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

30 subjects of old and middle age (28 male, 2 female) with obstructive sleep apnea syndrome (OSAS) and 20 normal subjects with matchable age and body weight (14 male, 6 female) as control were studied with nocturnal polysomnography for at least 7 hours. Right arm blood pressure was determined in supine position before and after sleep. Meantime, three 8-hour urine specimens, two collected while awake and one during sleep were examined for urinary levels of epinephrine (E) and norepinephrine (NE) with fluorometric method. All OSAS subjects (mean apnea index 42.9) had significant arterial oxygen desaturation (mean 63.9%). 12/30 OSAS subjects had definit history of essential hypertension. They described that hypertension appeared months or years after the onset of sleep disorders. Before sleep the blood pressure in OSAS subjects was higher than that in controls (mean 133/90 mmHg versus 118/77 mmHg P < 0.001). After 7 hours of sleep with apnea events, the blood pressure rose to 149/100 mmHg (P < 0.001). whereas in the controls there was no change of statistic significance (mean 115/77 mmHg). A diurnal rhythm in free catecholamines excretion was apparent for both NE and E (P < 0.05) in the controls, while in OSAS there was no normal diurnal rhythm. 24-hour values of NE were remarkably higher than those in controls. It is known that up to 40% of OSAS subjects is in the population of essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Obstructive sleep apnea syndrome and essential hypertension: diurnal variation of urinary catecholamines]. 130 54

Many different hemodynamic changes can be observed during obstructive apneas in the nocturnal sleep period. The most significant changes are observed whenever apneas occur in rapid succession. Systemic, pulmonary, and wedge pressure are modified. Many of these changes are mediated through cholinergic mechanisms. The mechanical effort of breathing against a partially or completely obstructed airway may also have an impact on hemodynamics. This impact must be dissociated from the impact of hypoxemia and blood gas changes. It has been questioned whether obstructive sleep apnea syndrome (OSAS) has any significant role in the development of 24-hour hypertension. In support of this theory, we found that tracheostomy does eliminate hypertension in obstructive sleep apneic children. In adults the issue is more complicated. Hypertension was eliminated in a subgroup of our patients treated with tracheostomy or nasal continuous positive airway pressure (CPAP), although the total group had no statistically significant blood pressure differences. Many variables that might dissociate treatment responders from nonresponders are not available. Hypertensive patients whose blood pressure normalized with OSAS treatment were significantly less overweight than the nonresponders in our series. Patients who remained hypertensive after treatment did, however, develop a normal circadian blood pressure trough during nocturnal sleep.
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PMID:Sleep-related hemodynamics and hypertension with partial or complete upper airway obstruction during sleep. 147 Aug 3

Symptoms and signs in 12 patients with severe obstructive sleep apnea (OSA) syndrome have been presented. The most common symptoms were snoring , increased motor activity during sleep and excessive daytime somnolence. The factors predisposing to OSA syndrome were obesity and anatomic abnormalities of the upper airway structure. In some cases the signs of OSA syndrome included hypertension, right heart failure, chronic alveolar hypoventilation and polycythemia. Polysomnography showed sleep fragmentation and the prevalence of light sleep stages. Obstructive sleep apneas repeated 73 +/- 23 times per hour of sleep. The mean apnea duration was 19 +/- 8 s. The mean arterial oxygen saturation during apnea was 72 +/- 14%.
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PMID:[Diagnosis of obstructive sleep apnea syndrome]. 148 56

