly recognized public health burden. OSA, consisting of apneas or hypopneas associated with respiratory efforts in the face of upper airway narrowing or collapse, is a common disorder that can be effectively treated with continuous positive airway pressure (CPAP). OSA not only results in daytime sleepiness and impaired executive function, but also has been implicated as a possible cause of systemic disease, particularly of the cardiovascular system. CSA, which may coexist with OSA, has gained attention because of the association of Cheyne-Stokes respiration with an ever-increasing prevalence of heart failure in an aging population. This article reviews some of the extensive literature on pathophysiologic mechanisms as they may relate to the development of cardiac and vascular disease and examine the evidence suggesting OSA as a specific cause of certain cardiovascular conditions. Available evidence regarding the implications of CSA in the context of heart failure is discussed.     

Herzinsuffizienz

Sleep-disordered breathing is highly prevalent in heart failure patients. This accounts for patients with heart failure due to reduced ejection fraction (HF-REF) or with preserved ejection fraction (HF-PEF). Independent of HF-REF or HF-PEF, prevalence of central sleep apnea (CSA) with Cheyne-Stokes respiration (CSR) increases with deterioration in cardiac function. While obstructive sleep apnea (OSA) represents a cardiovascular risk factor per se, CSA with CSR might reflect impairment in cardiac function. However, both entities seem to further impair cardiac function and patients’ prognosis. Continuous positive airway pressure (CPAP) therapy is recommended to treat OSA, while adaptive servoventilation (ASV) therapy seems to be the therapy of choice in heart failure patients with CSA. With these therapies, small studies show an improvement in symptoms quality of life, and cardiac performance. Thus, large randomized controlled trials investigating morbidity and mortality are underway, but first results will be expected not before end of 2015.     

Sleep-disordered breathing in heart failure: characteristics and implications

Sleep-disordered breathing, namely obstructive sleep apnea (OSA) and central sleep apnea (CSA), are both often encountered in the setting of heart failure (HF), and have distinct differences in terms of prevalence, pathophysiology and consequences. OSA is independently associated with an increased risk for cardiovascular disease and for congestive HF in the general population. It is conceivable that this breathing disorder may have particularly deleterious effects in patients with coexisting heart disease, especially in those with a failing heart. There are considerable data addressing the interaction between OSA and the cardiovascular system, which underscore the importance of an early detection of this breathing disorder, especially in patients with HF. CSA is generally considered a consequence rather than a cause of HF, and is correlated with the severity of hemodynamic impairment. However, when present, it is associated with increased arrhythmic risk and higher cardiac mortality. Potential mechanisms implicated in the genesis of this breathing pattern and the possible therapeutic options, which have been proven to be effective in the clinical setting, are discussed.     

Effect of supplemental nocturnal oxygen on gas exchange in patients with severe obstructive lung disease

We studied the effect of supplemental nocturnal oxygen on blood gases in 15 patients with severe but stable chronic obstructive lung disease (ratio of forced expired volume in one second to forced vital capacity, 37.2 +/- 1.8 [mean +/- S.E.] per cent of predicted; arterial oxygen tension, 50.7 +/- 1.4 mm Hg; and arterial carbon dioxide tension [PCO2], 53.1 +/- 1.5 mm Hg). Sleep variables and measures of gas exchange were determined on two consecutive nights; on the first night the subjects breathed supplemental oxygen, and on the second they breathed room air. Transcutaneous PCO2 was measured with an infrared sensor, and arterial oxygen saturation with an ear oximeter. Breathing of supplemental oxygen sufficient to keep oxygen saturation at or above 90 per cent was associated with only small increases (less than 6 mm Hg) in PCO2 throughout sleep, as compared with values while subjects were breathing room air. The increase in PCO2 occurred early in the night and was not progressive. Only three patients, who were found to have obstructive sleep apnea in addition to obstructive lung disease, had larger increases in PCO2 during sleep and reported morning headaches. We conclude that nocturnal oxygen does not induce clinically important increases in PCO2 during sleep in patients with stable obstructive lung disease and therefore can safely be used to prevent the dangerous consequences of hypoxia.     

