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

Obesity is associated with a number of medical conditions that lead to increased morbidity and increased mortality. Both the National Institutes of Health and the World Health Organization define obesity as a body mass index (BMI) > or = 30 kg/m2 and overweight as a BMI 25-30. The most common conditions associated with obesity are insulin resistance, diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, gallstones and cholecystitis, sleep apnea and other respiratory dysfunction, and the increased incidence of certain cancers. These are discussed below.
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PMID:The medical risks of obesity. 1196 7

By promoting atherosclerosis and thrombosis, a blood-clotting diathesis could contribute to excess cardiovascular morbidity and mortality in patients with systemic hypertension and/or obstructive sleep apnoea. Since psychological states affect haemostatic activity, we wondered about the contribution of behavioural factors to a hypercoagulable state in subjects with increased risk of cardiovascular disease. To tease apart the potential additive nature of cardiovascular disease risk, we examined four patient groups - hypertensives and normotensives, with and without sleep apnoea. The procoagulant molecules thrombin-antithrombin III complex, fibrin D-dimer and von Willebrand factor antigen were measured in 88 subjects (mean age 47 years; range 32-64 years) who underwent full polysomnography. Subjects completed the Center for Epidemiological Studies - Depression (CES-D) Scale, the Cook-Medley (CM) Hostility Scale, and the Profile of Mood States (POMS). Sleep apnoea, hypertension status, age, body mass index and psychological variables (CES-D, CM Stress, and POMS Vigour-Activity) together explained 29% of the variance in D-dimer, a marker of fibrin turnover ( r (2)=0.29, P =0.001). CES-D, CM Stress and POMS Vigour-Activity explained 17% of this variance even after controlling for sleep apnoea, hypertension status, age and body mass index (Delta r (2)=0.17, P =0.001). Thrombin-antithrombin III complex and von Willebrand factor were not significantly related to psychological variables, but this may reflect limited statistical power. Thus psychological factors are independently associated with D-dimer and explain as much of its variance as do traditional correlates (hypertension, sleep apnoea, age and body mass index). These results may provide a rationale for linking behavioural aspects with cardiovascular events.
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PMID:Independent contribution of psychological factors to fibrin turnover in subjects with sleep apnoea and/or systemic hypertension. 1224 29

Different pathophysiological mechanisms underlie the morbid associations observed between sleep apnea syndrome (SAS) and cardiovascular disease. Cardiovascular responses to apnea can be divided into acute cardiovascular modifications following each nocturnal respiratory event and chronic adaptations of the cardiovascular system. The same stimuli always trigger acute cardiovascular response: hypoxemia, hypercapnea, changes in the intra-thoracic pressure, micro-arousals. Each obstructive or central respiratory event is associated with a peak in blood pressure, changes in the heart rate, generally bradycardia at onset of apnea and tachycardia when respiration is renewed. Oxygen desaturation is the strongest stimulus explaining the observed acute cardiovascular responses. When these stimuli are repeated every night, the cardiovascular system adapts with a higher sympathetic tone and lower parasympathetic tone during the diurnal period. Baroreceptors also become less sensitive in apneic patients. Finally, endothelial function is altered in SAS patients with a desensitization of the alpha and beta-2 adrengeric receptors, altered NO-dependent vasodilatation, and hypersensitivity to vasoconstriction induced, for example, by angiotensin 2. The cardiovascular morbidity associated with SAS is currently thought to concern the development of diurnal hypertension (dose-effect response), left ventricular failure, higher risk of coronary or cerebral events. Very recently, epidemiological studies suggested that continuous positive pressure ventilation in SAS patients can reduce the cardiovascular risk.
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PMID:[Pathophysiology of cardiovascular risk in sleep apnea syndrome (SAS)]. 1238 23

Sleep and sleep disorders play a prominent role in hormone regulation. Given that sleep disordered breathing (SDB) and diabetes mellitus (DM) are thought to result from obesity, it has been assumed that when the two coexist, the diabetes was caused by the obesity. However, new data has shed light on the effects that SDB, sleep deprivation, and snoring have on glucose regulation. It now appears that in addition to causing daytime drowsiness, cardiovascular disease, mood and memory disturbances, impotence, and car wrecks, obstructive sleep apnea (OSA) also promotes insulin resistance. Though data is still sketchy on the optimum management of coexisting DM and OSA, large-scale studies will most likely prove that homeostatic glucose control in patients with sleep apnea will require aggressive treatment of their SDB.
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PMID:Sleep and the endocrine system: new associations to old diseases. 1239 57

