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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Recent studies of obstructive sleep apnea and its comorbidity with other systemic diseases have stimulated interest in the relationship of apnea to renal disease and hypertension. Polysomnographic sleep studies in patients on dialysis who complain of day-time fatigue or sleepiness reveal significant apnea in up to 73% of those studied. Abnormalities in respiratory controller mechanisms from chronic hypocarbia, metabolic acidosis, and uremic toxins have been blamed for the occurrence of apnea in this setting. Proteinuria and sometimes nephrotic syndrome have been recognized in morbidly obese patients with sleep apnea syndrome. Renal biopsies of such patients have shown glomerulomegaly and focal segmental sclerosis. It is postulated that these lesions may result from increased glomerular filtration and blood flow. Elevated urine output, sodium and chloride excretion, and atrial natriuretic peptide have been well demonstrated in obstructive apnea patients and correct to control levels with treatment of the apnea. Both acute (with each apnea) and chronic daytime blood pressure elevation are frequently observed in sleep apnea patients, and occult sleep apnea is postulated as one possible cause of "primary" hypertension in middle-aged men. In younger patients, such hypertension seems to be more reversible with the elimination of apnea. In older patients, however, the cure of systemic hypertension cannot be guaranteed with the elimination of the apnea, and asymptomatic apnea patients tend not to tolerate the bother and discomfort of apnea treatment with nasal continuous positive airway pressure. Therefore, aside from a careful history regarding sleep symptomatology, polysomnographic studies of clinic populations with primary hypertension to search for apnea as a cause cannot be recommended.
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PMID:Obstructive sleep apnea and the kidney. 830 38

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

A marked transient increase in blood pressure can occur at the end of each apneic period in patients with sleep apnea syndrome (SAS) and SAS may be a risk factor for cerebrovascular disease. To estimate blood pressure variability during apnea arterial blood pressure was directly and continuously recorded, and the transient increase in blood pressure in each sleep stage was assessed. Polysomnography was done in 5 men with SAS: arterial blood pressure, oxygen saturation, and respiratory curves were recorded. The maximum arterial blood pressure during the apneic period was compared with that at the end of apnea. The transient increase in blood pressure was 32.2 +/- 5.8 mmHg (mean +/- S.E.) for systolic pressure and 18.2 +/- 2.1 mmHg for diastolic pressure. During REM sleep, the values were 38.8 +/- 6.6 mmHg for systolic pressure and 23.4 +/- 2.2 mmHg for diastolic pressure. The increase in arterial blood pressure was significantly higher during REM sleep than during N-REM sleep (p < 0.05). This wide variation in blood pressure suggests that SAS is a risk factor for cerebrovascular disease, and that SAS may promote essential hypertension.
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PMID:[Relationship between sleep stage and blood pressure variability during apnea in patients with sleep apnea syndrome]. 853 85

It has been speculated for some time that various antihypertensive medications may have a deleterious effect on respiration during sleep and thereby enhance the apparent association between hypertension and sleep apnea/hypopnea (SAH). However, there are few data to support this contention. The present study used a double-blind, randomized, cross-over design to contrast the effects of 6 weeks treatment with alpha-methyldopa and the combination of hydrochlorothiazide and amiloride with that of amlodipine and the combined diuretics in a group of 24 newly diagnosed patients with primary hypertension. All-night polysomnography was performed before the initiation of therapy (baseline) and at the end of the two treatment periods. Respiratory variables failed to reveal any significant differences between the treatments and baseline, or between the two different treatment regimens. The two treatment regimens achieved similar reductions in blood pressure. The prevalence of SAH was 25% before treatment, which is comparable to a prevalence of 20% in a similar group drawn from the same population but receiving various antihypertensive medications. The findings of this study are in agreement with previous reports using other classes of antihypertensive drugs that also failed to detect any tendency for increases in nocturnal respiratory disturbance indices over assessment periods of 8 weeks or shorter.
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PMID:Short-term antihypertensive medication does not exacerbate sleep-disordered breathing in newly diagnosed hypertensive patients. 919 10

