Humans ; Sleep Apnea, Obstructive ; etiology

Atrial Fibrillation ; etiology ; Humans ; Recurrence ; Sleep Apnea, Obstructive ; complications

Humans ; Male ; Middle Aged ; Polycythemia ; etiology ; Sleep Apnea, Obstructive ; complications

Humans ; Respiratory System ; anatomy & histology ; Sleep Apnea, Obstructive ; etiology ; therapy

The obstruction localization methods of OSAHS patients were reviewed in this article. And the advantages and disadvantages of each method were analyzed. Clinical doctors need to choose suitable method according to patients situation.
Humans ; Practice Patterns, Physicians' ; Sleep Apnea, Obstructive ; diagnosis ; etiology

Obstructive sleep apnea syndrome (OSAS) is endangering human health seriously now. We had reviewed some typical animal model which had at least one OSAS character of intermittent hypoxia and/or hypercapnia, upper airway obstruction and sleep structure disorder. However, all of these models could not simulate clinical and pathological features of OSAS completely. Establishing a suitable animal model to study OSAS and related diseases is very important.
Airway Obstruction ; etiology ; Animals ; Disease Models, Animal ; Humans ; Hypercapnia ; etiology ; Hypoxia ; etiology ; Sleep Apnea, Obstructive ; complications

Obesity, with an increasing prevalence,has become one of the most common metabolic diseases. Obesity is associated with many respiratory diseases, especially sleep-related breathing disorders including obstructive sleep apnea-hypopnea syndrome, obesity hypoventilation syndrome, and overlap syndrome. This article reviews the association between obesity and these sleep-related breathing disorders.
Humans ; Obesity ; complications ; Obesity Hypoventilation Syndrome ; etiology ; Pulmonary Disease, Chronic Obstructive ; complications ; Sleep Apnea, Obstructive ; etiology

Obstructive sleep apnea (OSA), which is the most common sleep-related breathing disorder, is characterized as frequent upper airway collapse and obstruction. It is a treatable disorder but if left untreated is associated with complications in several organ systems. The health risk to OSA patients shows a strong association with acute cardiovascular events, and with chronic conditions. To the central nervous system, OSA causes behavioral and neuropsychologic deficits including daytime sleepiness, depression, impaired memory, mood disorders, cognition deficiencies, language comprehension and expression deficiencies, all of which are compatible with impaired hippocampal function. Furthermore, there exists a significant correlation between disease severity and cognitive deficits in OSA. Children with severe OSA have significantly lower intelligence quotient (IQ) and executive control functions compared to normal children matched for age, gender and ethnicity. This corroborates the findings of several pediatric studies of cognition in childhood OSA, where deficits are reported in general intelligence and some measures of executive function. In studies of OSA, it is difficult to differentiate the effects of its two main pathologic traits, intermittent hypoxia (IH) and sleep fragmentation. Many OSA studies, utilize IH as the only exposure factor in OSA studies. These approaches simplify research process and attain most of the academic goals. IH, continuous hypoxia and intermittent continuous hypoxia can all result in decreases in arterial O2. There are striking differences to them in the response of physiological systems. There are multiple studies showing that IH treatment in a rodent model of OSA can impair performance of standard water maze tests associated with deficits in spatial learning and memory which most likely are hippocampal-dependent. Cellular damage to the hippocampal cornuammonis 1 (CA1) region likely contributes to neuropsychological impairment among OSA patients, since neural circuits in the hippocampus are important in learning and memory. In this article, studies of hippocampal impairments from IH are reviewed for elucidating the mechanisms and relationships between hippocampal impairments and IH of OSA.
Hippocampus ; physiopathology ; Humans ; Hypoxia ; etiology ; physiopathology ; Sleep Apnea, Obstructive ; etiology ; physiopathology

Airway Obstruction ; complications ; surgery ; Continuous Positive Airway Pressure ; Humans ; Infant ; Male ; Sleep Apnea Syndromes ; etiology ; therapy ; Sleep Apnea, Obstructive ; etiology ; therapy ; Treatment Outcome

OBJECTIVETo review the current evidence about the prevalence of obstructive sleep apnea in patients with Marfan's syndrome, and discuss some proposed potential mechanisms for this relationship.

DATA SOURCESThe data in this review were mainly from Medline and PubMed articles published in English from 1990 to 2013. The search term was "Marfan's syndrome and sleep apnea".

STUDY SELECTIONClinical evidence about the epidemiology of obstructive sleep apnea in patients with Marfan's syndrome; the mechanism that causes obstructive sleep apnea; interventional therapy for patients with Marfan's syndrome, and coexisting obstructive sleep apnea.

RESULTSA high prevalence of obstructive sleep apnea exists in patients with Marfan's syndrome. The potential reasons are craniofacial abnormalities and lax upper airway muscles, which lead to high nasal airway resistance and upper airway collapse. Obstructive sleep apnea mechanically deteriorates aortic dilatation and accelerates progression of aortic aneurysms. The condition is reversible and rapid maxillary expansion and adequate continuous positive airway pressure therapy are possible effective therapies to delay the expansion of aortic diameter in patients with Marfan's syndrome.

CONCLUSIONSObstructive sleep apnea is strongly associated with Marfan's syndrome. Craniofacial abnormalities and lax upper airway are the main mechanisms. Untreated obstructive sleep apnea accelerates progression of aortic dissection and rupture. Effective therapies for obstructive sleep apnea could postpone the aortic dilatation in patients with Marfan's syndrome.