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

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

To investigate the impact of sleep-disordered breathing events on daytime hypertension (HT) in patients with increased upper airway resistance during sleep, we studied 191 male snorers aged 49.9 +/- 0.8 years. In 116 of them, an apnea-hypopnea index (AHI) above 10--defined as the presence of obstructive sleep apnea (OSA)--was found; the other 75 subjects had an AHI lower than 10 and were classified as habitual snorers (HSN). Prevalence of HT was not different between OSA (56 of 116 = 48 percent) and HSN (33 of 75 = 44 percent) and there was also no difference in systolic, diastolic, and mean blood pressures between the two groups. Hypertensive OSA patients had higher body mass index (BMI) than normotensive OSA subjects (31.4 +/- 0.7 vs 29.4 +/- 0.6; p less than 0.05), but there was no difference in age, AHI, and nocturnal oxygenation parameters. The same was true for the HSN group, with hypertensive subjects being more obese than normotensive subjects (BMI: 30 +/- 0.8 vs 27.3 +/- 0.8; p less than 0.05), but no difference in age and polysomnographic features. Discriminant analysis with HT as the classification variable and age, BMI, AHI, mean, and lowest nocturnal oxyhemoglobin saturation as independent variables, revealed an independent influence on HT only for BMI (F-prob = 0.001). Thus, our results stand against the hypothesis of a causal relationship between sleep-disordered breathing events and daytime hypertension. We conclude that the high prevalence of HT in male snorers is more directly linked to obesity than to sleep apnea, but an independent effect of snoring per se cannot be excluded.
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PMID:Systemic hypertension in snorers with and without sleep apnea. 164 15

Individuals weighing greater than 100 kg represent a small fraction of the population and yet pose a major health risk to themselves. It is proposed that individuals be classified according to their body mass index (BMI). Class 0 individuals have a BMI of 20-25 kg/m2 and are not obese; Class I individuals have a BMI of 25-30 kg/m2 and are at low risk from their obesity; Class II individuals have a BMI of 30-35 kg/m2 and have moderate risk; Class III individuals have a BMI of 35-40 kg/m2 and have high risk associated with their obesity; Class IV individuals have a BMI of greater than 40 kg/m2 and are at very high risk for illness. Class IV is the primary group for surgical consideration. The pathophysiologic consequences of excess weight result in large part from increased food intake and/or decreased physical activity. Individuals in Class IV have additional problems related to their weight, including cardiomyopathy, Pickwickian/sleep apnea syndrome, pituitary/gonadal dysfunction, acanthosis nigricans, and significant osteoarthritis.
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PMID:Pathophysiology of obesity. 173 17

The Pickwickian syndrome can be divided into two primary breathing disorders, which can affect patients alone or in combination: sleep apnea syndrome (SAS) and obesity hypoventilation syndrome (OHS). Between 1980 and 1990, 126 patients with respiratory insufficiency underwent gastric surgery for morbid obesity, 12.5% of the entire series. These patients weighed more (164 +/- 36 vs 135 +/- 25 kg, P less than 0.0001) and were more often men (62% vs 14%, P less than 0.001) than those without pulmonary dysfunction. Sixteen had OHS alone, 65 had SAS alone, and 45 had both. Of those with OHS, 38 have been followed for 5.8 +/- 2.4 y since surgery and 29 are currently asymptomatic. In the 12 patients in whom arterial blood gases were available greater than 5 y since surgery, the PaO2 increased from 54 +/- 10 to 68 +/- 20 mm Hg (P less than 0.0001) and PaCO2 fell from 53 +/- 9 to 47 +/- 11 mm Hg (P = 0.05). Of the 110 patients with SAS, 57 were available for follow-up an average of 4.5 +/- 2.3 y since surgery and 38 were completely asymptomatic, 15 had mild SAS, and 4 had both SAS and OHS. In 40 patients with pre- and post-weight reduction sleep polysomnograms, the sleep apnea index fell from 64 +/- 39 to 26 +/- 26 (P less than 0.0001). Although respiratory insufficiency of obesity patients had a higher operative mortality than did patients without pulmonary dysfunction (2.4% vs 0.2% after gastric bypass), weight loss was associated with significant improvements in sleep apnea, arterial blood gases, pulmonary hypertension, left ventricular dysfunction, lung volumes, and polycythemia.
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PMID:Long-term effects of gastric surgery for treating respiratory insufficiency of obesity. 173 36

