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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes the case of a 58 year old man who presented with an episode of acute respiratory failure and right heart decompensation. After recovery from the acute illness, hypoxaemia, hypercapnia and pulmonary arterial hypertension remained, the causes of which were not known. There was no airway obstruction, only a moderate restrictive ventilatory defect, a little weight increase and a unilateral diaphragmatic paralysis. Obstructive sleep apnoea was finally suspected and confirmed by sleep recording. The obstructive sleep apnoea probably explained the respiratory insufficiency and the pulmonary hypertension. Loss of weight was associated with the disappearance of hypercapnia and pulmonary hypertension. As a result of this study, the value of sleep recording is emphasized. When respiratory failure or pulmonary hypertension seem unexplained, think of obstructive sleep apnoea.
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PMID:[Value of sleep polygraph examination in the etiological diagnosis of apparently inexplicable respiratory insufficiency]. 404 63

In the case reported here, a 34-year-old man with severe obstructive sleep apnea syndrome had arterial hypertension and had had a stroke that caused right hemiplegia. A review of the literature reveals a surprisingly high occurrence of arterial hypertension in subjects with obstructive sleep apnea syndrome, including children. The cause of hypertension in these patients is not clear. Surgical procedures and a new nonsurgical treatment have been successful in relieving the symptoms of obstructive sleep apnea. Our patient's symptoms resolved completely after uvulopalatopharyngoplasty and tonsillectomy. However, his arterial hypertension persisted.
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PMID:Hypertension and stroke in a young man with obstructive sleep apnea syndrome. 405 36

Daytime blood pressure (BP) in 31 male patients with obstructive sleep apnea syndrome (OSAS) was measured and the effects of nasal continuous positive airway pressure (CPAP) treatment on daytime BP were studied. Subjects were 48 +/- 10 (mean +/- SD) years old and weighed 80 +/- 13 kg. The mean systolic BP and diastolic BP were 135 +/- 15 mmHg and 88 +/- 14 mmHg, respectively and daytime hypertension was present in 12 (38%) subjects. Apnea index (AI) and the lowest oxygen saturation during sleep were significantly more severe in the hypertensive (HT) than in the non-hypertensive (NHT) patients (p < 0.05). AI was significantly correlated with diastolic BP (p < 0.05) and the mean and lowest oxygen saturation during sleep were significantly correlated with both systolic (p < 0.05) and diastolic BP (p < 0.01). After nasal CPAP treatment for two weeks, both systolic and diastolic BP were significantly reduced; the former from 135 +/- 15 mmHg to 126 +/- 10 mmHg (p < 0.005) and the latter from 88 +/- 14 mmHg to 78 +/- 6 mmHg (p < 0.001). These data form direct evidence that daytime hypertension is partially induced by OSAS and is reversible with nasal CPAP treatment.
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PMID:Daytime hypertension and the effects of short-term nasal continuous positive airway pressure treatment in obstructive sleep apnea syndrome. 754 36

As a follow-up to a previous assessment of complications of sleep-disturbed breathing in 265 patients, we have reevaluated measures of sleepiness and hypertension in patients with obstructive sleep apnea (OSA) (n = 518), central sleep apnea (n = 50), and subclinical sleep-disordered breathing (SDB) (n = 107). Both subjective and objective (multiple sleep latency test [MSLT]) measures indicated that OSA patients were sleepier than those with subclinical SDB. The OSA patients weighed significantly more than the patients with central sleep apnea or subclinical SDB. They had a higher proportion of men, described more habitual sleepiness, and had a higher likelihood of feeling unrefreshed in the morning compared with the group with subclinical SDB. Among the OSA patients, there was a significant correlation between subjective and objective assessment of sleepiness, but this relationship was quantitatively very small. A forward stepwise regression analysis revealed that weight, and to a lesser degree waking time after sleep onset, could account for 65.5% of the variance in subjective sleepiness. Seventy-five percent of the variance of the mean sleep latency in the MSLT could be accounted for by the mean minimum arterial oxygen saturation in non-REM sleep and the nocturnal sleep latency. Diastolic BP was significantly higher in OSA patients compared with the patients with central sleep apnea and subclinical SDB. When covarying for weight, age, and gender, this effect lost significance. Among OSA patients taken by themselves, 98.3% of the variance in diastolic blood pressure could be accounted for by the mean minimum arterial oxygen saturation in non-REM sleep, with very small additional contributions of apnea/hypopnea index, weight, and age. In summary, among patients across a spectrum of SDB, differences in diastolic BP were primarily associated with weight, age, and gender. Among OSA patients, perhaps because of a more limited variance in weight, diastolic BP was associated with measures of SDB.
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PMID:The relationship of sleepiness and blood pressure to respiratory variables in obstructive sleep apnea. 755 70