Complex sleep apnea syndrome: is it a unique clinical syndrome?

STUDY OBJECTIVES: Some patients with apparent obstructive sleep apnea hypopnea syndrome (OSAHS) have elimination of obstructive events but emergence of problematic central apneas or Cheyne-Stokes breathing pattern. Patients with this sleep-disordered breathing problem, which for the sake of study we call the "complex sleep apnea syndrome," are not well characterized. We sought to determine the prevalence of complex sleep apnea syndrome and hypothesized that the clinical characteristics of patients with complex sleep apnea syndrome would more nearly resemble those of patients with central sleep apnea syndrome (CSA) than with those of patients with OSAHS. DESIGN: Retrospective review SETTING: Sleep disorders center. PATIENTS OR PARTICIPANTS: Two hundred twenty-three adults consecutively referred over 1 month plus 20 consecutive patients diagnosed with CSA. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Prevalence of complex sleep apnea syndrome, OSAHS, and CSA in the 1-month sample was 15%, 84%, and 0.4%, respectively. Patients with complex sleep apnea syndrome differed in gender from patients with OSAHS (81% vs 60% men, p < .05) but were otherwise similar in sleep and cardiovascular history. Patients with complex sleep apnea syndrome had fewer maintenance-insomnia complaints (32% vs 79%; p < .05) than patients with CSA but were otherwise not significantly different clinically. Diagnostic apnea-hypopnea index for patients with complex sleep apnea syndrome, OSAHS, and CSA was 32.3 +/- 26.8, 20.6 +/- 23.7, and 38.3 +/- 36.2, respectively (p = .005). Continuous positive airway pressure suppressed obstructive breathing, but residual apnea-hypopnea index, mostly from central apneas, remained high in patients with complex sleep apnea syndrome and CSA (21.7 +/- 18.6 in complex sleep apnea syndrome, 32.9 +/- 30.8 in CSA vs 2.14 +/- 3.14 in OSAHS; p < .001). CONCLUSIONS: Patients with complex sleep apnea syndrome are mostly similar to those with OSAHS until one applies continuous positive airway pressure. They are left with very disrupted breathing and sleep on continuous positive airway pressure. Clinical risk factors don't predict the emergence of complex sleep apnea syndrome, and best treatment is not known.     

Adaptive servoventilation versus noninvasive positive pressure ventilation for central, mixed, and complex sleep apnea syndromes

RATIONALE: Although continuous positive airway pressure (CPAP) is most often effective in patients with obstructive sleep apnea, optimal treatment of patients with predominantly mixed apneas, central sleep apnea syndrome/Cheyne-Stokes respiration (CSA/CSR), or complex sleep apnea (CompSAS) is less straightforward, and may require alternative ventilatory assist modalities. OBJECTIVES: To compare the efficacy of noninvasive positive pressure ventilation (NPPV) with adaptive servoventilation (ASV) in treating patients with centrally mediated breathing abnormalities. We hypothesized that NPPV and ASV would be equivalently efficacious in improving the apnea/hypopnea index (AHI) and respiratory arousal index (RAI). METHODS: Prospective randomized crossover clinical trial comparing NPPV with ASV in patients with CSA/CSR, predominantly mixed apneas, and CompSAS in an acute setting. MEASUREMENTS AND MAIN RESULTS: 21 patients (6 with CSA/CSR, 6 with predominantly mixed apneas, and 9 with CompSAS) with initial diagnostic AHI +/- standard deviation 51.9 +/- 22.8/hr and RAI 45.5 < or = 26.5/hr completed the study. Following optimal titration with CPAP (N = 15), disturbed breathing and disturbed sleep remained high with mean AHI = 34.3 +/- 25.7 and RAI = 32.1 +/- 29.7. AHI and RAI were markedly reduced with both NPPV (6.2 +/- 7.6 and 6.4 +/- 8.2) and ASV (0.8 +/- 2.4 and 2.4 +/- 4.5). Treatment AHI and RAI were both significantly lower using ASV (P < 0.01). CONCLUSION: These data confirm that in patients with CSA/CSR, mixed apneas, and CompSAS, both NPPV and ASV are effective in normalizing breathing and sleep parameters, and that ASV does so more effectively than NPPV in these types of patients.     