Eight obese patients (4 male, 4 female; mean age = 35.9 years) before [mean body mass index (BMI) = 37.1] and after (mean BMI = 31.4) weight loss by means of a mixed hypocaloric diet were compared with 8 lean subjects (4 male, 4 female; mean age = 37.1 years, mean BMI = 22.3) in a study of their nocturnal sleep patterns and sleep-related growth hormone (GH) secretions. Although no sleep disorders (in particular, sleep apnea and hypersomnia) were observed, GH secretion was markedly altered in obese patients that showed no sleep-related GH peaks. After weight loss, the sleep architecture in obese subjects was unchanged. On the contrary, GH peak appeared to be only partially restored and delayed until after stage III-IV of non-REM sleep. Our study on obese subjects suggests that the altered nocturnal GH secretion, probably related to a hypothalamic dysfunction, may be the result of the obesity per se.
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PMID:Sleep-related growth hormone secretion in human obesity: effect of dietary treatment. 175 83

Twenty-seven morbidly obese patients (13 men and 14 women) with body mass index greater than or equal to 40 kg m-2 were examined. The mean age of the subjects was 36.9 +/- 8.2 years (range 23-51 years), and the mean BMI was 50.2 +/- 6.2 kg m-2 (range 40.0-62.9 kg m-2). A whole-night sleep recording was made for all patients with signs or symptoms indicative of possible obstructive sleep apnoea syndrome (OSAS). If the first nocturnal sleep recording was abnormal, it was controlled after 1 year. Eleven (10 men and one woman) of the 27 patients had an oxygen desaturation index (ODI) of 10 h-1. They were symptomatic with excessive daytime sleepiness or other daytime symptoms of OSAS. The occurrence of OSAS in men and women was 76.9 and 7.1%, respectively. Arterial hypertension was associated with OSAS, but not with smoking or the degree of obesity. Antihypertensive treatment was received by nine of the 27 patients; six of them had OSAS. Thus six of the 11 (54.5%) patients with OSAS and three of the 16 (18.8%) nonapnoeic patients were treated for arterial hypertension (Fisher exact test, P = 0.042). The odds ratio of OSAS for arterial hypertension is 5.2 (95% CI, 0.71-43.6). Vertical-banded gastroplasty was performed in 14 patients, three of whom had OSAS. The selection of patients for gastroplasty was made without taking into account the results of sleep recordings. In the three OSAS patients, a 30-38% reduction in BMI was achieved by surgery. Eight patients with OSAS were treated with an intensified dietary regimen, and the reduction in BMI ranged from -2.6 to 33%. OSAS was either cured or significantly improved in six (55%) patients, with a mean reduction in BMI of 27%, while in patients with persistent OSAS the mean reduction in BMI was only 7%.
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PMID:Obstructive sleep apnoea syndrome in morbidly obese patients. 186 63

The pathogenesis of obesity hypoventilation is incompletely understood. We investigated 505 patients with sleep apnoea in respect of determinants that correlate with chronic hypercapnia. 14 patients (2.8 per cent) exhibited daytime hypercapnia (PCO2 greater than or equal to 45 mmHg). Compared with the entire group of patients, these patients showed heavier overweight (p less than 0.001) and their nightly respiratory dysregulation defined by the apnoea index was more severe (p less than 0.001). If these patients were compared with 14 normocapnic controls matched for apnoea index, weight and age, there was no difference in respect of lung function data. We conclude that overweight and the severity of sleep apnoea are determinants that predispose to chronic alveolar hypoventilation.
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PMID:[Which factors promote chronic alveolar hypoventilation in patients with obstructive sleep apnea?]. 186 1

