Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven patients with upper airway apnoea during sleep (one with SHY-Drager syndrome) were monitored polygraphically for wakefulness, sleep, and cardiovascular variables. Systemic hypertension and most of the severe arrhythmias recorded during sleep were secondary to repetitive obstructive apnonea and were mediated through the autonomic nervous system. Sleep related elevations of pulmonary arterial pressure were not influenced by atropine or impaired autonomic functions. Upper airway sleep apnoea is sleep related; the type of sleep (REM or NREM) is critical in the appearance of abnormalities. The distinction between two patient subgroups (total sleep dependent and NREM sleep dependent) has haemodynamic, and possibly long-term, implications. Sleep apnoea syndrome should be looked for in pateints with the Shy-Drager syndrome.
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PMID:Sleep apnoea syndrome: states of sleep and autonomic dysfunction. 19 9

A 67-year-old woman with acquired micrognathia developed severe daytime hypersomnia, loud snoring, nocturnal enuresis, encopresis, and hypertension. A polysomnogram demonstrated 564 sleep apneas, primarily obstructive, recurrent hypoxia, a bradytachycardia, and absent stages III, IV, and REM sleep. Endoscopy during sleep revealed recurrent active closure of the upper pharynx associated with loud snoring. A tracheoplasty was done because of severity of symptoms and failure of conservative therapy. Dramatic improvement in sleepiness and hypertension occurred within 48 hours. On postoperative night 15 a repeated polysomnogram showed only 23 apneas, no hypoxia or bradytachycardia, and long periods of stage II, IV, and REM sleep. Patients with the hypersomnia-sleep apnea syndrome should be provided with a tracheal opening during sleep when severe daytime somnolence, cardiac arrhythmias, and hypertension are present.
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PMID:Hypersomnia-sleep apnea due to micrognathia. Reversal by tracheoplasty. 20 45

A sleep apnea syndrome due to upper airway obstruction was diagnosed in 25 adult men (25 to 65 years of age) using nocturnal polygraphic monitoring. Excessive daytime somnolence, hypnagogic hallucinations, and automatic behavior, personality changes with abnormal behavioral outbursts, impotence, morning headaches, abnormal motor activity during sleep, nocturnal enuresis, and high blood pressure should suggest this diagnosis when any of the symptoms are associated with loud snoring. Respiratory monitoring during sleep and nocturnal cardiovascular evaluation bring prognostic information and indications for therapy. Three types of therapeutic trials, namely, diet, medications with or without diet, and surgery have been performed. Only surgery has been beneficial in these cases.
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PMID:Sleep apnea syndrome due to upper airway obstruction: a review of 25 cases. 55 14

A patient with autonomic insufficiency and extrapyramidal signs (Shy-Drager syndrome) and sleep apnea syndrome (SAS) underwent hemodynamic studies. In comparison to patients with SAS and intact autonomic reflexes, systemic hypertension was absent and marked sinus arrhythmia during sleep was blunted. Cyclical pulmonary hypertension associated with frequent apneic episodes during sleep persisted, reflecting a minor role of autonomic reflexes in the generation of this abnormality. Autopsy confirmed the Shy-Drager syndrome and multiple areas of degeneration were observed in areas of the CNS outside the medullary respiratory centers, suggesting their importance in the origin of the respiratory abnormalities in SAS.
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PMID:Sleep apnea syndrome in a patient with Shy-Drager syndrome. 62 49

Eight children, 5 to 14 years of age, were diagnosed by means of nocturnal polygraphic monitoring with a sleep apnea syndrome similar to that seen in adults. Excessive daytime sleepiness, decrease in school performance, abnormal daytime behavior, recent enuresis, morning headache, abnormal weight, and progressive development of hypertension should suggest the possibility of a sleep apnea syndrome when any of these symptoms is associated with loud snoring interrupted by pauses during sleep. Surgery may eliminate the clinical symptomatology.
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PMID:Sleep apnea in eight children. 93 81

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
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PMID:Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. 99 7

Periodic sleep apnea may be due to repeated episodes of upper airway obstruction in patients who have a short thick neck and/or large jowls. Apnea due to complete cessation of breathing may occur to a lesser extent. Anaylsis of the sleep electroencephalogram shows that these patients rarely achieve deep sleep and have less stage 1-REM sleep than normal subjects of comparable age. They are chronically sleep-deprived, a manifestation expressed by daytime somnolence, chronic fatigue and often by personality disturbances marked by paranoia, agitated depression and hostility. The definitive diagnosis of this syndrome may be established by monitoring during sleep, the electroencephalogram, measuring abdominal excursions through a mercury-in-Silastic-strain gauge and recording air flow at the nose by means of a thermocouple. As demonstrated by other investigators, chronic hypoventilation during sleep leads to both pulmonary and systemic arterial hypertension, which may produce generalized cardiac enlargement and congestive heart failure. The abnormalities in the periodic sleep apnea syndrome are abolished by establishing a patent airway either through tracheostomy or weight reduction.
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PMID:Periodic sleep apnea: chronic sleep deprivation related to intermittent upper airway obstruction and central nervous system disturbance. 111 91

Twenty-seven subjects with insomnia or diurnal hypersomnolence presented a sleep apnea syndrome when their respiration was systematically checked during sleep. These sleep-induced respiratory abnormalities were completely occult and pulmonary function tests performed during wakefulness were normal. The patients, all non-obese, presented serious pulmonary artery pressure changes which were directly connected with the repetitive sleep apneas. Half of the patients also had systemic hypertension. Two children (aged 11 and 15) underwent tracheostomies which by-passed the sleep-induced obstruction. Systemic hypertension was reduced after surgery.
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PMID:[Can an anomaly of the central nervous system be responsible for hemodynamic disorders]. 115 95

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

Voluntary end-expiratory apnoea in a 23-year-old asymptomatic mild hypertensive patient consistently elicited bradyarrhythmias (complete heart block and sinus pause) and sympathetic activation to muscle blood vessels, indicating simultaneous sympathetic and parasympathetic activation during apnoea. The sympathetic bradyarrhythmic response to apnoea was potentiated by hypoxia and eliminated by atropine. Baroreflex activation also attenuated the bradycardic response to apnoea. A 43-year-old hypertensive patient with sleep apnoea also exhibited bradyarrhythmias (sinus arrest for up to 10 s) and a fall in perfusion pressure to less than 50 mmHg during episodes of sleep apnoea. These cardiovascular changes were associated with a reduction in oxygen saturation to levels as low as 35%. Neither patient was on any medication. Simultaneous sympathetic and parasympathetic activation during episodes of apnoea may predispose to cardiovascular catastrophe. These chemoreflex mediated autonomic changes are inhibited by baroreflex activation. We propose that patients with impaired baroreflexes (patients with hypertension or heart failure and premature infants) may be especially susceptible to excessive autonomic responses to chemoreflex stimulation during periods of apnoea. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion and sympathetic activation during apnoea may predispose to sudden death.
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PMID:Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension. 149 63


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