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

Sleep-related breathing disorders can strain the cardiovascular system. Link-ups with arterial hypertension have been confirmed in obstructive or mixed sleep apnoea which is characterised by discontinuous nocturnal snoring. On the other hand, it is known that arterial hypertension is very frequently seen in snorers. The present study deals with short-term, breathing-related blood pressure patterns and blood pressure changes during the snoring phase. 18 obstructive snoring phases were identified in 4 male patients aged 50 years (42-65), Broca index 136 (119-171). Polysomnographic measurements were carried out in the sleep laboratory and the blood pressure was continuously recorded via the a. brachialis. The short-term breathing-dependent blood pressure changes were systolic 10.8 (10-30) mmHg at the beginning and 17.5 (10-30) mmHg at the end of the snoring phase (P less than 0.01). Diastolically there was a difference of 9.4 (5-15) mmHg versus 13.9 (5-25) mmHg (P less than 0.01). During the snoring phases the systolic blood pressure increased from 140.3 (120-190) mmHg to 170.0 (145-235) mmHg and the diastolic pressure from 69.7 (50-110) mmHg to 93.1 (70-120) mmHg. The study proves that blood pressure increases occur not only in apnoeic snoring but also in continuous obstructive snoring. It is suspected that these changes are responsible for the high frequency of arterial hypertension among continuous snorers.
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PMID:[Increase in blood pressure due to continuous obstructive snoring]. 186 14

15 patients with obstructive sleep apnea syndrome and arterial hypertension (H-OSAS), 25 normotensive patients with sleep apnea syndrome (N-OSAS) and 20 healthy age-matched controls (C) were included in this study. Ventilatory responses to activation (hypoxia) and inactivation (hyperoxia) of carotid chemoreceptors were studied in all subjects. Relationship between hypoxic ventilatory reactivity and nocturnal bradycardia during apnea-phases was analysed in both groups of patients. Results and conclusions. 1. We found an impairment of ventilatory response to hypoxia in H-OSAS and N-OSAS patients. However, the increase in ventilation in response to hypoxia was significantly greater in H-OSAS as compared to N-OSAS patients. 2. An augmented ventilatory response to inactivation of carotid chemoreceptors (the decrease in ventilation), observed in H-OSAS patients, indicates an increase in resting peripheral chemoreceptors drive in this group of patients. 3. The relationship between ventilatory response to hypoxia and nocturnal bradycaria in obstructive sleep apnea patients suggests, that hypoxic reactivity of arterial chemoreceptors might be involved in the origin of bradycardia during apnea events.
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PMID:Peripheral chemoreceptor reflex in obstructive sleep apnea patients; a relationship between ventilatory response to hypoxia and nocturnal bradycardia during apnea events. 186 15

To determine if a history of snoring is a risk factor for brain infarction, I conducted a case-control study of risk factors for ischemic stroke using 177 consecutive male patients aged 16-60 (mean 49) years with acute brain infarction. For each patient I chose an age-matched (+/- 6 years) male control. Arterial hypertension, coronary heart disease, snoring (habitually or often), and heavy drinking (greater than 300 g/wk) were risk factors in the stepwise multiple logistic regression analysis. The odds ratio of snoring for brain infarction was 2.13. By McNemar's test this association increased strongly if a history of sleep apnea, excessive daytime sleepiness, and obesity were all present with snoring (odds ratio 8.00). My study indicates that snoring may be a risk factor for ischemic stroke, possibly because of the higher prevalence of an obstructive sleep apnea syndrome among snorers than nonsnorers.
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PMID:Snoring and the risk of ischemic brain infarction. 186 48

1. Given the unexplained frequent association between systemic hypertension and obstructive sleep apnoea (OSA), the secretion of prostanoids during sleep was investigated (more specifically, the ratio of prostacyclin (PGI2) to thromboxane A2 (TxA2), since they have marked opposite effects on vascular tone). Prostacyclin has vasodilating effects, whereas thromboxane results in vasoconstriction. 2. In 11 OSA drug-free male patients (age 53 +/- 2 years, mean +/- s.e.m.; apnoea index 55 +/- 15 apnoeas/hour of sleep; body mass index 31 +/- 2 kg/m2), we measured the urinary excretion during sleep of 6-keto-PGF1-alpha and of thromboxane TxB2 (the stable metabolites of prostacyclin PGI2 and of thromboxane A2 respectively). This was done on two consecutive nights; one untreated, the other with nasal continuous positive airway pressure (CPAP) treatment. The results were compared with those of nine normal unobese male subjects. 3. The urinary ratio of 6-keto-PGF1-alpha to TxB2 was significantly (P less than 0.001) lower in the untreated OSA patients (1.7 +/- 0.2) than in the controls (3.1 +/- 0.3). It significantly increased with CPAP treatment to 2.3 +/- 0.2, P less than 0.02, which was no longer different from the controls. 4. These results suggest that OSA is associated with an abnormal release of prostanoids during sleep resulting in a decrease of the prostacyclin to thromboxane ratio which potentially has a vasoconstricting effect. The relationship between these changes and the systemic hypertension often observed in OSA patients remains to be established.
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PMID:Urinary excretion of prostanoids during sleep in obstructive sleep apnoea patients. 191 53