The aim of the presented pilot study was to compare urinary excretion of two plasma proteins similar in molecular mass and isoelectric point: albumin and alpha-1-antitrypsin (AAT) in patients with different forms of arterial hypertension and in healthy subjects. The 24-h urinary excretion of albumin and AAT were assessed in 52 patients, 29 with essential hypertension and 23 with secondary hypertension, caused by renovascular hypertension, adrenal phaeochromocytoma and obturative sleep apnoea syndrome. The concentrations of albumin and AAT were determined by rocket immunodiffusion. An increase of mean albumin and AAT urinary excretion was demonstrated, as compared to the control group, both in the patients with essential hypertension and with secondary hypertension. In 93.2% of the healthy subjects no AAT presence in urine was detected. No correlation was found between the excretion of albumin and AAT with urine.
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PMID:Comparison of urinary excretion of albumin and alpha-1-antitrypsin in patients with arterial hypertension. 1035 22

Obstructive sleep apnea syndrome is characterized by obesity, nocturnal breathing abnormalities, arterial hypertension, and an increased number of cardiovascular events. Sympathetic activity is increased during nocturnal apneic episodes, which may mediate the cardiovascular complications of sleep apnea. We studied 15 male subjects with obstructive sleep apnea syndrome and associated hypertension, 54 subjects with mild to moderate essential hypertension, and 25 healthy normotensive men. Cardiovascular autonomic control was assessed using frequency domain measures of heart rate variability (HRV) during a controlled breathing test and during orthostatic maneuver. Compared with normotensive and hypertensive groups, total power and low- and high-frequency components of HRV during controlled breathing were significantly (analysis of variance, p<0.0001) lower in the obstructive sleep apnea syndrome. During the orthostatic maneuver, the change in total power of HRV was different between the 3 groups (analysis of variance, p = 0.004). The total power of HRV tended to increase in the normotensive (4.11+/-12.29 ms2) and in hypertensive (2.31+/-12.65 ms2) groups, but decreased (1.13+/-1.23 ms2) in the hypertensive group with obstructive sleep apnea syndrome. According to multivariate regression analysis, age and sleep apnea were the major independent determinants of HRV. This study found that an abnormal response to autonomic nervous tests characterizes hypertension in overweight subjects with obstructive sleep apnea syndrome. This could be due to autonomic withdrawal or supersaturation of the end-organ receptors by excessive and prolonged sympathetic stimulation. Our results also show the reduced response of orthostatic maneuver and controlled breathing in the hypertensive group compared with the normotensive group.
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PMID:Comparison of autonomic withdrawal in men with obstructive sleep apnea syndrome, systemic hypertension, and neither condition. 1095 83

Sleep apnea syndrome (SAS) is an important cardiovascular risk factor in patients with hypertension or myocardial infarction (MI). We evaluated the influence of SAS on autonomic nervous activity and QT dispersion in patients with hypertension or coronary artery disease with old MI. A portable sleep polygraph was attached to 30 healthy volunteers (N group), 30 patients with essential hypertension (HT group), and 30 patients with old myocardial infarction (MI group) to serially record oronasal respiration, tracheal sound, thoracic respiratory movement, and percutaneous arterial oxygen saturation. In addition, a digital Holter ECG was used to examine heart rate variability during nighttime sleep. Heart rate variability was analyzed by obtaining low-frequency (LF) power, high-frequency (HF) power, the LF/HF ratio, and very low-frequency (VLF) power. Dispersion of QT intervals was obtained by CM5 and CM1 leads. VLF and LF powers were significantly higher in the HT-SAS group (hypertensive patients with SAS) than the N and HT-NSAS groups (hypertensive patients without SAS). The HF power was significantly lower in the HT-NSAS group than the N group, but the decrease in HF power in hypertension was not observed in the HT-SAS group. The LF/HF ratio was significantly higher in the HT-NSAS group than the N group, and this value was further increased in the HT-NSAS group. Percutaneous arterial oxygen saturation was decreased, and QT dispersion was significantly increased in the MI group during sleep apnea episodes. More severe autonomic nervous dysfunction and increased QTc dispersion were observed in hypertensive patients with SAS during episodes of apneas and hypopneas compared to those without SAS. These findings suggest that SAS may be associated with the future development of cardiac events.
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PMID:Influence of sleep apnea on autonomic nervous activity and QT dispersion in patients with essential hypertension and old myocardial infarction. 1513 67

