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

During 1976-1988 we diagnosed sleep apnea syndrome (SAS) in 1,620 adult men and women monitored in the Technion sleep laboratories. Their age at the time of diagnosis ranged between 21 and 79 years. Fifty-seven patients (53 men and 4 women) had died by 1990, 53% due to respiratory-cardiovascular causes. The observed/expected (O/E) mortality rates, calculated for men only, revealed excess mortality of patients under 70 years old. Excess mortality was significant in the fourth and fifth decades (3.33, p < 0.002; 3.23, p < 0.0002, respectively). In patients older than 70 O/E was 0.33 (p < 0.0007). Hierarchical multivariate analysis with four fixed variables [age, body mass index (BMI), hypertension and apnea index] and four additional variables added manually one at a time (heart disease, lung disease, diabetes, apnea duration) was used to determine the predictors of death from all causes, cardiopulmonary causes and from myocardial infarction (MI). All four major variables were found to be significant predictors of mortality from all causes, in addition to lung disease and heart disease. Only age and BMI were significant predictors of cardiopulmonary deaths in addition to lung disease. Age, BMI and hypertension predicted MI deaths in addition to lung disease. These results were interpreted to suggest that SAS affects death indirectly, most probably by being a risk factor for hypertension.
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PMID:Mortality in sleep apnea patients: a multivariate analysis of risk factors. 938 Oct 62

Much has been written about snoring and its affects on health, in particular its possible influence on cardiovascular disease. However, there are many assumptions made when linking the report of snoring to any consequences such as hypertension, heart disease or stroke. In particular it is not clear how snoring might influence the cardiovascular system, whether subjective reports of snoring are accurate, and snoring might only be acting as a marker for some common risk factor such as upper body obesity; a particular risk factor for cardiovascular disease, and through neck circumference, snoring. There is much better evidence that snoring is an important cause of sleepiness, even in the absence of conventional sleep apnoea.
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PMID:Epidemiology of snoring and its consequences. 761 44

In a group of 132 randomly selected male patients with the admission diagnosis arterial hypertension in a cardiological rehabilitation clinic, nightly monitoring was performed with Mesam 4 with records of the metabolism laboratory values and sleep disturbances longitudinally. Desaturation indexes of > or = 10/h after manual correction for plausibility revealed a total prevalence of 27.3% in the case of breathing disturbances. The prevalence increased to 52% in the over 55 year-old patients with a Broca index of > or = 120% in comparison to merely 15.4% in standard weighted, comparable age group. No differences were found in the laboratory values. These results again show the frequent occurrence of the combination adiposity, hypertension, and sleep apnea syndrome which has often been missed previously in specialist rehabilitation clinics.
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PMID:[Prevalence of sleep apnea syndrome with primary arterial hypertension in a cardiologic rehabilitation clinic]. 761 99

Numerous studies have suggested an alteration of sympathetic nervous system functioning in sleep apnea. However, most of these studies did not control for confounding factors such as diet, obesity, hypertension and anti-hypertensive medications. We examined plasma and urinary catecholamines in 43 patients, including hypertensive and normotensive individuals with and without sleep apnea. Hypertensive patients were studied at least 3 weeks following tapering of anti-hypertensive medication. All patients consumed similar diets and were of similar age and level of obesity. Twenty-four-hour urinary norepinephrine levels were significantly higher in apneics (58.2 ng vs. 40.2 ng in nonapneics, p < 0.002). Urinary norepinephrine in apneics was increased during both day and night. Plasma norepinephrine levels were not significantly elevated in apneic patients but were elevated in hypertensive patients both during sleep and in the morning (p < 0.05).
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PMID:The effect of sleep apnea on plasma and urinary catecholamines. 767 72