Arterial blood pressure patterns in 12 men with sleep apnea and arterial hypertension were studied at baseline and after 6 months' therapy with nasal continuous positive airway pressure (nCPAP). Preexisting antihypertensive medication was discontinued 1 week before baseline measurements. Weight did not change during the study period; body mass index was 29.3 (range, 25.4-38.5) vs. 29.3 (25.0-38.5). During therapy the apnea index decreased from 58 (range 30-73) to 2 (range 0-7) apneic episodes per hour (p less than 0.01). Intra-arterial systolic (BP sys.) and diastolic (BP dias.) blood pressure and heart rate decreased during therapy (p less than 0.001). Mean values +/- 95% confidence intervals were as follows: BP sys., 147.1 (+/- 1.6) mm Hg vs. 126.4 (+/- 1.5) mm Hg; BP dias., 81.6 (+/- 0.8) mm Hg vs. 69.4 (+/- 0.6) mm Hg; heart rate, 68.8 (+/- 0.7) beats/min vs. 65.4 (+/- 0.7) beats/min. Furthermore, the variability of these parameters decreased during therapy: variability BP sys., 53.8 (+/- 1.1) mm Hg vs. 25.6 (+/- 1.1) mm Hg; variability BP dias., 35.6 (+/- 0.7) mm Hg vs. 17.9 (+/- 0.7) mm Hg; variability of heart rate, 28.1 (+/- 0.7) beats/min vs. 14.9 (+/- 0.7) beats/min (p less than 0.001). During treatment we found that blood pressure scores already dropped during the awake phase, with a further decrease during non-REM and REM sleep (p less than 0.001). Our results, which demonstrate the reversibility of high blood pressure upon treatment of sleep apnea, indicate that sleep apnea can be an etiological factor in hypertension. Sleep apnea should therefore be considered in the differential diagnosis of arterial hypertension.
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PMID:Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy. 193 70

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)
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PMID:[Nocturnal continuous measurement of blood pressure in sleep apnea syndromes. Comparison between normotensive and hypertensive patients]. 195 62

To examine the hypothesis that sleep apnoea is a risk factor for ischaemic heart disease, overnight polysomnography was performed in 101 unselected male survivors of acute myocardial infarction (MI) aged less than 66 yr and in 53 male subjects of similar age without evidence of ischaemic heart disease. The apnoea index (AI, number of apnoea episodes per hour of sleep) was 6.9 (SEM 1.2) in the MI patients versus 1.4 (0.3) in the control subjects. After adjustment for age, body mass index, hypertension, smoking, and cholesterol level, multiple logistic regression analysis identified the top quartile of AI (greater than 5.3) as an independent predictor of MI patients. The relative risk for myocardial infarction between the highest and lowest quartiles of AI was 23.3 (95% confidence interval 3.9-139.9).
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PMID:Association of sleep apnoea with myocardial infarction in men. 197 82

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92

Ambulatory blood pressure monitoring can determine the average blood pressure level and the short- and long-term blood pressure variability (circadian rhythm). The circadian blood pressure rhythm appears to be mediated mainly by the circadian rhythm of the sympathetic tone which is linked to changes in physical and mental activity, e.g. the waking-sleeping cycle. A statistically significant circadian blood pressure rhythm was observed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, in patients with Cushing's syndrome, under glucocorticoid treatment, or with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, spinal cord injury, brainstem lesions, diabetic neuropathy, uremic neuropathy, etc), chronic renal failure, eclampsia, malignant hypertension, sleep apnea syndrome or systemic atherosclerosis, the normal circadian blood pressure rhythm appears to be eliminated or reversed, while in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, diabetes insipidus, acromegaly, hyperparathyroidism or hyperprolactinemia, the nocturnal blood pressure fall has been observed as in normal subjects. The alteration in the circadian blood pressure rhythm was observed with different pathophysiological conditions, although no specific pattern was observed for any condition. A disturbance in any part of the hierarchy of factors that regulate the circadian rhythm of sympathetic neural tone seems to disturb the circadian blood pressure rhythm. We conclude that ambulatory blood pressure monitoring is not critically important in the diagnosis of secondary hypertension although it does help in screening for secondary hypertension.
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PMID:Does ambulatory blood pressure monitoring improve the diagnosis of secondary hypertension? 208 1

The daily variation in blood pressure (circadian blood pressure rhythm) is characterized by a nocturnal fall and a diurnal rise. The circadian blood pressure rhythm seems to be mediated mainly by the circadian rhythm of sympathetic tone, linked to changes in physical and mental activities, e.g. the waking-sleeping cycle. Statistically significant circadian blood pressure rhythms have been confirmed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, the normal pattern of circadian blood pressure rhythm is reversed in elderly people and in those with Cushing's syndrome, those undergoing glucocorticoid treatment, and those with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, tetraplegia, diabetic or uremic neuropathy, etc), chronic renal failure, renal or cardiac transplantation, congestive heart failure, eclampsia, sleep apnea syndrome, malignant hypertension, systemic atherosclerosis and accelerated hypertensive organ damage. However, in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, or those with cardiac pacing, a nocturnal blood pressure fall is ordinarily observed. It may be that a fall in cardiac output rather than in peripheral resistance may be mainly responsible for the nocturnal fall in blood pressure. It also seems that a nocturnal heart rate fall is not responsible for it, since the nocturnal blood pressure fall remained unchanged in patients undergoing cardiac pacing and was disturbed in patients with Cushing's syndrome or hyperthyroidism in whom the circadian heart rate rhythm remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian blood pressure variations under different pathophysiological conditions. 209 80


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