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

In order to assess the complications of sleep apnea, we have reviewed a data base of 619 consecutive admissions to a university sleep disorders center. Although patients with obstructive sleep apnea (OSA) described more subjective sleepiness than patients with central sleep apnea (CSA) or primary snoring (PS), the multiple sleep latency test (MSLT) indicated similar levels of physiologic sleepiness in the two apneic groups, which was greater than among those with PS. There was no significant relationship between individual subjective estimates of habitual sleepiness and the MSLT values. Among the OSA patients the mean minimum arterial oxygen desaturation during REM sleep accounted for 65 percent of the variance of the mean sleep latency on the MSLT, with an additional, smaller, contribution of the disordered breathing rate per hour. Subjective reports of sleepiness were associated with sleep efficiency and the number of disordered breathing events in NREM sleep. Patients with OSA or CSA had similar diastolic blood pressures and frequencies of history of treatment for hypertension, which were significantly higher in OSA than in the PS group. In the OSA group the absolute minimum arterial oxygen desaturation during NREM sleep was the most significant contributor to waking diastolic blood pressure, with an additional small contribution by weight. A history of treatment for hypertension was most strongly associated with weight, without significant additional contributions by measures of disordered breathing events or oxygen desaturation; however, weight was highly intercorrelated with measures of the apnea/hypopnea index and minimum arterial oxygen desaturation. In summary, these data support recent findings which show a close relation of obesity to a history of hypertension in OSA, and extend to this group a previous observation that in regular heavy snorers, there may be a disparity between levels of physiologic and subjective sleepiness.
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PMID:Sleepiness and hypertension in obstructive sleep apnea. 155 54

An association between chronic high blood pressure and obstructive sleep apnea has been described. We hypothesized that repetitive episodic hypoxia patterned after the hypoxia seen in sleep apnea could contribute to diurnal elevation of blood pressure. Using 12-second infusions of nitrogen into daytime sleeping chambers, four groups of male rats (250-375 g) were subjected to intermittent hypoxia (3-5% nadir ambient oxygen) every 30 seconds, 7 hours per day for up to 35 days. In one group, blood pressure was measured weekly by the tail-cuff method in conscious animals during 5 weeks of episodic hypoxia. In the other three groups, blood pressure was measured in conscious animals via femoral artery catheters at baseline and after 20, 30, or 35 days of exposure. Additional groups served as controls: two sham groups housed in identical "hypoxia" chambers received compressed air instead of nitrogen (35 days) while two other groups remained unhandled in their usual cages (35 days). Both groups challenged with 35 days episodic hypoxia showed significant increases in blood pressure compared with controls: the tail-cuff rats showed a 21 mm Hg increase in systolic pressure (p less than 0.05) and the intra-arterially measured rats a 13.7 mm Hg increase in mean arterial pressure (p less than 0.05). The 30-day exposed rats also showed a 5.7 mm Hg increase in mean pressure over baseline (p less than 0.05). Blood pressure did not change significantly from baseline in the control groups. Left ventricle-to-body weight ratio was higher in both 35-day exposed groups than in unhandled or sham controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Repetitive, episodic hypoxia causes diurnal elevation of blood pressure in rats. 159 51

To investigate the long-term outcome of therapy and clinical symptoms of patients with OSAS (obstructive sleep apnea syndrome) in Japan, we studied 34 patients with OSAS who had been diagnosed by standard polysomnography more than one years (36.0 +/- 19.7 months: mean +/- SD) previously. They were 53.8 +/- 10.5 years old, body mass index was 27.8 +/- 5.2 kg/m2, and AHI (apnea & hypopnea index) was 50.0 +/- 24.2/h. The subjects had achieved weight loss (p less than 0.01), but had regained their initial weight at our follow-up. Eleven patients with OSAS were initially candidates for NCPAP (nasal continuous positive airway pressure), but only 5 patients used it for a prolonged time. The other 6 patients with OSAS could not use NCPAP because they did not wish to purchase a NCPAP instrument. One of 5 patients who used NCPAP for a long time died from lung cancer; thus, 4 patients used NCPAP continuously. Ten patients were commenced on ACZ (acetazolamide); however, only 5 patients took it continuously. ACZ resulted in some improvements in the sleep parameters (AHI index, desaturation time below SaO2 90%), but apnea & hypopnea duration and the difference in transcutaneous PCO2 between wake and sleep were not significantly improved by ACZ administration. ACZ was not as effective as NCPAP. Almost 60% of patients with OSAS had excessive daytime sleepiness. Hypertension was detected in about 60% of patients. Nine of 25 patients who had an automobile license had had more than one automobile accident. Nine patients who had had more than one automobile accident showed AHI greater than or equal to 30 in our study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy and clinical symptoms in patients with obstructive sleep apnea in Japan]. 160 58