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.
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PMID:Sleep disordered breathing and risk factors for cardiovascular disease. 1239 60

Cardiovascular and cerebrovascular disease are the most common life-threatening disease in the industrialized world. There is high interest in sleep apnea and cardiovascular disease: several studies have demonstrated an association between sleep apnea and cardiovascular and cerebrovascular events. The aim of this review is to critically appraise the possible adverse physiological consequences of sleep apnea on the cardiovascular system and to assess whether such adverse effects constitute a risk for the development of cardiovascular disease.
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PMID:["Bad" sleepers... Causes, effects, and diagnosis of sleep-related breathing disorders in cardiac patients]. 1241 29

There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function. Twenty-nine OSA patients and 12 control subjects were studied using technetium-99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP. A significantly lower LVEF was found in OSA patients, compared to control subjects, (53+/-7 versus 61+/-6%) along with a reduced LVPER (2.82+/-0.58 versus 3.82+/-0.77 end-diastolic volumes x s(-1)). Furthermore, OSA patients had significantly lower LVPFR (2.67+/-0.71 versus 3.93+/-0.58 end-diastolic volumes x s(-1)) and delayed TPFR (0.19+/-0.04 versus 0.15+/-0.03 s) in comparison with the control group. Six-months of CPAP treatment was effective in significantly improving LVEF, LVPER, LVPFR and TPFR. In conclusion, obstructive sleep apnoea patients without any cardiovascular disease seem to develop left ventricular systolic and diastolic dysfunction, which may be reversed, either partially or completely, after 6 months of continuous positive airway pressure treatment.
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PMID:Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome. 1244 80

The purpose of this article is to review the current state of knowledge on contributions of nocturnal urine overproduction and overactive bladder to the syndrome of nocturia. We review the recent literature and current state of the art in differential diagnosis, pathophysiology, and classification of nocturia. We found that multiple pathologic factors may result in nocturia, including cardiovascular disease, diabetes mellitus or insipidus, third spacing of fluid, sleep apnea, lower urinary tract obstruction, primary sleep disorders, and behavioral and environmental factors. Thus, nocturia may be attributed to nocturnal polyuria (nocturnal urine overproduction), diminished nocturnal bladder capacity, or both. Distinction between these conditions is made by a simple arithmetic analysis of the 24-hour voiding diary. Understanding the manifold origins of nocturia will lead to rational treatment of specific contributing pathophysiologic factors.
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PMID:Nocturnal polyuria versus overactive bladder in nocturia. 1249 48

The mechanisms underlying the link between obstructive sleep apnoea (OSA) and cardiovascular disease are not completely established. However, there is increasing evidence that autonomic mechanisms are implicated. A number of studies have consistently shown that patients with OSA have high levels of sympathetic nerve traffic. During sleep, repetitive episodes of hypoxia, hypercapnia and obstructive apnoea act through chemoreceptor reflexes and other mechanisms to increase sympathetic drive. Remarkably, the high sympathetic drive is present even during daytime wakefulness when subjects are breathing normally and no evidence of hypoxia or chemoreflex activation is apparent. Several neural and humoral mechanisms may contribute to maintenance of higher sympathetic activity and blood pressure. These mechanisms include chemoreflex and baroreflex dysfunction, altered cardiovascular variability, vasoconstrictor effects of nocturnal endothelin release and endothelial dysfunction. Long-term continuous positive airway pressure treatment decreases muscle sympathetic nerve activity in OSA patients. The vast majority of OSA patients remain undiagnosed. Unrecognized OSA may contribute, in part, to the metabolic and cardiovascular derangements that are thought to be linked to obesity, and to the association between obesity and cardiovascular risk. Furthermore, acting through sympathetic neural mechanisms, OSA may contribute to or augment elevated levels of blood pressure in a large proportion of the hypertensive patient population.
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PMID:Sympathetic nerve activity in obstructive sleep apnoea. 1260 10

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


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