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

This report describes an unusual case of severe obstructive sleep apnea and alveolar hypoventilation leading to hypersomnolence and cor pulmonale, which were corrected by tracheostomy. Four years later, after a 22.5-kg weight gain, nocturnal apneas of similar frequency, duration, and depth of desaturation reappeared but were totally central in origin. The central apneas were eliminated with home nocturnal positive-pressure ventilation via cuffed tracheostomy tube. Each time the patient's apneas were corrected (obstructive: tracheostomy; central: mechanical ventilation), daytime alveolar hypoventilation disappeared rapidly. Yearly right heart catheterizations and radionuclide ejection fractions documented pulmonary hypertension and right heart failure, with resolution following tracheostomy and recurrence after appearance of central apneas. The changes in hemodynamic status corresponded to the patient's weight, presence of apnea, daytime alveolar hypoventilation, and treatment of nocturnal oxyhemoglobin desaturation. This case illustrates the theory of a common etiology of both central and obstructive apnea through abnormal respiratory controller gain and points to several roles obesity may play in apnea.
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PMID:Recurrence of sleep apnea syndrome following tracheostomy. A shift from obstructive to central apnea. 273 81

Sleep apnoea syndromes are a frequent disease, with an incidence of more than 1% in the adult population, a strong male predominance, and a maximal frequency between 40 and 60 years. Their clinical manifestations are dominated by snoring and daytime sleepiness, at times associated with morning headaches, intellectual deficiency, sexual impotence. Obesity, hypertension and polycythemia are not uncommon. These patients are at risk for accidents due to sleepiness, sudden death due to sleep apnoea-related cardiac arrhythmias, ischemic attacks related to hypertension and polycythemia and right heart failure secondary to pulmonary hypertension and alveolar hypoventilation. The most frequent form of sleep apnoea syndromes include obstructive and mixed apnoeas. Their mechanism involves both anatomic factors (upper airway narrowing) and functional factors (defective activation of upper airways dilatory muscles) which lead to upper airway occlusion upon inspiration during sleep. Two therapeutic strategies are possible: a surgical one, uvulopalatopharyngoplasty, the efficacy of which is inconstant and unpredictable and nasal continuous positive airway pressure, which is constantly efficacious but constraining. Central sleep apnoea syndromes are rare, less clearly defined and more difficult to treat.
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PMID:[Sleep apnea syndromes in adults]. 332 Dec 51

Risk factors related to increased mortality were determined on the basis of 329 aortocoronary bypass operations. They were: (1) emergency surgery, (2) poor left ventricular function, (3) reoperation, and (4) pulmonary hypertension. Angina pectoris, recent myocardial infarction, age over 65 years, obesity, significant systemic disturbances, smoking, arterial hypertension, and sex were without effect.
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PMID:[The relation between risk factors and mortality in aortocoronary bypass operations]. 348 57

Mefenorex, N-(3-chloropropyl)-alpha-methylphenethylamine, (RONDIMEN), is included in the list of centrally acting stimulants and/or hallucinogens or related compounds to be considered by a World Health Organization (WHO) Expert Committee in 1985 for possible scheduling under the Convention on Psychotropic Substances, 1971. The therapeutic efficacy of mefenorex as an adjunctive support in the treatment of obesity for limited periods of time, as well as its ability to be well tolerated, has been amply demonstrated. There have been no reports of actual abuse. There have been no reports of illicit trafficking, falsification of packages or materials, or clandestine laboratories manufacturing the compound. Data from preclinical and clinical studies do not suggest a potential for abuse similar to that of amphetamine or related compounds. Moreover, the lack of pulmonary hypertension with mefenorex has been demonstrated in both preclinical and clinical studies. There have been no reports of any public health or social problems associated with mefenorex use. The compound is a well-tolerated anorectic agent with little central stimulant activity.
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PMID:Mefenorex (Rondimen). 374 6

Hypoxia is the major cause of pulmonary hypertension and right ventricular hypertrophy in chronic obstructive pulmonary disease, cystic fibrosis, kyphoscoliosis, chronic mountain sickness, and the obesity-hypoventilation and sleep apnea syndromes. Pulmonary hypertension develops in these patients because the long-standing vasoconstriction produced by hypoxia causes muscular hypertrophy of the pulmonary arteries and arterioles. These pathologic changes may regress if alveolar hypoxia is corrected and hypoxic pulmonary vasoconstriction is continuously inhibited. Intermittent inhibition of hypoxic pulmonary vasoconstriction does not reverse these pathologic changes. Since patient noncompliance with oxygen therapy makes it difficult to achieve continual relief of alveolar hypoxia, a drug that inhibits hypoxic vasoconstriction may be useful. Experimental findings indicate that hypoxic pulmonary vasoconstriction requires calcium influx and can be inhibited by certain slow-channel calcium blockers. Studies also demonstrate that slow-channel calcium antagonists can attenuate the pulmonary hypertension and right ventricular hypertrophy produced in rats by chronic hypoxia. Recently, two studies have shown that nifedipine inhibits hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease. If further studies demonstrate that these short-term effects are sustained, certain slow-channel calcium blockers may become a useful adjuvant to low-flow oxygen therapy in the treatment of hypoxic pulmonary hypertension.
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PMID:Calcium channel blockers in hypoxic pulmonary hypertension. 397 91