Obstructive sleep apnea (OSA) occurs in about 10% of the middle-aged population but in about 30% of the hypertensive population of the same age. About 20% of the middle-aged population has hypertension but about 50% of patients with OSA have hypertension. Despite this close relationship between these two entities, previous attempts to determine whether the respiratory abnormalities in OSA were responsible for the hypertension were inconclusive, particularly because of the confounding effect of obesity which is common to both conditions. Data from recent observational and intervention studies, however, have succeeded in avoiding many of the pitfalls of earlier studies and it is now becoming evident that OSA may be a major cause of hypertension--responsible for about 30% of all cases. Successful treatment of OSA by any means has been shown in most studies to cause significant reductions in blood pressure throughout the 24 h period, while at the same time alleviating the vast array of symptoms and clinical abnormalities associated with this common and serious condition. Despite the encouraging results of these recent data, more studies are urgently required which should include larger numbers of patients and controls in order to clarify further the relationship between OSA and hypertension.
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PMID:Is obstructive sleep apnea a common cause of essential hypertension? 755 81

Patients with obstructive sleep apnea and other sleep-related breathing disorders that cause sleep disruption frequently present with abnormal circadian blood pressure patterns or frank hypertension. Ambulatory blood pressure monitoring has been useful in research documenting nocturnal hypertension and the normalization of blood pressure when sleep apnea is treated. In practice, similar measurements can provide a clue to the presence of an undiagnosed sleep disorder and can be valuable in following the blood pressure response to the treatment of sleep-disordered breathing.
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PMID:Ambulatory monitoring of blood pressure in patients with sleep-disordered breathing. 760 23

Platelet function and fibrinolytic activity was studied during rest and after ergometric exercise in 13 hypertensive or normotensive patients with obstructive sleep apnea (OSA) and in 10 sex- and weight-matched controls. All patients had undergone a complete polysomnography for the diagnosis of OSA. The controls did not undergo any sleep investigation but had no history of snoring or witnessed apneas during sleep. On antihypertensive drug wash-out, two of the patients were normotensive, whereas 11 had mild to moderate hypertension. Platelet aggregation measured by adenosine 5'-diphosphate- or adrenaline-induced aggregation, platelet factor-4 or beta-thromboglobulin did not differ between patients and controls. During exercise beta-thromboglobulin decreased significantly in both OSA patients and controls. Plasma tissue plasminogen activator activity was similar in OSA patients and controls and increased significantly in both groups after exercise. Plasminogen activator inhibitor type 1 (PAI-1) was 18.4 +/- 3.6 IU/ml in OSA patients compared with 8.2 +/- 1.7 IU/ml in controls (p < 0.029) during rest, indicating decreased fibrinolytic activity. The difference between groups remained after exercise (p < 0.017). Blood pressure elevation was more common and body mass index (BMI) was higher in patients with OSA, but there was no direct relation between blood pressure level or BMI and PAI-1. Nevertheless, differences between groups were smaller when blood pressure and obesity were accounted for. It is concluded that patients with OSA may exhibit decreased fibrinolytic activity. Low fibrinolytic activity may represent a confounding pathophysiological mechanism behind the high incidence of myocardial infarction and stroke in patients with OSA.
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PMID:Platelet function and fibrinolytic activity in hypertensive and normotensive sleep apnea patients. 761 Mar 15