To determine if a history of snoring is a risk factor for brain infarction, I conducted a case-control study of risk factors for ischemic stroke using 177 consecutive male patients aged 16-60 (mean 49) years with acute brain infarction. For each patient I chose an age-matched (+/- 6 years) male control. Arterial hypertension, coronary heart disease, snoring (habitually or often), and heavy drinking (greater than 300 g/wk) were risk factors in the stepwise multiple logistic regression analysis. The odds ratio of snoring for brain infarction was 2.13. By McNemar's test this association increased strongly if a history of sleep apnea, excessive daytime sleepiness, and obesity were all present with snoring (odds ratio 8.00). My study indicates that snoring may be a risk factor for ischemic stroke, possibly because of the higher prevalence of an obstructive sleep apnea syndrome among snorers than nonsnorers.
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PMID:Snoring and the risk of ischemic brain infarction. 186 48

Fifty-seven patients with obstructive sleep apnoea (OSA) were treated for at least six months with nasal continuous positive airway pressure (CPAP). At follow-up, sleep studies were performed in which CPAP was not used for the first half of the night. We compared the severity of OSA at follow-up without CPAP to the severity of OSA during the patient's initial diagnostic study. Apnoea and hypopnoea index (AHI) fell from 41.4 +/- 7.5 (mean +/- 95% CI) to 34.8 +/- 7.9 (p = 0.06 by Wilcoxon test) and minimum oxygen saturation rose from 71.6 +/- 3.2 to 78.5 +/- 2.6 (p less than 0.001). Some of this change may have been due to reduced REM sleep in the follow-up study (10.5 +/- 2.1% Total Sleep Time vs 7.4 +/- 2.4% TST, p less than 0.05). Long-term nasal CPAP was not associated with any reduction of obesity (BMI before CPAP 31.9 +/- 1.0, after CPAP 31.7 +/- 1.0 (p = 0.39). Systolic arterial pressure fell (before CPAP 143.0 +/- 4.5 mmHg, after CPAP 136.3 +/- 4.6, p less than 0.05) but diastolic pressure did not (before CPAP 88.5 +/- 3.0 mmHg, after CPAP 85.6 +/- 2.9 mmHg, p = 0.11). We concluded that the effect of CPAP treatment for six or more months was a small fall in AHI and a small rise in minimum SaO2, but that this would be of marginal clinical significance, and may be artefactual.
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PMID:Long-term nasal CPAP does not ameliorate obstructive sleep apnoea. 187 51

In order to study the frequency and the mechanisms of daytime pulmonary hypertension (PH) in obstructive sleep apnoea syndrome (OSAS) lung function tests, blood gas analysis and right-heart catheterization were performed in 46 consecutive patients. OSAS was assessed by polysomnography. 9 patients only (20%) had PH (mean pulmonary artery pressure (Ppa) greater than or equal to 20 mmHg). Patients with PH had lower daytime PaO2 (60.8 +/- 7.6 vs. 76.2 +/- 9.4 mmHg; p less than 0.001), higher daytime PaCO2 (44.8 +/- 4.2 vs. 38.0 +/- 4.0 mmHg; p less than 0.001), lower forced vital capacity (FVC) and forced expiratory volume (FEV1) (p less than 0.001), but the severity of OSAS was not different whether PH was present or not (apnoea index: 62 +/- 34 hour in the PH group vs. 65 +/- 40 hour, apnoea + hypopnoea index 102 +/- 33 hour in the PH group vs. 86 +/- 36 hour, lowest sleep SaO2: 59 +/- 21% in the PH group vs. 66 +/- 18%). There were significant correlations between Ppa and: daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), FEV1 (r = -0.52; p less than 0.001) but not between Ppa and apnoea index, apnoea + hypopnoea index, lowest sleep SaO2. PH and daytime hypoxaemia were associated either with chronic airway obstruction or with severe obesity.
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PMID:Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome. 191 66


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