Energy based feature extraction for classification of sleep apnea syndrome

In this paper it is aimed to classify sleep apnea syndrome (SAS) by using discrete wavelet transforms (DWT) and an artificial neural network (ANN). The abdominal and thoracic respiration signals are separated into spectral components by using multi-resolution DWT. Then the energy of these spectral components are applied to the inputs of the ANN. The neural network was configured to give three outputs to classify the SAS situation of the subject.The apnea can be mainly classified into three types: obstructive sleep apnea (OSA), central sleep apnea (CSA) and mixed sleep apnea (MSA). During OSA, the airway is blocked while respiratory efforts continue. During CSA the airway is open, however, there are no respiratory efforts. In this paper we aim to classify sleep apnea in one of three basic types: obstructive, central and mixed. A significant result was obtained.     

Adaptive servo-ventilation and deadspace: effects on central sleep apnoea

Central Sleep Apnoea (CSA) occurs commonly in heart failure. Adaptive servo-ventilation (ASV) and deadspace (DS) have been shown in research settings to reverse CSA. The likely mechanism for this is the increase of PaCO(2) above the apnoeic threshold. However the role of increasing FiCO(2) on arousability remains unclear. To compare the effects of ASV and DS on sleep and breathing, in particular effects on Arousal Index (ArI), ten male patients with heart failure and CSA were studied during three nights with polysomnography plus measurements of PetCO(2). The order of the interventions control (C), ASV and DS was randomized. ASV and DS caused similar reductions in apnoea-hypopnoea index [(C) 30.0 +/- 6.6, (ASV) 14.0 +/- 3.8, (DS) 15.9 +/- 4.7 e h(-1); both P < 0.05]. However, DS was associated with decreased total sleep time compared with C (P < 0.02) and increased spontaneous ArI compared to C and ASV (both P < 0.01). Only DS was associated with increased DeltaPetCO(2) from resting wakefulness to eupnic sleep [(C) 2.1 +/- 0.9, (ASV) 1.3 +/- 1.0, (DS) 5.6 +/- 0.5 mmHg; P = 0.01]. ASV and DS both stabilized ventilation however DS application also increased sleep fragmentation with negative impacts on sleep architecture. We speculate that this effect is likely to be mediated by increased PetCO(2) and respiratory effort associated with DS application.     

Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: an update for 2007. An American Academy of Sleep Medicine report

These practice parameters are an update of the previously published recommendations regarding the use of autotitrating positive airway pressure (APAP) devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. Continuous positive airway pressure (CPAP) at an effective setting verified by attended polysomnography is a standard treatment for obstructive sleep apnea (OSA). APAP devices change the treatment pressure based on feedback from various patient measures such as airflow, pressure fluctuations, or measures of airway resistance. These devices may aid in the pressure titration process, address possible changes in pressure requirements throughout a given night and from night to night, aid in treatment of OSA when attended CPAP titration has not or cannot be accomplished, or improve patient comfort. A task force of the Standards of Practice Committee of the American Academy of Sleep Medicine has reviewed the literature published since the 2002 practice parameter on the use of APAP. Current recommendations follow: (1) APAP devices are not recommended to diagnose OSA; (2) patients with congestive heart failure, patients with significant lung disease such as chronic obstructive pulmonary disease; patients expected to have nocturnal arterial oxyhemoglobin desaturation due to conditions other than OSA (e.g., obesity hypoventilation syndrome); patients who do not snore (either naturally or as a result of palate surgery); and patients who have central sleep apnea syndromes are not currently candidates for APAP titration or treatment; (3) APAP devices are not currently recommended for split-night titration; (4) certain APAP devices may be used during attended titration with polysomnography to identify a single pressure for use with standard CPAP for treatment of moderate to severe OSA; (5) certain APAP devices may be initiated and used in the self-adjusting mode for unattended treatment of patients with moderate to severe OSA without significant comorbidities (CHF, COPD, central sleep apnea syndromes, or hypoventilation syndromes); (6) certain APAP devices may be used in an unattended way to determine a fixed CPAP treatment pressure for patients with moderate to severe OSA without significant comorbidities (CHF, COPD, central sleep apnea syndromes, or hypoventilation syndromes); (7) patients being treated with fixed CPAP on the basis of APAP titration or being treated with APAP must have close clinical follow-up to determine treatment effectiveness and safety; and (8) a reevaluation and, if necessary, a standard attended CPAP titration should be performed if symptoms do not resolve or the APAP treatment otherwise appears to lack efficacy.     

