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

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

The obstructive sleep apnoea-hypopnoea syndrome (OSAHS) is a sleep-related breathing disorder characterised by repetitive pharyngeal collapse. OSAHS is associated with a reduced quality of life. A high OSAHS prevalence has been reported in patients treated for head and neck cancer (HNC). The aim of the present study was to identify the prevalence of OSAHS within a Dutch population of patients treated for HNC. Consecutive HNC patients with a follow-up of 6 months to 5 years after treatment of an oral or oropharynx carcinoma were eligible for inclusion. Two questionnaires were used to assess the presence of OSAHS-related complaints. Subsequently, polysomnography was used in patients with OSAHS-related complaints to confirm the diagnosis of OSAHS. Four out of 33 included patients were diagnosed with OSAHS, yielding a prevalence of 12%. Since recognition and treatment of OSAHS might play an important role in improving quality of life of HNC patients, we suggest screening all patients with an oral or oropharynx carcinoma for the presence of OSAHS-related complaints prior to and following HNC treatment.
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PMID:Prevalence of obstructive sleep apnoea following head and neck cancer treatment: a cross-sectional study. 1615 Jun 32

Sleep is a complex behavioral state that occupies one-third of the human life span. Although viewed as a passive condition, sleep is a highly active and dynamic process. The sleep-related decrease in muscle tone is associated with an increase in resistance to airflow through the upper airway. Partial or complete collapse of the airway during sleep can lead to the occurrence of apneas and hypopneas during sleep that define the syndrome of sleep apnea. Sleep apnea has become pervasive in Western society, affecting approximately 5% of adults in industrialized countries. Given the pandemic of obesity, the prevalence of Type 2 diabetes mellitus and metabolic syndrome has also increased dramatically over the last decade. Although the role of sleep apnea in cardiovascular disease is uncertain, there is a growing body of literature that implicates sleep apnea in the pathogenesis of altered glucose metabolism. Intermittent hypoxemia and sleep fragmentation in sleep apnea can trigger a cascade of pathophysiological events, including autonomic activation, alterations in neuroendocrine function, and release of potent proinflammatory mediators such as tumor necrosis factor-alpha and interleukin-6. Epidemiologic and experimental evidence linking sleep apnea and disorders of glucose metabolism is reviewed and discussed here. Although the cause-and-effect relationship remains to be determined, the available data suggest that sleep apnea is independently associated with altered glucose metabolism and may predispose to the eventual development of Type 2 diabetes mellitus.
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PMID:Disorders of glucose metabolism in sleep apnea. 1622 61

Obstructive sleep apnea syndrome is characterized by recurrent total or partial upper airway collapse during sleep. Although this disease affects more than 5% of general population, it remains largely undiagnosed. It is associated with an increase in cardiovascular risk and with a decrease in sustained attention that may cause automobile accidents or occupational injuries. Several simplified diagnostic tools (polysomnography) now allow easier diagnosis in a sleep laboratory or on an outpatient basis. Nasal continuous positive airway pressure remains the reference treatment, acting as a pneumatic splint that maintains airway patency. CPAP is effective in reducing daytime somnolence and controlling cardiovascular risk. Prosthetic management is an alternative to CPAP in cases of moderate sleep apnea with or without retrognathism in normal-weight patients. The effectiveness of surgery has not been proven, and it is indicated only in exceptional cases.
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PMID:[Obstructive sleep apnea syndrome]. 1630 67

Sleep disordered breathing is a common condition within the general community. Mostly this is represented by obstructive sleep apnoea (OSA), a condition characterized by repetitive occlusions of the upper airway due to retro-positioning of the tongue and pharyngeal collapse during sleep. This article covers the key evidence relating OSA to both causation and progression of congestive heart failure and cardiovascular disease including hypertension. The results of recent studies are summarized, and the authors conclude that whilst progress has been made, there remain many gaps in our knowledge in relation to the contribution to the burden of cardiac disease produced by associated conditions such as OSA. Larger studies with important primary endpoints will be required to demonstrate the merit of screening and treating this disorder.
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PMID:Obstructive sleep apnoea, congestive heart failure and cardiovascular disease. 1635 81

Obstructive sleep apnea is a common disorder characterized by repetitive collapse of the pharyngeal airway during sleep. The disorder results primarily from an anatomically small upper airway in conjunction with pharyngeal dilator muscles that can compensate for the anatomic deficiency awake, but not asleep. Ventilatory control instability and a low arousal threshold may contribute to the disorder as well. The consequences of sleep apnea fall into two domains: (1) neurocognitive dysfunction (sleepiness and decreased quality of life) resulting from sleep fragmentation and (2) cardiovascular disease (hypertension, stroke, myocardial infarction, and heart failure) likely resulting from the intermittent hypoxia. The disorder is generally diagnosed in the sleep laboratory over the course of a night, although alternative approaches in the home are also utilized. A number of treatment options are available. Continuous positive airway pressure remains the most consistently effective approach, although oral appliances (generally mandibular-advancing devices) and a number of surgical procedures have some demonstrated efficacy. Thus, therapy must be individualized to the patient's desires and the severity of the apnea.
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PMID:Sleep apnea. 1649 60

