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

The frequent association of sleep apnea syndrome and essential hypertension led to think of sleep apnea as an etiology of hypertension, especially as a good correlation has been found between the severity of both diseases. Moreover, treating the apnea syndrome results in a decrease of blood pressure. The aim of our study is to depict the outlines of a severe hypertensive individual with sleep apnea by comparing 9 men primarily referred to the hypertension clinic with refractory hypertension and finally found to have sleep apnea (study group) to 23 men whose diagnosis of sleep apnea was made in the pulmonary unit (controls). Fifteen of these were hypertensives. Mean age of the study group was 47 +/- 7 years vs 60 +/- 11. Controls were less overweighted: BMI = 33 +/- 6 kg/m3 vs 39 +/- 5. Mean blood pressure was 171 +/- 16/107 +/- 4 mmHg in the study group vs 157 +/- 19/92 +/- 12 mmHg in controls. Prevalence of glucose metabolism disorders was significantly greater in the study group: 6 patients with maturity onset diabetes and 3 with proven glucose intolerance, vs respectively 4 and 6 controls. Triglycerides were elevated in both groups whereas mean cholesterol was slightly above normal values. Six patients of the study group could have an echocardiogram which showed left ventricular hypertrophy (mean left ventricular mass index = 206 +/- 31 g/m2 after the Penn convention).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1991 Aug
PMID:[Should arterial hypertension in sleep apnea syndrome be stressed?]. 183 55

Sleep apnea syndrome and systemic hypertension are frequently associated but their causal relationship is unclear. We compared the oscillations of systemic blood pressure and heart rate during polysomnography in 8 normotensive subjects (2 females) and 5 hypertensive (supine awake blood pressure: 165 +/- 7/96 +/- 5 mmHg) without treatment. Their ages (normotensive: 52.1 +/- 11.0 yrs, hypertensive: 51.2 +/- 6.4 yrs) and body mass indices (32.6 +/- 9.6 kg/m2 vs 33.2 +/- 5.2 kg/m2 respectively) were not statistically different. Systemic blood pressure was continuously monitored by a non invasive digital plethysmography (Finapres). Both groups had similar respiratory events indices (normotensive: 45.2 +/- 18.1/hr, hypertensive: 48.4 +/- 20.5/hr) and minimal oxygen saturations (79.4 +/- 9.1% vs 82.4 +/- 7.0% respectively). During apneas in slow-wave sleep were observed the minimal values for systolic and diastolic pressures which were significantly higher in hypertensive than in normotensive (138.2 +/- 9.6/83.2 +/- 16.1 mmHg vs 105.9 +/- 11.1/60.5 +/- 10.9 mmHg respectively). During resumption of ventilation maximal blood values were recorded which were also higher in hypertensive than in normotensive (185.0 +/- 13.8/113.2 +/- 21.5 mmHg vs 155.9 +/- 19.8/88.7 +/- 17.1 mmHg respectively) (p less than 0.05). Although absolute variations of blood pressure were similar, relative changes in systolic pressure were significantly higher in normotensive (p less than 0.05). Maximal heart rate was 76.8 +/- 6.2 bpm in normotensive and 76.6 +/- 3.9 bpm in hypertensive during resumption of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1991 Aug
PMID:[Nocturnal continuous measurement of blood pressure in sleep apnea syndromes. Comparison between normotensive and hypertensive patients]. 195 62

The Arnold-Chiari malformation (MAC), ectopic medulla of the cerebral hemispheres, may be the basis of respiratory problems provoked by compression of the respiratory centre. It is associated with numerous respiratory problems in children; there are however few publications related to the association of MAC and ventilatory problems in adults. It was recently suggested and subsequently shown that the syndrome of sleep apnoea (SAS) could occur in relation to MAC. We report a new observation documenting the association of MAC and SAS. The surgical cure of MAC enabling a remission of SAS suggests the existence in this case of a causal relation between the two pathologies. A search for such a malformation by imagery of the occipito-medullary crest should be a part of the work up in SAS when the cause remains undetermined.
Rev Mal Respir 1990
PMID:[Sleep apnea syndromes and Arnold-Chiari malformation]. 232 Jul 86