This study examined the relationship between sleep apnea and beta 2-adrenergic receptor characteristics. Using standard polysomnography, individuals were classified as either apneic (n = 15) or mild to nonapneic (n = 15) according to their respiratory disturbance index (RDI). Subjects were similar in terms of sodium excretion and blood pressure. Apneic subjects showed a decrease in beta 2-adrenergic receptor sensitivity (p = 0.01) [as determined by isoproterenol-stimulated cyclic adenosine 5'-monophosphate (AMP) production in lymphocytes] and an increased binding affinity to the beta receptor antagonist [125I]iodopindolol (p < 0.001). beta receptor density was also diminished in apneics, but not significantly (p = 0.08). Forskolin-stimulated cyclic AMP was not significantly different between the groups, indicating a similarity in postreceptor Gs-adenylate cyclase activation. Across all subjects, RDI was negatively correlated with beta receptor sensitivity (r = -0.35, p = 0.05) and Kd (r = -0.54, p < 0.01) and positively correlated with systolic blood pressure (r = 0.37, p < 0.05). The findings indicate that sleep apnea is associated with a diminished beta 2-adrenergic receptor function but no change in postreceptor components and suggest a mechanism for the high comorbidity between sleep apnea and hypertension.
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PMID:Beta 2-adrenergic receptor characteristics in sleep apnea patients. 776 41

Sleep pattern and breathing in humans are altered following cerebrovascular accidents involving the brainstem. Sleep apnea is a well-established complication of stroke involving the brainstem. On the other hand, the effect of cerebral stroke on sleep and breathing has not been well defined. The diffuse cerebral symptoms such as cognitive deficits, depression or fatigue, after hemispheric stroke mimic those present in patients with sleep apnea. To define the breathing pattern in patients with stroke involving cerebral hemispheres without brainstem lesion and without the prior history of sleep-disordered breathing, we studied 10 patients within 1 year of their stroke. The data collected during polysomnography from the stroke patients were compared with a group of subjects matched for age, body mass index, presence of hypertension, and smoking history without stroke. Patients with stroke had an abnormal sleep architecture with significantly lower slow wave sleep and rapid eye movement (REM) sleep when compared with controls. Sleep was fragmented because of the presence of increased respiratory disturbances. Stroke patients had a respiratory disturbance index of 52 +/- 10 events per hour when compared with 3 +/- 1 in controls (p < .05). Majorities of respiratory events were obstructive apneas and were associated with arterial oxygen desaturations and arousals. The pathogenic mechanism of sleep-disordered breathing in patients with hemispheric stroke seems to be related to the physiological effect of sleep on already compromised upper airway muscle control. Patients with stroke and diffuse cerebral symptoms should be investigated for the possibility of sleep-disordered breathing.
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PMID:Sleep apnea in patients with hemispheric stroke. 781 Nov 79

It has long been known, that irregular, heavy snoring and daytime sleepiness are common features of acromegaly. Only recently has the high incidence (30-60%) and clinical relevance of the sleep apnoea underlying these symptoms been recognized. Both diseases have a group of common symptoms and prognostic features: Increased cardiovascular and respiratory mortality, elevated incidence of hypertension, daytime sleepiness, decreased vitality, headaches and depression. These are very prominent in sleep apnoea and often reversible under treatment. In acromegaly their etiology has been widely unexplained and they commonly persist even when human growth hormone (hGH) levels remain normal after operative treatment. We report on 2 patients presenting with excessive daytime sleepiness and severe obstructive sleep apnoea caused by acromegaly. Both had macroglossia and hypertrophy of hypopharyngeal tissues regressive after surgical therapy. The average hGH-levels were 20 and 31 ng/ml before and 3 and 1.7 ng/ml several months after operation respectively. Apnoea indices and minimal oxygen saturations (SO2) were 59/h and 55/h, and 60% and 58% initially and improved postoperatively to 40/h and 50/h, and 72% and 70%. Polysomnographic parameters were normalized by NCPAP-therapy pre- and postoperatively and daytime sleepiness improved dramatically. In one patient the NCPAP-pressure could be decreased postoperatively. Since patients with sleep apnoea have an increased perioperative risk of hypoxia and because transsphenoidal operation and postoperative nasal tamponade were performed, both patients were tracheostomized perioperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnoea in acromegaly--prevalence, pathogenesis and therapy. Report on two cases. 783 Dec 13