A number of predisposing factors (obesity, nasal obstruction, adenoidal hypertrophy, macroglossia, etc) have been related to obstructive sleep apnea syndrome (OSAS). In addition hypothyroidism and large goitres have been reported to be associated to OSAS, but this association has not been adequately studied. We describe an obese patient with euthyroid goitre associated with OSAS. The patient showed a body mass index (BMI) of 47 and a large neck with a circumference of 60 cm. The flow-volume curve demonstrated an expiratory plateau suggesting an intrathoracic upper airway obstruction. Arterial blood gas analysis results were: pH 7.39; PCO2 54.2 mmHg; P O2 47 mmHg. Nocturnal polisomnography showed an apnea/hypopnea index (AHI) of 31 episodes/hour. Upper airway collapse was overcome by a nasal continuous positive airway pressure (nCPAP) of 14 cmH2O. Weight loss obtained by a hypocaloric diet was not accompanied by any OSAS improvement. After thyroidectomy, a nCPAP of 4 cmH2O was sufficient to prevent upper airway closure. Discontinuation of nCPAP treatment for 4 consecutive nights did not determine worsening of sleep apnea symptoms, nor a worsening of overnight oxymetry. A new polysomnography carried out after 4 nights off nCPAP showed an AHI of 33 episodes/hour. OSAS should be suspected in patients with large goitres. Decisions regarding discontinuation of nCPAP treatment after thyroidectomy should be based on polisomnographic results.
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PMID:Euthyroid goitre and sleep apnea. 1670 Jan 96

Obstructive sleep apnea is caused by pharyngeal occlusion due to alterations in upper airway mechanical properties and/or disturbances in neuromuscular control. The objective of the study was to determine the relative contribution of mechanical loads and dynamic neuromuscular responses to pharyngeal collapse during sleep. Sixteen obstructive sleep apnea patients and sixteen normal subjects were matched on age, sex, and body mass index. Pharyngeal collapsibility, defined by the critical pressure, was measured during sleep. The critical pressure was partitioned between its passive mechanical properties (passive critical pressure) and active dynamic responses to upper airway obstruction (active critical pressure). Compared with normal subjects, sleep apnea patients demonstrated elevated mechanical loads as demonstrated by higher passive critical pressures [-0.05 (SD 2.4) vs. -4.5 cmH2O (SD 3.0), P = 0.0003]. Dynamic responses were depressed in sleep apnea patients, as suggested by failure to lower their active critical pressures [-1.6 (SD 3.5) vs. -11.1 cmH2O (SD 5.3), P < 0.0001] in response to upper airway obstruction. Moreover, elevated mechanical loads placed some normal individuals at risk for sleep apnea. In this subset, dynamic responses to upper airway obstruction compensated for mechanical loads and maintained airway patency by lowering the active critical pressure. The present study suggests that increased mechanical loads and blunted neuromuscular responses are both required for the development of obstructive sleep apnea.
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PMID:Neuromechanical control of upper airway patency during sleep. 1708 60

Although neuroplasticity is an important property of the respiratory motor control system, its existence has been appreciated only in recent years and, as a result, its functional significance is not completely understood. The most frequently studied models of respiratory plasticity is respiratory long-term facilitation (LTF) following acute intermittent hypoxia and enhanced LTF following chronic intermittent hypoxia. Since intermittent hypoxia is a prominent feature of sleep-disordered breathing, LTF and/or enhanced LTF may compensate for factors that predispose to sleep-disordered breathing, particularly during obstructive sleep apnoea (OSA). Long-term facilitation has been studied most frequently in rats, and exhibits interesting properties consistent with a role in stabilizing breathing during sleep. Specifically, LTF: (1) is prominent in upper airway respiratory motor activity, suggesting that it stabilizes upper airways and maintains airway patency; (2) is most prominent during sleep in unanaesthetized rats; and (3) exhibits sexual dimorphism (greatest in young male and middle-aged female rats; smallest in middle-aged male and young female rats). Although these features are consistent with the hypothesis that upper airway LTF minimizes the prevalence of OSA in humans, there is little direct evidence for such an effect. Here we review advances in our understanding of LTF and its underlying mechanisms and present evidence concerning a potential role for LTF in maintaining upper airway patency, stabilizing breathing and preventing OSA in humans. Regardless of the relationship between LTF and OSA, a detailed understanding of cellular and synaptic mechanisms that underlie LTF may guide the development of new drugs to regulate upper airway tone, thereby offsetting the tendency for upper airway collapse characteristic of heavy snoring and OSA.
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PMID:Is there a link between intermittent hypoxia-induced respiratory plasticity and obstructive sleep apnoea? 1709 64

Obstructive sleep apnea (OSA) affects a large portion of the population and is associated with repeated airway collapse leading to chronic intermittent hypoxia, exaggerated swings in intrathoracic pressure and post apneic arousal. OSA is associated with heightened sympathoadrenal tone and is a risk factor for cardiovascular mortality and morbidity. In addition to well-known mechanical and autonomic effects, OSA appears to be associated with systemic inflammation. This could provide one mechanism leading to cardiovascular disease (CVD). A central factor in the inflammatory cascade is nuclear factor kappa B (NF-kappaB), which is involved in the transcription of numerous genes involved in the inflammatory cascade. The object of this article is to review recent literature on some of the aspects of OSA related to a proinflammatory state and the possible role of NF-kappaB as one mechanism providing a link between sleep apnea and CVD.
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PMID:Obstructive sleep apnea, cardiovascular disease, and inflammation--is NF-kappaB the key? 1738 Mar 55


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