The aim of this study was to test the efficacy of nocturnal oximetry as a means of continuous recording of SaO2 in the identification of apnoeic events in the recognition of non-apnoeic desaturation. The oscillations of SaO2 in relation to successive periods of apnoea during the course of the sleep apnoea syndrome (SAS) or with apnoeic episodes in patients with chronic airflow obstruction (BPCO) or restricted disease, were identified using a new delta index quantifying the variations of SaO2 during the night. 26 successive patients in whom there was an indication for nocturnal oximetry were included in a prospective study comparing nocturnal oximetry and polysomnography during 34 nights. In the apnoeic patients we found a strong correlation (r = .85. p. less than .01) between the apnoeic period and the delta index. In BPCO the number of apnoea was correlated with the delta index (r = .96. p. less than .01). A minimal threshold of the delta index fixed at 1.5 was satisfactory for detecting apnoea if the initial SaO2 was less than 93%. The value of the adequate for affected detection ought to be fixed at .8 (95% sensitivity) when the initial SaO2 was greater than 93%. A detection of apnoeic events thus seems possible by this method.
Rev Mal Respir 1990
PMID:[Can oximetry contribute to the detection of apnea? The use of a mathematical analysis of the oximetry signal]. 236 65

The results at three months of uvulopalatopharyngoplasty (UPPP) have been evaluated in thirty adult patients with an obstructive sleep apnoea syndrome (SAOS). For the group overall the mean apnoea index (IA) decreased from 57 apnoeas per hour and the mean maximal desaturation decreased to 60% post operatively. However in the overall results different individual facts overlap. 20 of the 30 patients, or 67%, have an IA post operatively of less than 50% of the pre-operative value (responders). 14 of these or 47% have a post operative IA of less than 10 apnoeas per hour, a value considered as non pathological. Finally 33% of the patients have no improvement in their post operative IA (non responders). A stricking diminution of nocturnal desaturation and of the disorganisation of sleep was seen in responders to UPPP. No predictive factor for the results of UPPP could be determined. This study shows that UPPP is an effective treatment in a large number of patients having SAOS at the price of minor and transitory complications.
Rev Mal Respir 1989
PMID:[Effects after 3 months of uvulopalatopharyngoplasty in the treatment of obstructive sleep apnea syndromes in adults]. 269 Feb 12

Amyloid is defined by its affinity for Congo red, which gives it a characteristic green birefringence in polarised light. This peculiarity is the result of its structure in beta-fibrillary folds, which is common to all biochemical varieties of amyloidosis whatever the origins of the immunoglobulin, reactive AA or prealbumin for example. Tracheobronchial amyloidosis exists in two forms: a pseudotumoral mass of a few millimeters in diameter discovered by chance at endoscopy without producing any clinical signs; and multi-focal sub-mucosal plaques which lead to bronchial stenosis and which can be destroyed by laser. Parenchymal amyloid can be nodular, or diffuse and interstitial. The amyloid nodules are single or multiple and their size varies from a few millimeters to several centimeters; they lead to few symptoms and do not require any treatment in the majority of cases if the diagnosis has been achieved by transparietal puncture for example (but the diagnosis is made above all by the excision of a mass which is presumed to be neoplastic). Diffuse interstitial parenchymal amyloid involves the alveolar region: it is a not uncommon finding at necropsy when it only infiltrates the vessels, it can give rise to the symptomatology of an interstitial pneumonia when there is widespread infiltration of the alveolar-capillary zone. The distinction between this type of diffuse interstitial amyloid and the miliary micro-nodular amyloidosis is sometimes difficult with overlapping between these two entities. Amyloid may also involve the pleura, the mediastinal nodes, the respiratory muscles and in particular the diaphragm; macroglossia may be responsible for obstructive sleep apnoea. Tracheobronchial amyloid and pulmonary nodules are generally localised to the respiratory system, whereas diffuse interstitial amyloid is combined in a group along with systemic amyloid. There is no specific treatment for amyloidosis.
Rev Mal Respir 1989
PMID:[Amyloidosis and amyloid deposits. Amyloidosis of the lower respiratory tract]. 264 9