This article provides an in-depth overview of the relationship between primary hypertension and adult obstructive sleep apnea syndrome. The background data and research are taken from the English-language literature through 1993. Primary hypertension is a common cause of major medical illnesses, including stroke, heart disease, and renal failure, in middle-aged males. Its prevalence in the United States is around 20%, with the rate of newly diagnosed hypertensive patients being about 3% per year. Sleep apnea syndrome is common in the same population. It is estimated that up to 2% of women and 4% of men in the working population meet criteria for sleep apnea syndrome. The prevalence may be much higher in older, non-working men. Many of the factors predisposing to hypertension in middle age, such as obesity and the male sex, are also associated with sleep apnea. Recent publications describe a 30% prevalence of occult sleep apnea among middle-aged males with so called "primary hypertension." Is this association fortuitous, related to a high prevalence of both diseases in the same population, or is it caused by a factor common to both diseases, such as obesity? Should the diagnosis of apnea be actively sought with sleep studies in hypertensive populations? If a diagnosis of "asymptomatic" sleep apnea is made in a hypertensive person, should the apnea be treated? Current research data provide only partial answers to these and other questions regarding the association of apnea and hypertension. Logic dictates that clinically symptomatic patients in hypertensive clinics should receive appropriate evaluation for apnea, but broad populations of hypertensive individuals should not be referred for sleep studies.
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PMID:The relationship between systemic hypertension and obstructive sleep apnea: facts and theory. 784 28

The association between snoring and blood pressure is still a matter for debate, partly because of uncertainty about the definition of snoring and partly because confounding factors may affect systemic blood pressure such as obesity, sleep apnoea, and nocturnal hypoxaemia. To isolate the contribution of each of these factors, 1415 patients (389 females, 1026 males) referred to a sleep disorders centre were studied. A full history was obtained with particular attention to cardiovascular disease and medications. The patients had nocturnal polysomnography including objective measurement of snoring, and blood pressure was measured in the morning. 18% of non-snores had hypertension as did 20% of heavy snores (not significantly different). Multivariate linear regression analysis showed that snoring was not a significant determinant of blood pressure. Only age, male sex, apnoea/hypopnoea index, and body mass index contributed significantly to the variability of blood pressure. We conclude that snoring in the absence of sleep apnoea is not associated with raised blood pressure.
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PMID:Blood pressure, snoring, obesity, and nocturnal hypoxaemia. 791 47

Nocturnal polysomnography, the standard diagnostic test for sleep apnea, is an expensive and limited resource. In order to help identify the urgency of need for treatment, we determined which clinical features were most useful for establishing an accurate estimate of the probability that a patient had sleep apnea. Of 263 physician-referred patients, 200 were eligible for the study and 180 (90%) completed it. All patients had their histories recorded with a standard questionnaire, and underwent anthropomorphic measurements and nocturnal polysomnography. Sleep apnea was defined as more than 10 episodes of apnea or hypopnea per hour of sleep. Multiple linear and logistic regression models predictive of sleep apnea were compared with physicians' subjective impressions and previously reported models. Likelihood ratios were calculated for several levels of a sleep apnea clinical score produced by one of the linear models. Predictors of sleep apnea in the final model (R2 = 0.34) included neck circumference, hypertension, habitual snoring, and bed partner reports of nocturnal gasping/choking respirations. This model was superior to physician impression, slightly inferior to more detailed linear and logistic models, and comparable to previously reported models. A sleep apnea clinical score of less than 5 had a likelihood ratio of 0.25 (95% CI: 0.15 to 0.42) and a corresponding posttest probability of 17%, while a score of greater than 15 had a likelihood ratio of 5.17 (95% CI: 2.54 to 10.51) and posttest probability of 81%. These likelihood ratios can simply and accurately determined the probability of whether a patient has sleep apnea.
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PMID:Likelihood ratios for a sleep apnea clinical prediction rule. 795 53


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