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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea syndrome (OSAS) is the most common organic disorder of excessive daytime somnolence. In cross-sectional studies the minimum prevalence of OSAS among adult men is about one per cent. Prevalence is highest among men aged 40-65 years. The highest figures for this age group indicate that their prevalence of clinically significant OSAS may be 8.5% or higher. Habitual snoring is the most common symptom of OSAS (70-95%). The most significant risk factor for OSAS is obesity, especially upper body obesity. Other risk factors for snoring, and for OSAS, are male gender, age between 40 and 65 years, cigarette smoking, use of alcohol, and poor physical fitness. Upper airway obstruction with snoring or sleep apnea are commonly seen in children of all ages. Snoring is very common among infants and children with Pierre Robin syndrome and among infants with nasal obstruction. Snoring and obstructive sleep apnea are also very common in men with acromegaly. Many other syndromes or diseases exist in which the upper airway is narrowed. Prevalence of snoring and sleep apnea is increased in all such situations. It has been suggested that sleep apnea may be one mechanism contributing to sleep-related mortality. The prevalence of every night snoring seems to decrease after the age of 65. However, more than 25% of persons over 65 have more than five apneas per hour of sleep. It remains to be seen whether this finding has clinical significance. Partial upper airway obstruction, even without apneas, may influence pulmonary arterial pressure and may cause daytime sleepiness and some health consequences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of obstructive sleep apnea syndrome. 147 Aug

The prevalence and mechanisms of daytime pulmonary hypertension were examined in 24 cases of obstructive sleep apnea syndrome (OSAS). All patients were free from chronic lung disease. They underwent pulmonary function tests and blood gas analysis in the sitting and supine position, hypercapnic ventilatory response test, exercise test and right heart catheterization. Elevation of mean pulmonary arterial pressure (m-PAP) above 20 mmHg was observed in 5 out of 24 cases (20.8%). The group with pulmonary hypertension (PG+: m-PAP = 22.2 +/- 2.7 mmHg) showed marked obesity (p < 0.001), significant decrease of supine FRC/TLC (p < 0.05), increase of supine CC/FRC (p < 0.01), decrease of supine PaO2 (p < 0.02) and desaturation during exercise (p < 0.05) in comparison with the group without pulmonary hypertension (PH-: 13.9 +/- 3.1 mmHg). m-PAP was positively correlated with %IBW and desaturation during exercise (p < 0.01, p < 0.02) and negatively correlated with supine PaO2 (p < 0.01). Various changes in pulmonary function and pulmonary hemodynamics due to obesity seem to lead to daytime pulmonary hypertension of OSAS.
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PMID:[Pulmonary function and pulmonary hemodynamics in obstructive sleep apnea syndrome]. 148 30

Symptoms and signs in 12 patients with severe obstructive sleep apnea (OSA) syndrome have been presented. The most common symptoms were snoring , increased motor activity during sleep and excessive daytime somnolence. The factors predisposing to OSA syndrome were obesity and anatomic abnormalities of the upper airway structure. In some cases the signs of OSA syndrome included hypertension, right heart failure, chronic alveolar hypoventilation and polycythemia. Polysomnography showed sleep fragmentation and the prevalence of light sleep stages. Obstructive sleep apneas repeated 73 +/- 23 times per hour of sleep. The mean apnea duration was 19 +/- 8 s. The mean arterial oxygen saturation during apnea was 72 +/- 14%.
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PMID:[Diagnosis of obstructive sleep apnea syndrome]. 148 56

A variety of imaging techniques have been used to assess upper airway size and function in patients with OSA. Each technique has certain advantages and limitations. Many of the imaging techniques study awake and upright patients, whereas OSA typically occurs while the patient is asleep in the supine position. Upper airway imaging may identify specific upper airway abnormalities that cause OSA. Furthermore, the majority of patients with OSA have a narrow and more collapsible airway in the velopharynx. Upper airway occlusion during sleep usually starts in the velopharynx and extends caudally. Obesity results in both extrinsic upper airway narrowing and soft tissue enlargement. Upper airway edema may occur secondary to OSA and subsequently exacerbate the OSA by causing further upper airway narrowing. Upper airway imaging provides some insights into the mechanism of action of certain treatments and is increasingly used to help direct treatment. Weight loss reduces upper airway collapsibility. Nasal CPAP increases upper airway size and reduces upper airway edema. UPPP enlarges the oropharynx and reduces upper airway collapsibility. Patients with a narrow upper airway, particularly relative to tongue size, have a good response to UPPP.
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PMID:Upper airway imaging in relation to obstructive sleep apnea. 152 9