Effect of Continuous Positive Airway Pressure on Sleep Structure in Heart Failure Patients with Central Sleep Apnea

Study Objectives:

At termination of obstructive apneas, arousal is a protective mechanism that facilitates restoration of upper airway patency and airflow. Treating obstructive sleep apnea (OSA) by continuous positive airway pressure (CPAP) reduces arousal frequency indicating that such arousals are caused by OSA. In heart failure (HF) patients with central sleep apnea (CSA), however, arousals frequently occur several breaths after apnea termination, and there is uncertainty as to whether arousals from sleep are a consequence of CSA. If so, they should diminish in frequency when CSA is attenuated. We therefore sought to determine whether attenuation of CSA by CPAP reduces arousal frequency.

Design:

Randomized controlled clinical trial.

Patients and Setting:

We examined data from 205 HF patients with CSA (apnea-hypopnea index [AHI] ≥ 15, > 50% were central) randomized to CPAP or control who had polysomnograms performed at baseline and 3 months later.

Measurements and Results:

In the control group, there was no change in AHI or frequency of arousals. In the CPAP-treated group, the AHI decreased significantly (from [mean ± SD] 38.9 ± 15.0 to 17.6 ± 16.3, P < 0.001) but neither the frequency of arousals nor sleep structure changed significantly.

Conclusion:

These data suggest that attenuation of CSA by CPAP does not reduce arousal frequency in HF patients. We conclude that arousals were not mainly a consequence of CSA, and may not have been acting as a defense mechanism to terminate apneas in the same way they do in OSA.

Citation:

Ruttanaumpawan P; Logan AG; Floras JS; Bradley TD. Effect of Continuous Positive Airway Pressure on Sleep Structure in Heart Failure Patients with Central Sleep Apnea. SLEEP 2009;32(1):91-98.     

A mechanism of central sleep apnea in patients with heart failure.

BACKGROUND: Breathing is controlled by a negative-feedback system in which an increase in the partial pressure of arterial carbon dioxide stimulates breathing and a decrease inhibits it. Although enhanced sensitivity to carbon dioxide helps maintain the partial pressure of arterial carbon dioxide within a narrow range during waking hours, in some persons a large hyperventilatory response during sleep may lower the value below the apneic threshold, thereby resulting in central apnea. I tested the hypothesis that enhanced sensitivity to carbon dioxide contributes to the development of central sleep apnea in some patients with heart failure. METHODS: This prospective study included 20 men who had treated, stable heart failure with left ventricular systolic dysfunction. Ten had central sleep apnea, and 10 did not. The patients underwent polysomnography and studies of their ventilatory response to carbon dioxide. RESULTS: Patients who met the criteria for central sleep apnea had significantly more episodes of central apnea per hour than those without central sleep apnea (mean [+/-SD], 35+/-24 vs. 0.5+/-1.0 episodes per hour). Those with sleep apnea also had a significantly larger ventilatory response to carbon dioxide than those without central sleep apnea (5.1+/-3.1 vs. 2.1+/-1.0 liters per minute per millimeter of mercury, P=0.007), and there was a significant positive correlation between ventilatory response and the number of episodes of apnea and hypopnea per hour during sleep (r=0.6, P=0.01). CONCLUSIONS: Enhanced sensitivity to carbon dioxide may predispose some patients with heart failure to the development of central sleep apnea.     

