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

The mechanism of pathogenesis of hypertension in patients with obstructive sleep apnea (OSA) is unknown. Many investigators point to the high sympathetic nervous system activity (SNS) observed in OSA patients. However, there is no clear explanation as to the mechanism for the development of SNS hyperactivity in these patients. A common feature of patients with OSA is repetitive bouts of transient hypoxemia during sleep. Repetitive transient hypoxemia in rats has resulted in hypertension. In OSA patients, resolution of nocturnal hypoxemia with CPAP has corrected nocturnal and diurnal hypertension. Also, exposure to hyperoxia reduces blood pressure and sympathetic activity in OSA patients, but not in normals. These data suggest a significant role of peripheral chemoreceptors in the regulation of vascular tone. We hypothesize that peripheral chemoreceptors significantly contribute to the pathogenesis of hypertension in patients with OSA and that this is associated with chemoreceptor hyperactivity. This implies that correcting the intermittent nocturnal hypoxemia alone may prevent the cardiovascular morbidity associated with obstructive sleep apnea.
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PMID:Obstructive sleep apnea and hypertension: are peripheral chemoreceptors involved? 1113 49

In the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of repetitive episodes of hypoxia, hypercapnea, arousals, and a striking surge in sympathetic excitation, and altered baroreflex control during sleep. Obstructive sleep apnea (OSA) may lead to the cardiac arrhythmias and myocardial ischemia and it is a possible risk factor for stroke. We confirmed that nasal CPAP has been shown to lower blood pressure in some hypertensive OSA patients. Early recognition and treatment of sleep-apnea may improve cardiovascular function.
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PMID:[Nasal CPAP treatment and hypertension and altered cardiovascular variability associated with obstructive sleep apnea (OSA)]. 1139 3

Daytime pulmonary hypertension (PH) is relatively common in obstructive sleep apnea (OSA) and is thought to be associated with pulmonary vascular remodeling (PRm). The extent to which PH is reversible with treatment is uncertain. To study this, we measured pulmonary hemodynamics (Doppler echocardiography) in 20 patients with OSA (apnea-hypopnea index [AHI] 48.6 +/- 5.2/h, mean +/- SEM) before and after 1 and 4 mo of CPAP treatment (compliance 4.7 +/- 0.5 h/night). Patients had normal lung function, and no cardiac disease or systemic hypertension. Doppler studies were performed at three levels of inspired oxygen concentration (11%, 21%, and 50%) and during incremental increases in pulmonary blood flow (10, 20, and 30 microg/kg/min dobutamine infusions). Treatment resulted in a decrease in pulmonary artery pressure (Ppa, 16.8 +/- 1.2 mm Hg before CPAP versus 13.9 +/- 0.6 mm Hg after 4 mo CPAP, p < 0.05) and total pulmonary vascular resistance (231.1 +/- 19.6 versus 186.4 +/- 12.3 dyn. s. cm(-)(5), p < 0.05). The greatest treatment effects occurred in the five patients who were pulmonary hypertensive at baseline. The pulmonary vascular response to hypoxia decreased after CPAP (DeltaPpa/DeltaSa(O(2)) 10.0 +/- 1.6 mm Hg before versus 6.3 +/- 0.8 mm Hg after 4 mo CPAP, p < 0.05). The curve of Ppa versus cardiac output (Q), derived from the incremental dobutamine infusion, shifted downward in a parallel fashion during treatment. Systemic diastolic blood pressure also fell significantly. Improvements in pulmonary hemodynamics were not attributable to changes in left ventricular diastolic function or Pa (O(2)). We conclude that CPAP treatment reduces Ppa and hypoxic pulmonary vascular reactivity in OSA and speculate that this may be due to improved pulmonary endothelial function.
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PMID:Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. 1250 85

