Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to investigate the effects of obstructive sleep apnoea on: (i) PaCO2 levels; (ii) coagulation systems (plasma fibrinogen levels and whole blood viscosity); and (iii) heat shock proteins (HSPs) levels, which are also called stress proteins, in patients with obstructive sleep apnoea syndrome (OSAS). Patients treated with or without nasal continuous positive airway pressure (NCPAP) had arterial blood gases, plasma fibrinogen, haematocrit, serum total protein and changes in PaCO2 (estimated by transcutaneous PaCO2) measured before and after polysomnography. Heat shock protein 72 levels in peripheral blood mononuclear cells were also measured during sleep with and without NCPAP. OSAS patients with hypercapnia demonstrated significant increases in PaCO2 in the morning compared with the previous night. In such OSAS patients, treatment with NCPAP resulted in a normalization of the 20 mg/dL increase in fibrinogen levels which had been seen previously in the morning after sleep. Basal HSP 72 levels (08.00 pm before sleep) were high in OSAS patients compared to normal subjects and progressively decreased during sleep in the absence of NCPAP therapy. NCPAP relieved disabling day-to-day symptoms in addition to improving cardiovascular morbidity in patients with OSAS. Therefore it is important to understand the effects of OSAS on various organ systems as the prevalence of patients with OSAS is high.
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PMID:New insights into the therapy and pathophysiology of patients with obstructive sleep apnoea syndrome. 969 24

Sleep-related breathing disorders (SRBDs) represent a spectrum of abnormalities that range from simple snoring to upper airway resistance syndrome to sleep apnea. The clinical presentation may include obesity, snoring, neuropsychological dysfunction, and daytime hypersomnolence and tiredness. The acute hemodynamic alterations of obstructive sleep apnea include systemic and pulmonary hypertension, increased right and left ventricular afterload, and increased cardiac output. Earlier reports attributed the coexistence of SRBDs with cardiovascular diseases to the shared risk factors such as age, sex, and obesity. However, recent epidemiologic data confirm an independent association between SRBDs and the different manifestations of cardiovascular diseases. Possible mechanisms may include a combination of intermittent hypoxia and hypercapnia, repeated arousals, sustained increase in sympathetic tone, reduced baroreflex sensitivity, increased platelet aggregation, and elevated plasma fibrinogen and homocysteine levels. The strength of the association, its pathogenesis, and the impact of treatment of SRBDs on the health outcome of patients with cardiovascular diseases are issues to be addressed in future studies.
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PMID:Cardiovascular consequences of sleep-related breathing disorders. 1235 Feb 42

