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Central sleep apnea (CSA) comprises a variety of breathing patterns and clinical entities. They can be classified into 2 categories based on the partial pressure of carbon dioxide in the arterial blood. Nonhypercapnic CSA is usually characterized by a periodic breathing pattern, while hypercapnic CSA is based on hypoventilation. The latter CSA form is associated with central nervous, neuromuscular, and rib cage disorders as well as obesity and certain medication or substance intake. In contrast, nonhypercapnic CSA is typically accompanied by an overshoot of the ventilation and often associated with heart failure, cerebrovascular diseases, and stay in high altitude. CSA and hypoventilation syndromes are often considered separately, but pathophysiological aspects frequently overlap. An integrative approach helps to recognize underlying pathophysiological mechanisms and to choose adequate therapeutic strategies. Research in the last decades improved our insights; nevertheless, diagnostic tools are not always appropriately chosen to perform comprehensive sleep studies. This supports misinterpretation and misclassification of sleep disordered breathing. The purpose of this article is to highlight unresolved problems, raise awareness for different pathophysiological components and to discuss the evidence for targeted therapeutic strategies. [ABSTRACT FROM AUTHOR]

Background: Obstructive sleep apnea (OSA) is a common disorder resulting in a myriad of adverse vascular risks, including altered inflammatory/anti-inflammatory adipokine balance. Recent studies are yet to agree on how this balance responds to the OSA severity. As it is customary in these studies to obtain a single blood sample in participants after completion of the nocturnal polysomnogram (PSG), we hypothesized that these adipokines' early ultradian pulsatility might contribute to the reported contradictory results. Methods: Fasting serum leptin and adiponectin were measured every 15 minutes for one hour in the morning after the diagnostic PSG for 13 adults recruited consecutively from the Salem VAMC Sleep Clinic between September 2006 and October 2007. Results: No differences in the timed paired samples of leptin (P=0.30) and adiponectin (P=0.28) were found in OSA participants (mean apnea-hypopnea index 21.1). Conclusion: Customary protocol of obtaining a single blood sample for leptin and adiponectin after nocturnal PSG seems appropriate. [ABSTRACT FROM AUTHOR]

The inflammatory state caused by obesity increases the level of adipokines, such as leptin, with a direct impact on the central respiratory regulation. The present study addresses this problem by evaluation of the association of sleep apnea diagnosis in relation to body fat measured by dual-energy X-ray absorptiometry (DXA), anthropometric parameters and biochemical variables. All patients carried out overnight polysomnography, anthropometric evaluations [Body Mass Index (BMI), neck and waist circumference], body composition analyzed by DXA and blood sample collection (lipid profile, fasting glycemia, insulin, glycated hemoglobin, C-reactive protein and serum leptin levels). Obstructive sleep apnea-hypopnea syndrome (OSAHS) was defined by the apnea-hypopnea index (AHI) from the overnight polysomnography. According to the AHI, the women were divided into two groups: with and without apnea. Twenty-seven of them had OSAHS (AHI = 22.04 ± 17.55). The main results are the following: (a) BMI was not capable of predicting OSAHS in this study ( p = 0.204); (b) for each 1 % increase in TBF %, the probability of having sleep apnea increased by 12.8 %; (c) comparing all variables (anthropometrics, DXA and blood sample), serum leptin was the only variable with a significant difference between the groups ( p = 0.0257). The results reinforce the role of total body fat and leptin in the etiology of OSAHS and the need to include the evaluation of corporal composition measures by DXA in studies of sleep apnea. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. Increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease--related mortality, but it still largely unclear whether this association is causative or simply speculative and epidemiological. Basically, reliable clinical evidence supports the hypothesis that OSAS might be associated with essential and resistant hypertension, as well as with an incremental risk of developing stroke, cardiac rhythm perturbations (e.g., atrial fibrillation, bradyarrhythmias, supraventricular and ventricular arrhythmias), coronary artery disease, acute myocardial infarction, and heart failure. Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes, and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intrathoracic pressure, micro-arousal, sympathetic hyperactivity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulability, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders. In this article we discuss the different aspects of the relationship between OSAS and pathogenically different conditions such as systemic hypertension, coronary artery disease, stroke, metabolic abnormalities, arrhythmias, and heart failure, and we also discuss the kaleidoscope of phenomena implicated in the pathogenesis of this challenging disease. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) has long been recognized as a disorder characterized by snoring and frequent cessations of breathing resulting in fragmentation of sleep, which eventually leads to cumulative sleep debt in affected patients. Until two decades ago, snoring and apneas drew attention mainly as a social curiosity and sleep apnea was not thought of as a serious disorder with multisystem involvement. Impairment of quality of work and high incidence of motor vehicle accidents associated with OSA were recognized toward the end of the last century. Since the turn of this millennium physicians have become increasingly aware of the various cardiovascular complications, metabolic disturbances, and neuropsychologic deficits. It has become very clear in the last decade that patients with OSA have a high recurrence of atrial fibrillation after elective cardioversion if their sleep apnea is not treated with continuous positive airway pressure (CPAP). Poor control of diabetes mellitus and resistant hypertension in the setting of OSA has also been recognized and significant progress in our understanding in this area has been accomplished. Unless physicians include sleep in their system review, many cases will go undiagnosed, which will eventually result in cardiovascular complications. Patients are also not readily forthcoming with the symptoms of sleep apnea, as they often assume that symptoms, such as snoring and daytime sleepiness, are not something serious to be discussed with their physician. In this review, the characteristics, the pathophysiology, and epidemiology of OSA are discussed. Furthermore, the mechanisms by which OSA affects the cardiovascular, endocrine, and metabolic functions have been explored. [ABSTRACT FROM AUTHOR]