Between 1991-2000 2052 patients (81% men and 19% women) were referred to our Sleep Laboratory because of OSA suspision. In 1194 (58%) subjects (88% men and 12% women) diagnosis of obstructive sleep apnoea (OSA, AHI > 10) was confirmed. In 430 of them (36%) mild OSA (AHI 11-25), in 243 (20%) moderate OSA (AHI 26-40), and in 521 (44%) severe OSA (AHI > 40) was diagnosed. Epworth sleepiness scale score in those groups was 10.4, 10.5 and 13.0 points respectively. 908 (76%) of patients with OSA were submitted to nCPAP treatment. Effective CPAP pressure ranged from 5 to 20 milibars, mean 8.4 mbars. In 21 patients upper airway resistance syndrome (UARS) was diagnosed. Central sleep apnoea, most frequently of Cheyne-Stokes respiration type was diagnosed in 13 patients. The most common diseases accompanying OSA were: systemic hypertension (46%), coronary heart disease (29%), diabetes (12%), and COPD (9%). Majority of OSA patients (61%) were obese (BMI > 30 kg/m2), 32% were over weight (BMI 25-30 kg/m2). Only 7% had normal body weight (BMI 20-25 kg/m2). Long-term (more than one year) compliance to treatment was found in 70% of patients prescribed CPAP.
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PMID:[Ten years experience of the sleep laboratory at the Institute of Tuberculosis and Lung Disease in Warsaw]. 1192 60

Beginning with modest clinical observations in 1984, a picture has evolved suggesting that sympathetic nervous system over activity may be responsible in part for the elevated blood pressure seen in obstructive sleep apnea patients. Early studies of urinary and plasma catecholamines indirectly suggested sympathetic over activity carried to daytime, non-apneic conditions. Later intra-neuronal recordings of muscle sympathetic nerve activity directly demonstrated both acute and diumal (non-apneic) sympathetic over activity. Most importantly, diurnal sympathetic over activity has been shown to diminish with adequate treatment of apnea using nasal CPAP. Norepinephrine and angiotensin II are both released with increased peripheral sympathetic activity and are parallel vascular growth-promoting factors. Thus, one would expect alterations in vascular structure and function in a state of chronic sympathetic over activity. While changes in peripheral vascular structure have not been demonstrated in hypertension of sleep apnea, changes in peripheral vascular responsiveness have. There is reduced response to acetylcholine and isoproterenol vasodilation, and to norepinephrine and angiotensin vasoconstriction in humans with sleep apnea. Some of these vascular reactivity changes are shown to reversed with chronic nasal CPAP treatment. Finally, complimentary to the above evidence in humans, there is indirect evidence of sympathetic over activity as well as differences in vascular reactivity in intermittent hypoxia challenged rats. We have made significant strides in the past 15-20 years towards understanding systemic hypertension related to sleep apnea, especially the role of the sympathetic nervous system. Future research will need to look at exact mechanism of sympathetic nervous system over activity, particularly how central nervous system pathways may undergo facilitation, leading to daytime over activity. Furthermore, the mechanisms of sustained hypertension in sleep apnea patients is almost certainly of multiple etiologies. There is no marker for separating sleep apnea patients with hypertension derived solely from intermittent hypoxia from other secondary causes. Perhaps endothelial cell molecular markers could help to identify patients at risk for cardiovascular change associated with snoring and apnea, as well to guide treatment. Finally, studies demonstrating microvascular changes in blood vessels are extremely difficult to do, but promise to yield important knowledge about cellular mechanisms and results of long-term treatment of sleep apnea on cardiovascular disease.
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PMID:Sympathetic over activity in the etiology of hypertension of obstructive sleep apnea. 1262 27