Increasing evidence suggests that snoring and sleep apnea are associated with cerebrovascular diseases. Several other factors may be involved in this association because many established or potential risk factors for stroke are related to snoring and sleep apnea. These include arterial hypertension, coronary heart disease, age, obesity, smoking, and alcohol consumption. Recent epidemiologic and clinical studies indicate, however, that snoring can increase the risk of stroke independently of these confounding factors. Accumulating epidemiologic evidence of long-term harmful effects of the obstructive sleep apnea syndrome appears to be related to increasing vascular morbidity and mortality. Potential mediators among snoring, obstructive sleep apneas, and stroke include cardiac arrhythmias and other hemodynamic disturbances, increased levels of catecholamines, and disturbances in cerebral blood flow caused by sleep apneas, as well as hypoxemic periods that may potentiate atherosclerosis.
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PMID:Snoring, sleep apnea syndrome, and stroke. 163 Jun 43

To investigate the impact of sleep-disordered breathing events on daytime hypertension (HT) in patients with increased upper airway resistance during sleep, we studied 191 male snorers aged 49.9 +/- 0.8 years. In 116 of them, an apnea-hypopnea index (AHI) above 10--defined as the presence of obstructive sleep apnea (OSA)--was found; the other 75 subjects had an AHI lower than 10 and were classified as habitual snorers (HSN). Prevalence of HT was not different between OSA (56 of 116 = 48 percent) and HSN (33 of 75 = 44 percent) and there was also no difference in systolic, diastolic, and mean blood pressures between the two groups. Hypertensive OSA patients had higher body mass index (BMI) than normotensive OSA subjects (31.4 +/- 0.7 vs 29.4 +/- 0.6; p less than 0.05), but there was no difference in age, AHI, and nocturnal oxygenation parameters. The same was true for the HSN group, with hypertensive subjects being more obese than normotensive subjects (BMI: 30 +/- 0.8 vs 27.3 +/- 0.8; p less than 0.05), but no difference in age and polysomnographic features. Discriminant analysis with HT as the classification variable and age, BMI, AHI, mean, and lowest nocturnal oxyhemoglobin saturation as independent variables, revealed an independent influence on HT only for BMI (F-prob = 0.001). Thus, our results stand against the hypothesis of a causal relationship between sleep-disordered breathing events and daytime hypertension. We conclude that the high prevalence of HT in male snorers is more directly linked to obesity than to sleep apnea, but an independent effect of snoring per se cannot be excluded.
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PMID:Systemic hypertension in snorers with and without sleep apnea. 164 15

Recent studies about renal function and volume regulating hormones in obstructive sleep apnea (oSAS) indicate complex disturbances in volume homeostasis. Increased nocturnal secretion of atrial natriuretic peptide (ANP) and decreased renin secretion during apnea looks similar to a situation seen during hypervolemia or increased cardiac volume load. Increased venous return induced by pathologically high negative intrathoracic pressure during obstructive apnea may be the cause. Since during wakefulness no true hypervolemia is present, a "pseudohypervolemia" or "central hypervolemia" must exist caused by volume shift from the peripheral to the central compartment during apnea. Since volume homeostasis and blood pressure regulation are complexly connected the question arises whether disturbances in volume homeostasis play a role in the pathogenesis of arterial hypertension in sleep apnea. In a subgroup of hypertensive patients hypertension is salt-sensitive and volume dependent; it is called volume-expanded or low-renin hypertension. An inhibitor of the Na+/K(+)-ATPase acting via the digitalis receptor - called digitalis like factor (DLF) - is regarded as the causative agent for the development of hypertension in these cases. From this background, we were interested in the question whether DLF may be the linkage between disturbances in volume homeostasis and the pathogenesis of hypertension in sleep apnea. We could demonstrate a decrease of nocturnal urinary excretion of DLF during nasal continuous positive air pressure (nCPAP) therapy. Since a positive correlation between changes in diuresis respectively natriuresis and DLF excretion was found, we suggested DLF to be involved in changes of renal function in sleep apnea besides ANP. In 3 patients we measured nocturnal plasma levels of DLF and renin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbances in volume regulating hormone system--a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome? 165 Sep 45


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