Obesity and associated medical conditions may have an impact on morbidity and even mortality in patients with psychiatric disorders. The authors present the results of a survey of the prevalence of obesity and selected medical conditions among 420 consecutively admitted psychiatric inpatients at a long-stay facility and compare these data with those reported in the literature. Female psychiatric subjects had considerably higher rates of being either overweight or obese (69%) as compared to women in the general U.S. population (51%). Male psychiatric subjects did not differ significantly from their counterparts in the general population in being overweight or obese (nearly 55%). The majority of psychiatric subjects with essential hypertension, diabetes mellitus, dyslipidemias, cardiovascular disease, or sleep apnea were either overweight or obese (72%-87%). In this cross-sectional study, no associations could be deduced between psychotropic drug classes and specific medical conditions. No specific psychiatric diagnostic category was associated with a significantly greater prevalence of any specific medical condition, except that subjects with schizoaffective disorder appeared to have a higher prevalence of type II diabetes mellitus (11.6%). Subjects with predominant substance or alcohol abuse or dependence disorders had a lower prevalence of obesity and associated medical conditions.Obesity-either independently or additively along with a sedentary lifestyle, unhealthy dietary habits, and nicotine dependence-may have a serious impact on coexisting medical comorbidity in psychiatric patients. Judicious monitoring for obesity and rapid pharmacological and nonpharmacological intervention, where appropriate, by concerned clinicians may improve several coexisting medical conditions in psychiatric patients and thereby improve patients' overall quality of life.
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PMID:Obesity and medical illnesses in psychiatric patients admitted to a long-term psychiatric facility. 1599 May 58

The insulin resistance syndrome (IRS) is considered to be a new target of risk-reduction therapy. The IRS is a cluster of closely associated and interdependent abnormalities and clinical outcomes that occur more commonly in insulin-resistant/hyperinsulinemic individuals. This syndrome predisposes individuals to type 2 diabetes, cardiovascular diseases, essential hypertension, certain forms of cancer, polycystic ovary syndrome, nonalcoholic fatty liver disease, and sleep apnea. In patients at high risk for cardiovascular diseases, endothelial dysfunction is observed in morphologically intact vessels even before the onset of clinically manifest vascular disease. Indeed, there are several lines of evidence that indicate that endothelial function is compromised in situations where there is reduced sensitivity to endogenous insulin. It is well established that a decreased bioavailability of nitric oxide (NO) contributes to endothelial dysfunction. Furthermore, NO may modulate insulin sensitivity. Activation of NO synthase (NOS) augments blood flow to insulin-sensitive tissues (i.e. skeletal muscle, liver, adipose tissue), and its activity is impaired in insulin resistance. Inhibition of NOS reduces the microvascular delivery of nutrients and blunts insulin-stimulated glucose uptake in skeletal muscle. Furthermore, induction of hypertension by administration of the NOS inhibitor NG-monomethyl-L-arginine is also associated with insulin resistance in rats. Increased levels of asymmetric dimethylarginine (ADMA) are associated with endothelial vasodilator dysfunction and increased risk of cardiovascular diseases. An intriguing relationship exists between insulin resistance and ADMA. Plasma levels of ADMA are positively correlated with insulin resistance in nondiabetic, normotensive people. New basic research insights that provide possible mechanisms underlying the development of insulin resistance in the setting of impaired NO bioavailability will be discussed.
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PMID:Insulin resistance: potential role of the endogenous nitric oxide synthase inhibitor ADMA. 1644 67


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