Although clinical experience has suggested for more than two decades that OSA is associated with impairment of cognition, emotional state, and quality of life and that treatment with nasal CPAP produces significant improvements in these areas, sound empirical evidence to support this view, especially regarding treatment outcome, has been lacking. More recent investigations have begun to provide this support from randomized, adequately controlled studies. These assessments suggest that some degree of cognitive dysfunction is associated with OSA. The effects are most apparent in the severe cases, whereas results in mild cases are more equivocal. Reported impairments include global intellectual dysfunction and deficits in vigilance, alertness, concentration, short- and long-term memory, and executive and motor function. Considerable discrepancy exists across studies with respect to type and degree of dysfunction, however. Disturbances in general intellectual function and executive function show strongest correlations with measures of hypoxemia. Not unexpectedly, alterations in vigilance, alertness, and, to some extent, memory seem to correlate more with measures of sleep disruption. Although many inadequately controlled investigations have demonstrated reversibility of most or all of these deficits with effective treatment, more recent placebo-controlled studies have raised doubts regarding whether the observed changes are truly a function of treatment. This issue requires further systematic exploration with adequate controls and step-wise analysis of treatment duration effects. A similar set of considerations exists with respect to the relationship between psychological disturbance, primarily depression, and OSA. Although several studies suggest significant depression in these patients, the results are mixed. Placebo-controlled treatment trials fail to demonstrate consistently a difference in mood improvement between active treatment groups and controls, although several methodologic considerations suggest that these results should be interpreted with caution. Numerous investigations leave little doubt about the issue of quality of life impairment among persons with OSA. Further characterization of impairment, particularly in areas specific to this population, will provide clearer understanding of the problem. Preliminary investigations of treatment response in controlled studies indicate significantly greater improvement of quality of life in response to CPAP. Although patients with OSA commonly report disturbances in cognitive and psychological function and general quality of life, the increased rates of obesity, hypertension, diabetes, cardiovascular disease, medication use, and related psychosocial complications present a host of potential etiologies that might explain the impairments noted. There can be little doubt that these covariants do, in some cases, contribute to neuropsychological dysfunctions. It is essential that future studies continue to define those disturbances that are specific to OSA, the relationship between levels of severity and impairment, the role of treatment in reversing these dysfunctions, and the correlation between test results and significant day-to-day social and occupational functional impairment.
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PMID:Neuropsychological impairment and quality of life in obstructive sleep apnea. 1280 Jul 82

To assess the knowledge of general physicians about the diagnosis and management of obstructive sleep apnea (OSA), a self-administered questionnaire, containing 15 questions, was distributed to 160 doctors attending a pulmonary CME program in March 2002. After 15 minutes of response time, the questionnaires were collected. The data were entered and analyzed using SPSS (Version 10.0) software. One hundred and twenty (75%) questionnaires were returned. Only 41% of responders had ever read an article about OSA and 36% had suspected it at least once in their practice. The majority (61-77%) of responders were aware of the common symptoms of OSA, but 55% did not recognize its association with hypertension. A significant number of doctors were not aware that OSA could occur in non-obese individuals (33%), women (42%) and children (39%). Only 25% of responders recognized that a history and blood tests were insufficient to make a reliable diagnosis of OSA. Half of the responders were aware of CPAP therapy for OSA, whereas 18% would have prescribed sedatives to treat sleep disturbances in OSA.
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PMID:General physicians' perspective of sleep apnea from a developing country. 1297 74

About 1.9 % of the population suffer from an obstructive sleep apnea syndrome (OSAS). At the age of between 30 and 60 years it occurs in 3 %. Patients with OSAS develop more frequently such disorders as arteriosclerosis, cardiac arrhythmias and arterial hypertension. A host of pathophysiological changes can be diagnosed. The elevated sympathic activity, recurrent hypoxemias, stress, disturbances in the microvascular milieu, endothelial dysfunction, elevated oxidative capacity as well as a reduced vascular reagibility are deemed to be factors connected to arteriosclerosis. Different biochemical markers, which are seen as risk factors or as markers of cardiovascular diseases, are altered in patients with OSAS (high-sensitive CRP, Interleukin(IL)-6, IL-8, IL-10, TNF-alpha, VGEF, ICAM-1, VCAM-1 and L-Selectin). Patients with OSAS exhibit signs of an impaired insulin sensitivity. Disturbances in microcirculation are also evident. Patients with OSAS have, compared to patients without sleep apnea, elevated blood pressure measurements, even given other common risk factors. The incidence of coronary heart diseases is increased in patients with OSAS. Morbidity and mortality, especially of arteriosclerotic diseases are elevated. Many of the aforementioned disturbances can be improved by a CPAP-therapy.
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PMID:[Cardiovascular diseases and sleep-disordered breathing]. 1525 73

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognized condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of few techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalizing respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long-term cardiovascular morbidity is not established.
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PMID:Obstructive sleep apnoea and the autonomic nervous system. 1531 May 3

The use of CPAP to control excessive daytime sleepiness in OSAHS probably also produces a substantial reduction in vascular risk. This is reviewed with particular reference to hypertension.
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PMID:Sleep . 6: obstructive sleep apnoea/hypopnoea syndrome and hypertension. 1556 10


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