Relationship of sleep apnea to functional capacity and length of hospitalization following stroke

STUDY OBJECTIVES: Recent evidence indicates that sleep apnea is common in patients with stroke. We hypothesized that the presence of sleep apnea among stroke patients would be associated with a greater degree of functional disability and longer hospitalization following stroke. DESIGN: Prospective study. SETTING AND PATIENTS: Sixty-one stroke patients admitted to a stroke rehabilitation unit. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Sleep studies were performed on all patients, and sleep apnea was defined as an apnea-hypopnea index of 10 or more per hour of sleep. Patients underwent functional assessments, including the Functional Independence Measure. Sleep apnea was found in 72% of patients; 60% had predominantly obstructive sleep apnea, while 12% had predominantly central sleep apnea. Although the severity of stroke was similar in the 2 groups, compared to patients without sleep apnea, those with sleep apnea had lower functional capacity [Functional Independence Measure score (mean +/- SEM) 80.2 +/- 3.6 versus 94.7 +/- 4.3, p < 0.05 at admission, and 101.5 +/- 2.8 versus 112.9 +/- 2.7, p < 0.05 at discharge] and spent significantly more days in rehabilitation (45.5 +/- 2.3 versus 32.1 +/- 2.7 days, p < 0.005). In addition, multiple regression analysis showed that obstructive sleep apnea was significantly and independently related to functional impairment and length of hospitalization. CONCLUSIONS: Sleep apnea is very common among stroke patients undergoing rehabilitation, and its presence is associated with worse functional impairment and a longer period of hospitalization and rehabilitation. These data suggest that sleep apnea may be contributing to functional impairment and prolonged hospitalization following stroke.     

Non-linear dynamics of human periodic breathing and implications for sleep apnea therapy

A mathematical model of non-obstructive human periodic breathing (Cheyne–Stokes respiration) or central sleep apnea (CSA) is described which focused on explaining recently reported non-linear behavior. Evidence was presented that CHF (chronic heart failure)–CSA and ICSA (idiopathic central sleep apnea) both involved limit cycle oscillations. The validity of applying linear control theory for stabilization must then be re-examined. Critical threshold values and ranges of parameters were predicted which caused a change (bifurcation) from limit cycle periodic breathing to stable breathing. Changes in lung volume were predicted to form a bifurcation during CHF–CSA where stability and instability can involve a lung volume change as small as 0.1 l. CSA therapy based on reducing control loop gain was predicted to be relatively ineffective during stable limit cycle oscillation. The relative ratios of durations of ventilation to apnea (T _v/T _a) during periodic breathing were primarily determined by peripheral chemoreceptor dynamics during crescendo, de-crescendo, and apnea phases of CSA.     

Acute effects of paroxetine on genioglossus activity in obstructive sleep apnea

STUDY OBJECTIVE: To determine the acute effects of paroxetine on genioglossus activity during NREM sleep. DESIGN: A single dose of Paroxetine (40 mg) or placebo was administered four hours before bedtime on nights separated by one week in a double blind randomized crossover manner. The moving time average of genioglossus muscle activity (EMGgg) expressed as a percentage of maximum was measured using a mouthpiece electrode customized for each subject. The peak inspiratory and tonic values of EMGgg and the corresponding esophageal pressure deflections (DP) during the last three occluded breaths of obstructive apneas during NREM sleep were analyzed. SETTING: NA. PARTICIPANTS: 8 adult men with severe obstructive sleep apnea (OSA). INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Paroxetine increased the peak inspiratory EMGgg (29.8+/-2.4 (SE) versus 24.4+/-2.7 % max, p<0.05) and peak EMGgg/DP ratio (0.78+/-0.12 versus 0.65+/-0.11 % max/cm H2O, p<0.01) but not the tonic EMGgg (11.6+/-0.9 versus 9.8+/-0.7 % max) nor the DP (39.4+/-2.2 versus 38.2+/-2.8 cm H2O). Linear regression analysis of the peak inspiratory EMGgg versus DP relationship showed that paroxetine increased the slope (0.62+/-0.11 versus 0.49+/-0.09 % max/cm H2O, p<0.01). However, the apnea + hypopnea index (paroxetine: 75.2+/-5.5 versus placebo: 73.7+/-6.9 events/hour) did not differ. CONCLUSIONS: Paroxetine augmented peak inspiratory genioglossus activity during NREM sleep but this effect was not sufficient to decrease the frequency of obstructive apnea in this group with severe OSA.     

Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration

INTRODUCTION: The influence of sleeping position on obstructive sleep apnea severity is well established. However, in central sleep apnea with Cheyne Stokes respiration (CSA-CSR) in which respiratory-control instability plays a major pathophysiologic role, the effect of position is less clear. STUDY OBJECTIVES: To examine the influence of position on CSA-CSR severity as well as central and mixed apnea frequency. METHODS: Polysomnograms with digitized video surveillance of 20 consecutive patients with heart failure and CSA-CSR were analyzed for total apnea-hypopnea index, mean event duration, and mean oxygen desaturation according to sleep stage and position. Position effects on mixed and central apnea index, mean apnea duration, and mean desaturation were also examined in non-rapid eye movement sleep. RESULTS: Data are presented as mean +/- SEM unless otherwise indicated. Group age was 59.9 +/- 2.3 years, and total apnea-hypopnea index was 26.4 +/- 3.0 events per hour. Compared with supine position, lateral position reduced the apnea-hypopnea index in all sleep stages (Stage 1, 54.7 +/- 4.2 events per hour vs 27.2 +/- 4.1 events per hour [p < .001]; Stage 2, 43.3 +/- 6.1 events per hour vs 14.4 +/- 3.6 events per hour [p < .001]; slow-wave sleep, 15.9 +/- 6.4 events per hour vs 5.4 +/- 2.9 events per hour [p < .01]; rapid eye movement sleep, 38.0 +/- 7.3 events per hour vs 11.0 +/- 3.0 events per hour [p < .001]). Lateral position attenuated apnea and hypopnea associated desaturation (supine 4.7% +/- 0.3%, lateral 3.0% +/- 0.4%; p < .001) with no difference in event duration (supine 25.7 +/- 2.8 seconds, lateral 26.9 +/- 3.4 seconds; p = .921). Mixed apneas were longer than central (29.1 +/- 2.1 seconds and 19.3 +/- 1.1 seconds; p < .001) and produced greater desaturation (6.1% +/- 0.5% and 4.5% +/- 0.5%, p = .003). Lateral position decreased desaturation independent of apnea type (supine 5.4% +/- 0.5%, lateral 3.9% < or = 0.4%; p = .003). CONCLUSIONS: Lateral position attenuates severity of CSA-CSR. This effect is independent of postural effects on the upper airway and is likely to be due to changes in pulmonary oxygen stores. Further studies are required to investigate mechanisms involved.     

Association between atrial fibrillation and central sleep apnea

BACKGROUND: We previously described an association between atrial fibrillation and central sleep apnea in a group of patients with congestive heart failure. We hypothesized that the prevalence of atrial fibrillation might also be increased in patients with central sleep apnea in the absence of other cardiac disease. METHODS AND RESULTS: We compared the prevalence of atrial fibrillation in a series of 60 consecutive patients with idiopathic central sleep apnea (apnea-hypopnea index > 10 events per hour, > 50% central events) with that in 60 patients with obstructive sleep apnea (apnea-hypopnea index > 10, > 50% obstructive events) and 60 patients without sleep apnea (apnea-hypopnea index < 10), matched for age, sex, and body mass index. Subjects with a history of congestive heart failure, coronary artery disease, or stroke were excluded from the study. The prevalence of atrial fibrillation among patients with idiopathic central sleep apnea was found to be significantly higher than the prevalence among patients with obstructive sleep apnea or no sleep apnea (27%, 1.7%, and 3.3%, respectively, P < .001). However, hypertension was most common and oxygen desaturation most extreme among patients with obstructive sleep apnea. CONCLUSIONS: We conclude that there is a markedly increased prevalence of atrial fibrillation among patients with idiopathic central sleep apnea in the absence of congestive heart failure. Moreover, the high prevalence of atrial fibrillation among patients with idiopathic central sleep apnea is not explainable by the presence of hypertension or nocturnal oxygen desaturation, since both of these were more strongly associated with obstructive sleep apnea.     