AIM: The aim of this study was to investigate the relationship among plasma leptin, ghrelin, adiponectin, resistin levels, and obstructive sleep apnea syndrome (OSAS). METHODS: Fifty-five consecutive newly diagnosed OSAS patients and 15 age-matched nonapneic controls were enrolled in this study. After sleep study between 8:00 AM and 9:00 AM on the morning, venous blood was obtained in the fasting state to measure ghrelin and adipokines. RESULTS: Serum ghrelin levels of OSAS group were significantly (P < 0.05) higher than those of the control group. No significant difference was noted in the levels of leptin, adiponectin, and resistin in OSAS group when compared to controls. There was a significant positive correlation between ghrelin and apnea-hypopnea index (AHI) (r = 0.237, P < 0.05) or the Epworth sleepiness scale (ESS) (r = 0.28, P < 0.05). There was also a significant positive correlation between leptin and body mass index (r = 0.592, P < 0.0001). No significant correlation was observed between leptin, adiponectin, resistin, and any polysomnographic parameters. CONCLUSION: Our findings demonstrated that serum ghrelin levels were higher in OSAS patients than those of control group and correlated with AHI and ESS. Further studies are needed to clarify the complex relation among OSAS, obesity, adipokines, and ghrelin. [ABSTRACT FROM AUTHOR]

Obesity is becoming a major medical concern in several parts of the world, with huge economic impacts on health-care systems, resulting mainly from increased cardiovascular risks. At the same time, obesity leads to a number of sleep-disordered breathing patterns like obstructive sleep apnea and obesity hypoventilation syndrome (OHS), leading to increased morbidity and mortality with reduced quality of life. OHS is distinct from other sleep- related breathing disorders although overlap may exist. OHS patients may have obstructive sleep apnea/hypopnea with hypercapnia and sleep hypoventilation, or an isolated sleep hypoventilation. Despite its major impact on health, this disorder is under-recognized and under-diagnosed. Available management options include aggressive weight reduction, oxygen therapy and using positive airway pressure techniques. In this review, we will go over the epidemiology, pathophysiology, presentation and diagnosis and management of OHS. [ABSTRACT FROM AUTHOR]

As the prevalence of obesity increases in both the developed and the developing world, the respiratory consequences are often underappreciated. This review discusses the presentation, pathogenesis, diagnosis and management of the obstructive sleep apnoea, overlap and obesity hypoventilation syndromes. Patients with these conditions will commonly present to respiratory physicians, and recognition and effective treatment have important benefits in terms of patient quality of life and reduction in healthcare utilisation. Measures to curb the obesity epidemic are urgently required. [ABSTRACT FROM AUTHOR]

Background: Leptin levels have been reported to be higher in patients with obstructive sleep apnea (OSA) than in control subjects with matching age and body mass index (BMI). Although animal studies have shown that leptin augments hypercapnic ventilatory response (HCVR), the effect of leptin on HCVR has not been clarified in OSA. Objectives: To investigate whether leptin could augment HCVR during wakefulness in patients with OSA. Methods: Of 134 consecutive patients with OSA, 13 eucapnic and 16 hypercapnic patients with OSA, and 12 control subjects matched for sex, age, and BMI were selected. Fasting serum leptin levels were collected, and HCVR during wakefulness assessed by the slope between minute ventilation and end-tidal PCO2. Results: There was a significant positive relationship between serum leptin levels and HCVR in the group including control subjects and eucapnic patients with OSA (r = 0.42, p < 0.05). Subgroup analyses suggest that serum leptin levels and HCVR were significantly higher in eucapnic patients with OSA than in control subjects. On the other hand, hypercapnic patients had lower HCVR than eucapnic patients (p < 0.05), whereas serum leptin levels were similar between the two OSA subgroups. Conclusion: Leptin levels and HCVR are correlated as long as the eucapnic condition is maintained. We speculate that a stimulating effect of leptin on HCVR may be masked by the hypoventilation state. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article reports on studies of the causes of hypercapnia on patients with obstructive sleep apnea (OSA). A study showed that leptin deficiency may be responsible for hypercapnia in OSA particularly when it occurs with obesity and led to examinations of leptin levels in patients with OSA. Some studies showed that leptin is increased by obesity and by hypoxia.