Improved case identification of children with upper airway obstruction during sleep should result if physicians are aware of such signs and symptoms as excessive daytime sleepiness, loud snoring, restless sleep, recurrent nocturnal enuresis, systemic and pulmonary hypertension, undergrowth or obesity, and cor pulmonale. Furthermore, partial airway obstruction during wakefulness may be a risk factor for the development of sleep apneas or hypopneas. In suspected cases, polysomnography is a useful method for confirming and quantitating the type (central, obstructive, or mixed) and extent of ventilatory disturbance during sleep and its functional significance (such as arterial oxyhemoglobin desaturation or cardiac arrhythmia). Other methods may be employed to yield similar data. There seem to be at least two groups of children reported in the literature, those in whom there is a specific surgically correctable lesion (such as adenotonsillar hypertrophy) versus those who eventually need tracheotomy because of collapse of upper airway musculature during sleep. In the latter group of children, it is necessary to hypothesize an additional defect in the CNS regulation of respiration during sleep. Further research is necessary to define the boundary between normal and abnormal breathing during sleep, and to understand more thoroughly the effects of intermittent hypoventilation on daytime functioning.
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PMID:Sleep disorders associated with upper airway obstruction in children. 731 58

Pulmonary hypertension was diagnosed in a 41-year-old woman after 16 months' use of fenfluramine as a treatment for obesity. Despite discontinuation, pulmonary pressure remained elevated. Drug-induced pulmonary hypertension is rare but has been reported relatively often after use of the sympathicomimetic agent aminorexfumarate, but also, although more rarely, of fenfluramine.
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PMID:[Pulmonary hypertension following use of fenfluramine for obesity]. 780 76

Patients with obstructive sleep apnea syndrome (OSAS) may have daytime pulmonary hypertension (PH). Transient and sometimes severe elevations of pulmonary arterial pressure during sleep as a result of intermittent upper airway obstruction may lead to daytime PH. We sought to study the factors involved in the development of daytime PH. Right-heart catheterization, pulmonary function tests, and arterial blood gas measurements were done in 25 patients in whom OSAS was diagnosed by whole-night polysomnography. Eight of the patients (32%) had PH, defined by a mean pulmonary arterial (PA) pressure > or = 20 mmHg. For the group as a whole, mean PA pressure was positively and significantly correlated with daytime PaCO2 (r = 0.79), percent of ideal body weight (r = 0.45), and Hb (r = 0.40). Mean PA pressure was negatively and significantly correlated with PaO2 (r = -0.54), FEV 1% (r = -0.52), and %FVC (r = -0.68). In contrast, mean PA pressure was not significantly correlated with apnea index or with sleep desaturation. These data indicate that daytime PH was not directly related to sleep-disordered breathing, but was related to daytime hypoxemia, daytime hypercapnia, obesity, obstructive and restrictive respiratory impairments, and secondary polycythemia.
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PMID:[Daytime pulmonary hypertension in the obstructive sleep apnea syndrome]. 854 78

A 32-year-old woman was hospitalized with recurrent left-sided chest pain and dyspnea on exertion, which had progressed for approximately 10 years. Since age 18 she had been spending more than twelve hours per day in a predominantly seated position on a floor mat, engaged in Japanese dressmaking. A chest roentgenogram showed marked dilation of the main pulmonary arteries, bilateral oligemia in the upper lung fields and a peripheral infiltration in the middle field of the left lung. The (99m)Tc-MAA perfusion lung scan showed multiple defects in both lungs, but no abnormal findings were detected on a 133Xe ventilation scan. A pulmonary angiogram showed multiple occlusions of pulmonary arteries in both lungs. Because recurrent chest pain and dyspnea had been present for a long time, and because ultrasonic cardiography revealed pulmonary hypertension repeatedly for several years, pulmonary thromboembolism was considered to be chronic and recurrent. The patient had none of the following risk factors for pulmonary emboli: malignancy, neurological disease, heart disease, obesity, pregnancy, or a congenital coagulative abnormality such as deficiency of AT-III, protein C, protein S, or plasminogen. Because no other cause could be found, the chronic recurrent pulmonary thromboembolism most likely resulted from extensive sedentary work that caused stagnation of venous return and deep vein thrombosis.
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PMID:[Chronic recurrent pulmonary thromboembolism associated with sedentary work]. 862 76

"Cor pulmonale" is a classic feature of the "Pickwickian syndrome". Earlier studies have reported a high prevalence of pulmonary hypertension (PH) in obstructive sleep apnoea (OSA) patients, but this has not been confirmed by recent studies with a more adequate methodology, including larger groups of patients. The first part of this review is devoted to the prevalence of PH in OSA; most recent studies agree on prevalence of 15-20%. The second (and major) part of the study deals with the causes and mechanisms of PH in OSA. Pulmonary hypertension is rarely observed in the absence of day-time hypoxaemia, and the severity of nocturnal events (apnoea index (AI), apnoea+ hypopnoea index (AHI) does not appear to be the determining factor of PH. Diurnal arterial blood gas disturbances and PH are most often explained by the presence of severe obesity (obesity-hypoventilation syndrome) and, principally, by association of OSA with chronic obstructive pulmonary disease (the so called "overlap syndrome"). Bronchial obstruction is generally of mild-to-moderate degree and may be asymptomatic. The final part of the review analyses the therapeutic consequences of the presence of PH in OSA patients. Pulmonary hypertension, which is generally mild-to-moderate, does not need a specific treatment. When nasal continuous positive airway pressure (CPAP) fails to correct sleep-related hypoxaemia, supplementary oxygen must be administered. In patients with marked daytime hypoxaemia (arterial oxygen tension (Pa,O2), < or = 7.3 kPa (55 mmHg) conventional O2 therapy (nocturnal + diurnal) is required.
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PMID:Pulmonary hypertension in the obstructive sleep apnoea syndrome: prevalence, causes and therapeutic consequences. 872 47


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