Schlafbezogene Atmungsstörungen und zerebrovaskuläre Erkrankungen

Sleep-related breathing disorders comprise obstructive sleep apnea (OSA), central sleep apnea (CSA), Cheyne–Stokes respiration (CSR), and central alveolar hypoventilation. OSA is significantly associated with known cardiovascular risk factors, e.g., arterial hypertension, atrial fibrillation, and carotid atheromatosis. In addition, OSA has been shown to independently increase stroke risk. Thus, OSA is a direct and indirect risk factor of ischemic stroke, and early diagnosis and treatment of OSA may be crucial for stroke prevention. Acute ischemic stroke may cause any type of sleep-related breathing disorder in an affected patient. Nocturnal breathing abnormalities may be present transiently or persist for a longer period of time, affecting both neurological outcome and the risk of recurrent stroke. Sleep-disordered breathing is highly prevalent in patients with large supratentorial or bihemispheric infarctions, brainstem and cerebellar infarctions. It is associated with worse prognosis, increased disability, and higher mortality. Recently, several interventional studies showed that early implementation of continuous positive airway pressure (CPAP) treatment overnight is feasible and significantly improves neurological outcome in patients with ischemic stroke even if overall mortality may not be significantly reduced.     

Arterial stiffness increases during obstructive sleep apneas

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.     

Effects of nasal O2 on sleep-related disordered breathing in ambulatory patients with stable heart failure

OBJECTIVE: The purpose of this study was 1) to determine the effects of nasal O2 on periodic breathing, arterial oxyhemoglobin desaturation and nocturnal ventricular arrhythmias in patients with heart failure and 2) determine the characteristics of patients whose periodic breathing will be reversed by O2 administration; our hypothesis was that patients with more severe periodic breathing and desaturation, will respond more favorably to oxygen. DESIGN: Prospective study. SETTING: Referral sleep laboratory of a Department of Veterans Affairs Medical Center. PARTICIPANTS: 36 ambulatory male patients with heart failure whose initial polysomnograms showed periodic breathing with fifteen or more episodes of apnea (A) and hypopnea (H) per hour (AH index, AHI) were treated with nasal O2 during the subsequent full night polysomnography. INTERVENTIONS: Oxygen. MEASUREMENTS AND RESULTS: Arterial blood gases and hydrogen ion concentrations were measured, and cardiac radionuclide ventriculography, Holter monitoring, and polysomnography were done. The studies were scored blindly. Treatment with O2 resulted in a significant reduction in AHI (49+/-19 vs 29+/-29, means+/-SD), central apnea index (28+/-23 vs 13+/-18 per hour), and the percent of total sleep time below an arterial oxyhemoglobin saturation of 90% (23+/-21% vs 0.8+/-2.3%). In spite of virtual normalization of saturation with O2 therapy, the number of ventricular arrhythmias during sleep did not change significantly. In 39% of the patients (14 out of 36), O2 therapy resulted in reversal of central sleep apnea (defined by a reduction in AHI to less than 15/hr). In this group, the AHI decreased by 78% which was significantly (p=0.0001) more than improved (22%) in AHI of the remaining patients (n=22). The main differences between baseline characteristics of the two groups was a significantly higher mean PaCO2 in patients who did respond fully to O2 (39.3+/-5.4 vs 36.1+/-4.2 mm Hg, p=0.03). In both groups, however, O2 administration resulted in significant and similar improvement in arterial oxyhemoglobin saturation (saturation <90%, percent total sleep time 0.1+/-0.3% vs 1+/-3%). CONCLUSION: In patients with stable heart failure, administration of nasal O2 significantly improves periodic breathing and virtually eliminates clinically significant arterial oxyhemoglobin desaturation. The beneficial effects of O2, however, may be modulated by the level of arterial PCO2. Acute O2 therapy has important benefits on sleep apnea and nocturnal arterial oxyhemoglobin desaturation in heart failure patients. Long term benefits of O2 therapy in heart failure and sleep apnea need to be determined.