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

In order to assess the complications of sleep apnea, we have reviewed a data base of 619 consecutive admissions to a university sleep disorders center. Although patients with obstructive sleep apnea (OSA) described more subjective sleepiness than patients with central sleep apnea (CSA) or primary snoring (PS), the multiple sleep latency test (MSLT) indicated similar levels of physiologic sleepiness in the two apneic groups, which was greater than among those with PS. There was no significant relationship between individual subjective estimates of habitual sleepiness and the MSLT values. Among the OSA patients the mean minimum arterial oxygen desaturation during REM sleep accounted for 65 percent of the variance of the mean sleep latency on the MSLT, with an additional, smaller, contribution of the disordered breathing rate per hour. Subjective reports of sleepiness were associated with sleep efficiency and the number of disordered breathing events in NREM sleep. Patients with OSA or CSA had similar diastolic blood pressures and frequencies of history of treatment for hypertension, which were significantly higher in OSA than in the PS group. In the OSA group the absolute minimum arterial oxygen desaturation during NREM sleep was the most significant contributor to waking diastolic blood pressure, with an additional small contribution by weight. A history of treatment for hypertension was most strongly associated with weight, without significant additional contributions by measures of disordered breathing events or oxygen desaturation; however, weight was highly intercorrelated with measures of the apnea/hypopnea index and minimum arterial oxygen desaturation. In summary, these data support recent findings which show a close relation of obesity to a history of hypertension in OSA, and extend to this group a previous observation that in regular heavy snorers, there may be a disparity between levels of physiologic and subjective sleepiness.
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PMID:Sleepiness and hypertension in obstructive sleep apnea. 155 54

A sample of 84 adult male patients with obstructive sleep apnea (OSA) were classified by a cluster analysis on the basis of apnea index (AI) and body mass index (BMI). Demographic, cephalometric, tongue, soft palate, and upper airway-size data were evaluated for the two subgroups of OSA patients and for 18 control subjects. One OSA group consisted of 43 patients with a high AI and low BMI ratio, the other group was comprised of 41 patients with a low AI and high BMI ratio. The patients with a high AI and low BMI ratio had retruded mandibles with high mandibular plane angles and proclined lower incisors. The patients with a low AI and high BMI ratio had inferior hyoid bones and large soft palates. A multiple regression analysis was performed between AI (the dependent variable) and the other variables (independent variables) for each of the subgroups. In the patients with a high AI and low BMI ratio, a high AI was related to a large skeletal anteroposterior discrepancy, a steep mandibular plane, and an inferoanterior position of the hyoid bone. In the patients with a low AI and high BMI ratio, a high AI was related to a large tongue and a small upper airway. In both groups, BMI was the major contributor to AI. In conclusion, these two groups may represent distinct subgroups of OSA patients and provide some insight into the contribution of obesity to the pathogenesis of OSA. The patients with a high AI and low BMI ratio have a skeletal mismatch, whereas the patients with a low AI and high BMI have atypical soft tissue structures.
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PMID:Obstructive sleep apnea subtypes by cluster analysis. 159 93

A retrospective study was conducted to determine which types of children might have polysomnographic findings that are most compatible with obstructive sleep apnea (OSA). The charts of 93 patients who were aged 18 months to 12 years were examined. All 93 patients had symptoms that were initially suggestive of OSA, and they underwent polysomnography. The types of presenting symptoms and associated illnesses were noted. Physical findings, including height, weight, and tonsil size, were examined. Of 93 patients with symptoms that were suggestive of OSA, 34 met sleep study criteria for OSA. In 44 patients, OSA was not demonstrated, and 15 patients had other results. On the basis of age, sex, and symptoms, no significant differences could be found between the group with OSA and the group with normal polysomnographic findings. Cor pulmonale, tonsil hypertrophy, and failure to thrive were associated with OSA. Surprisingly, obesity was not significantly associated with OSA.
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PMID:Polysomnographic and clinical findings in children with obstructive sleep apnea. 162 96

Increasing evidence suggests that snoring and sleep apnea are associated with cerebrovascular diseases. Several other factors may be involved in this association because many established or potential risk factors for stroke are related to snoring and sleep apnea. These include arterial hypertension, coronary heart disease, age, obesity, smoking, and alcohol consumption. Recent epidemiologic and clinical studies indicate, however, that snoring can increase the risk of stroke independently of these confounding factors. Accumulating epidemiologic evidence of long-term harmful effects of the obstructive sleep apnea syndrome appears to be related to increasing vascular morbidity and mortality. Potential mediators among snoring, obstructive sleep apneas, and stroke include cardiac arrhythmias and other hemodynamic disturbances, increased levels of catecholamines, and disturbances in cerebral blood flow caused by sleep apneas, as well as hypoxemic periods that may potentiate atherosclerosis.
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PMID:Snoring, sleep apnea syndrome, and stroke. 163 Jun 43


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