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

Fifty-one middle-aged male patients with obstructive sleep apnea syndrome (OSAS) were evaluated using two-dimensional echocardiography, 24-h blood pressure measurements, polysomnography, and plasma norepinephrine (NE) measurements. Among these patients, left ventricular hypertrophy (LVH) (left ventricular posterior wall thickness [LVPWT] or interventricular septal thickness [IVST] > or = 12 mm) and right ventricular hypertrophy (RVH) (right ventricular wall thickness [RVT] > or = 5 mm) were present in 41.2% (21/51) and 11.8% (6/51). LVH was present in 50.0% of group 2 patients (apnea index > or = 20) and in 30.5% of group 1 patients (apnea index < 20). All patients with LVH had hypertension. RVH was present in 21.4% of group 2 patients and none of the group 1 patients. IVST, LVPWT, LV mass, LV mass/body surface area (BSA), and obesity index were significantly greater in group 2 than in group 1. Apnea index and the duration in which nocturnal oxygen saturation was decreased under 90% (duration of SaO2 < 90%), were significantly correlated with LV mass/BSA and 24-h mean blood pressure. Apnea index, number of apneas, duration of nocturnal oxygen saturation less than 90%, weight, and obesity index were significantly greater in patients with both LVH and RVH than in patients without LVH and RVH, or those with only LVH. Plasma NE after waking significantly increased compared with that before sleep (p < 0.05). The ratio of plasma NE levels after waking to those before sleep was significantly correlated with the duration of SaO2 < 90% (r = 0.83, p < 0.05), but not with apnea index. These results suggest that frequent episodes of oxygen desaturation and/or arousal responses caused by apnea may contribute to the complication of LVH and RVH in the long term, and apnea-induced cyclical increases in blood pressure and the resulting sustained elevation in blood pressure associated with the increase in afterload and sympathetic activity may play a role in the development of LVH.
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PMID:Cardiac hypertrophy in obstructive sleep apnea syndrome. 778 43

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

Obstructive sleep apnea syndrome (OSAS) is a major health problem, not only because of its consequences in terms of morbidity and mortality, but also because of its social impact in the form of car accidents and industrial accidents. These facts stress the necessity of screening OSAS among the population, particularly in patients suffering from obesity or hypertension, diseases frequently associated with OSAS. This review will focus on the epidemiology and the pathophysiology of this syndrome, its clinical features with a view to screening OSAS, and the main examination used to confirm the diagnosis. The management of OSAS will be discussed.
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PMID:Obstructive sleep apnea syndrome: a frequent complication of obesity. 799 78

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53

1. Obstructive sleep apnoea and snoring are associated with daytime hypertension. It is uncertain whether this association is directly due to the disturbed sleeping respiration or the result of confounding variables, particularly obesity, smoking and alcohol intake. 2. Ambulatory blood pressure and echocardiographic left ventricular muscle mass were measured in 19 patients with obstructive sleep apnoea, 19 men who snore without apnoea and 38 control subjects matched for age, sex, body mass index, smoking and alcohol intake. Ambulatory blood pressure was also measured before and after treatment in 11 patients with obstructive sleep apnoea and their matched control subjects. 3. Compared with matched control subjects, untreated obstructive sleep apnoea and snoring were not associated with an increase in daytime blood pressure. A daytime elevation of either systolic or diastolic blood pressure of > 3.8 mmHg due to obstructive sleep apnoea or snoring was excluded with 95% confidence in each of the study groups. Daytime blood pressure was also unchanged when obstructive sleep apnoea was treated with nasal continuous positive airway pressure. Night-time blood pressure was not significantly different in the patients with obstructive sleep apnoea or the snorers when compared with their matched control subjects. However, a fall in night-time systolic blood pressure was seen in the patients with obstructive sleep apnoea after treatment [fall in systolic blood pressure -6.3 (SD 8.2) mmHg, P < 0.02]. 4. Left ventricular diameter, wall thickness and calculated mass were similar in each of the study groups and their matched control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ambulatory blood pressure and left ventricular hypertrophy in subjects with untreated obstructive sleep apnoea and snoring, compared with matched control subjects, and their response to treatment. 816 36

Obstructive sleep apnea affects millions of individuals. It usually is due to pharyngeal collapse during sleep, resulting in daytime somnolence. This can have grave consequences on everyday life and in the long term can lead to pulmonary and systemic hypertension, myocardial disease, and stroke. Non-structural obstructive sleep apnea can be relieved by tracheostomy and continuous positive airway pressure, two methods that bypass the overly compliant pharyngeal musculature during inspiration. It may well be desirable to exchange a dynamic and more physiologic approach to obstructive sleep apnea for these purely static solutions. This approach should restore disturbed cyclical stiffening of the upper airway by electronically stimulating the appropriate muscles, timed by information originating during the inspiratory effort. The open-loop systems proposed here are based upon principles pioneered by us for the rehabilitation of the paralyzed larynx that are now well within practical reach of current technologies.
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PMID:The potential for neurostimulation in obstructive sleep apnea. 818 85

A 60-year-old obese woman was admitted for evaluation of excessive daytime sleepiness, loud snoring, cyanosis, systemic edema, hypertension and diabetes mellitus. Laboratory examination showed severe hypoxemia, hypercapnea, metabolic alkalosis, hypokalemia and hyperaldosteronism. CT scan showed a left adrenal tumor. A diagnosis of obstructive sleep apnea syndrome associated with primary aldosteronism was established. Metabolic alkalosis, hypokalemia and sodium retention due to hyperaldosteronism were thought to be factors exacerbating her sleep apnea.
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PMID:[A case report of obstructive sleep apnea syndrome associated with primary aldosteronism]. 818 53

Sleep disordered breathing has increasingly been recognised as a frequent cause of ill-health in the community. Moderate or severe forms of the most common condition, obstructive sleep apnea (OSA), occur in up to 12% of the adult male population. A substantial body of literature has been published on the potential relationship between OSA and cardiovascular disease. In particular, OSA has been associated with cardiac failure, stroke, myocardial infarction and hypertension. Part of this association may be explained by other confounders, mainly obesity, which is common in OSA patients. The present review was prepared following a workshop aimed to critically review available scientific evidence suggesting that hypertension is a direct consequence of OSA. In addition, pathophysiologic mechanisms that may be involved in the relationship between OSA and cardiovascular disease, particularly brief intermittent elevation of blood pressure and sustained systemic hypertension, are discussed.
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PMID:Obstructive sleep apnea and blood pressure elevation: what is the relationship? Working Group on OSA and Hypertension. 820 10

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, cranio-facial 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 cardio-circulatory 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 apneas. A clinical and laboratory study]. 828 15

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


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