Each of 51 patients (42 male, 9 female) examined by polysomnography for suspected obstructive sleep apnea syndrome (OSAS) was subjected to a glucose load test with 75 g glucose and determination of blood sugar and blood insulin levels (at 0, 30, 60, 120 and 180 min). The patients were divided into 4 groups; with and without excess weight (Broca index < or = > 110%), and with and without pathological apnea index (< or = > 10). There was no significant difference between the groups with respect to age. The corresponding groups did not show any significant differences with regard to Broca index or apnea index. However, the patient group with a Broca index > or = 110% and a pathological apnea index > or = 10 was significantly different to all other groups with regard to glucose and insulin level after 60 min. This group was also significantly different to all other groups with regard to systolic and diastolic blood pressure. The reduced glucose tolerance and increased insulin resistance in combination with arterial hypertension in this patient group is indicative that a combination of adiposity and OSAS represents a particularly high risk factor for the development of arterial hypertension even though the pathological mechanism responsible for the development of arterial hypertension is also present in members of both the normal weight OSAS group and the overweight group without OSAS who exhibit a metabolic predisposition for the development of hypertension. A synergetic interaction of both pathomechanisms favors the development of arterial hypertension. Overweight patients with OSAS thus constitute a high-risk group for the development of cardiovascular diseases.
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PMID:[Glucose tolerance, insulin resistance and arterial hypertension in patients with obstructive sleep apnea syndrome]. 761 95

Our study included 42 patients with obstructive sleep apnea (OSAS) confirmed by polysomnography. In these patients we investigated the clinical manifestations, the results of the laboratory examinations, including polysomnography, ORL observations and tests of pulmonary function, as well as the therapeutic results. Our patients presented a serious set of symptoms which included excessive daytime sleepiness, snoring, obesity, craniofacial abnormalities, systemic hypertension, cardiac arrhythmias, incapacity to work with precocious retirement, marital conflicts and high incidence of accidents, namely traffic accidents. An adequate treatment, mostly with nasal CPAP (continuous positive airway pressure), induced marked relief of the symptoms; some patients had an advantage in surgical treatment and weight reduction. OSAS is a frequent entity, affecting mostly male adults after the 5th decade. The lack of knowledge about this entity and the common social acceptance of some of its cardinal symptoms induces considerable delays in its diagnosis. The severity of the symptoms, the personal and social risks of excessive daytime sleepiness, the cardiocirculatory effects and the risk of sudden death during sleep justify an early diagnosis in order to prevent the severe evolution of the disease. Its complex physiopathology and multiple etiological factors justify a multidisciplinary approach.
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PMID:Obstructive sleep apnea. Clinical and laboratory studies. 765 80

The National Commission on Sleep Disorders Research, in its report to Congress, concluded that the primary care community generally does not understand sleep disorders. Obstructive sleep apnea carries a risk of substantial morbidity and mortality. Excessive daytime sleepiness results from fragmented sleep and microarousals associated with apneic events. It causes poor work performance and increases the incidence of automobile accidents due to driving while drowsy. The commission estimates that the loss of productivity in the United States from excessive daytime sleepiness is more than $20 billion per year. Obstructive sleep apnea is strongly associated with hypertension, myocardial infarction, and stroke. Risk factors for obstructive sleep apnea include male sex, obesity, older age, craniofacial anomalies, and familial risk. Treatment is based on documenting the disorder by polysomnography. Medical management of the syndrome includes weight loss and nasal continuous positive airway pressure. A network of follow-up and support is necessary to maintain compliance. Surgical treatment is reserved for those for whom nasal airway pressure treatment fails. A surgical protocol is presented that demonstrates efficacy equal to nasal airway pressure treatment. Primary care physicians should assume the responsibility of identifying patients at risk for obstructive sleep apnea and refer them appropriately.
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PMID:Obstructive sleep apnea. Trends in therapy. 772 98


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