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.
Rev Mal Respir 1989
PMID:[Physiopathology of obstructive sleep apneas]. 269 Feb 8

The occurrence of episodes of desaturation during sleep in patients suffering from chronic airflow obstruction is well known. The severity of nocturnal hypoxaemia depends, in part, on the level of the diurnal PaO2. Hypoventilation linked to sleep is the principle mechanism responsible for the decrease in PaO2 and the desaturation which results and depends on the level of oxyhaemoglobin saturation (SaO2) during wakefulness. However, it is not possible to predict the severity of nocturnal desaturation solely on the basis of diurnal oxyhaemoglobin saturation. Numerous factors may contribute to a worsening of nocturnal desaturation. In some patients it may be associated with hypoventilation and a worsening of the ventilation perfusion inequalities. A fall in the ventilatory response to hypoxaemia and hypercapnea contributes equally to the severity of desaturation. The awake response to hypoxia is variable according to the stage of their respiratory failure but may play a role in worsening nocturnal hypoxia. Snoring and obstructive apnoea are responsible for severe desaturation in chronic airflow obstruction presenting as hypoxaemia which may be moderated during the day. At present the value of systematic nocturnal polygraphic recordings in the "work-up" of chronic airflow obstruction has not been demonstrated. Its principle practical interest is in research into the associated sleep apnoea syndrome. It should be recognised in a patient with chronic airflow obstruction who snores and is somnolent with hypoxaemia and/or poorly explained hypercapnea. The therapeutic approach in respiratory failure should take account of nocturnal desaturation and the oxygen flow at night should be superior to the one to two litres which are required to correct the diurnal hypoxaemia.
Rev Mal Respir 1988
PMID:[Frequency and severity of hypoxemia during sleep in COPD. Clinical and therapeutic impact]. 317 63

A syndrome of sleep apnoea may appear 15 to 29 years after acute anterior poliomyelitis (PAA). It is generally a mixed syndrome with an association of central type and obstructive apnoea in variable proportions. We report such a case occurring in a patient who had presented 30 years before with PAA, and presenting on this occasion with resting pulmonary artery hypertension, polycythaemia but without disturbance of blood gases. Treatment with positive pressure ventilation was given by the nasal route at 10 cm of water leading to an improvement with a significant decrease in the number and duration of apnoeic episodes and a disappearance of desaturation. The sleep apnoea syndrome (SAS) should be considered as a possible late sequel of PAA.
Rev Mal Respir 1988
PMID:[Sleep apnea syndrome: late sequela of poliomyelitis]. 318 71

The soft palate is a muscular fold suspended from the posterior border of the bony palate and extending downwards and backwards into the oropharynx. Usually, the soft palate and tongue are in tight apposition, closing the oropharyngeal isthmus; the soft palate can however rise and touch the posterior pharyngeal wall, closing the nasopharynx: thus the soft palate regulates the flow of air through nose and/or mouth. During oronasal breathing (as during exercise, speech or smoking) the impedance of naso and oropharynx respectively is determined by the position of the soft palate. Hence partitioning of the airflow through nose and mouth will depend on the latter. This is true in both adults and babies. Babies are not obligatory nasal breathers (as was previously thought). This applies as well as to near miss for sudden infant death syndrome babies. The soft palate is also involved in the genesis of snoring and the sleep apnea syndrome.
Rev Mal Respir 1988
PMID:[The role of the soft palate in respiration]. 336 31


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