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

Insulin-mediated glucose disposal varies widely in apparently healthy human beings, and the more insulin resistant an individual, the more insulin they must secrete in order to prevent the development of type 2 diabetes. However, the combination of insulin resistance and compensatory hyperinsulinemia increases the likelihood that an individual will be hypertensive, and have a dyslipidemia characterized by a high plasma triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) concentration. These changes increase risk of cardiovascular disease (CVD), and in 1988, this cluster of related abnormalities was designated as comprising a syndrome (X). Several other clinical syndromes are now known to be associated with insulin resistance and compensatory hyperinsulinemia. For example, polycystic ovary syndrome appears to be secondary to insulin resistance and compensatory hyperinsulinemia. More recently, studies have shown that the prevalence of insulin resistance/hyperinsulinemia is increased in patients with nonalcoholic fatty liver disease, and there are reports that certain forms of cancer are more likely to occur in insulin resistant/hyperinsulinemic persons. Finally, there is substantial evidence of an association between insulin resistance/hyperinsulinemia, and sleep disordered breathing. Given the rapid increase in the number of clinical syndromes and abnormalities associated with insulin resistance/hyperinsulinemia, it seems reasonable to suggest that the cluster of these changes related to the defect in insulin action be subsumed under the term of the insulin resistance syndrome. In addition to the identification of additional clinical syndromes related to insulin resistance/hyperinsulinemia, a number of new risk factors have been recognized that would increase CVD risk in these individuals. Thus, in addition to a high TG and a low HDL-C, the atherogenic lipoprotein profile in insulin resistant/hyperinsulinemic individuals also includes the appearance of smaller and denser low density lipoprotein particles, and the enhanced postprandial accumulation of remnant lipoproteins; changes identified as increasing risk of CVD. Elevated plasma concentrations of plasminogen activator inhibitor-1 (PAI-1) have been shown to be associated with increased CVD, and there is evidence of a significant relationship between PAI-1 and fibrinogen levels and both insulin resistance and hyperinsulinemia. Evidence is also accumulating that sympathetic nervous system (SNS) activity is increased in insulin resistant, hyperinsulinemic individuals, and, along with the salt sensitivity associated with insulin resistance/hyperinsulinemia, increases the likelihood that these individuals will develop essential hypertension. The first step in the process of atherogenesis is the binding of mononuclear cells to the endothelium, and mononuclear cells isolated from insulin resistant/hyperinsulinemic individuals adhere with greater avidity. This process is modulated by adhesion molecules produced by endothelial cells, and there is a significant relationship between degree of insulin resistance and the plasma concentration of the several of these adhesion molecules. Further evidence of the relationship between insulin resistance and endothelial dysfunction is the finding that asymmetric dimethylarginine, an endogenous inhibitor of the enzyme nitric oxide synthase, is increased in insulin resistant/hyperinsulinemic individuals. Finally, plasma concentrations of several inflammatory markers are elevated in insulin resistant subjects. It is obvious that the cluster of abnormalities associated with insulin resistance and compensatory hyperinsulinemia contains many well-recognized CVD risk factors, choosing which one, or ones, that are primarily responsible for the accelerated atherogenesis that characterizes this syndrome is not a simple task. Indeed, efforts to try to do so by the use of multiple regression analysis of epidemiological data may be more misleading than helpful.
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PMID:Insulin resistance, the insulin resistance syndrome, and cardiovascular disease. 1648 19

This study tested whether obstructive sleep apnoea syndrome (OSAS) influenced clinical characteristics and outcomes after successful percutaneous coronary intervention (PCI) in 123 consecutive patients with acute coronary syndrome (ACS). Patients with an apnoea-hypopnea index (AHI) >or= 5 were considered as having OSAS. Carotid ultrasonography and echocardiography were performed, and C-reactive protein (CRP) and fibrinogen were measured. Co-existence of ACS and OSAS occurred in 76 patients (61.8%) and patients with OSAS had a greater interventricular septum thickness (IVST) and higher levels of CRP than non-OSAS patients. In an elderly subpopulation (>or= 75 years of age), two-vessel disease was significantly more common and fibrinogen levels were significantly higher in OSAS than non-OSAS patients. Carotid intima-media thickness (IMT) correlated with the AHI in ACS patients. In elderly ACS patients, IMT, Gensini score and fibrinogen correlated with AHI. Patients were followed up for 1 year for major adverse cardiac events (MACEs) and no significant difference in major MACEs was found after this period between OASAS and non-OSAS patients. This study indicates that OSAS is associated with inflammation and increased IVST in ACS patients after successful PCI and, in elderly ACS patients, also with CAD severity and enhanced blood coagulability.
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PMID:Impact of obstructive sleep apnoea on clinical characteristics and outcomes in patients with acute coronary syndrome following percutaneous coronary intervention. 1993 Aug 39

Sleep-disordered breathing (SDB) has a prognostic impact in patients with cardiac diseases. We included 257 patients with preserved left ventricular function and angiographically proven coronary artery disease (CAD). All patients underwent cardiorespiratory polygraphy. In 251 patients high-sensitive C-reactive protein and fibrinogen were measured. SDB was documented in 188 patients (apnea-hypopnea-index [AHI] 16.4+/- 1.9/h): 58 patients presented central sleep apnea (CSA) and 130 patients obstructive sleep apnea (OSA). All patients (73%) with SDB had higher blood fibrinogen levels than those without SDB (p = 0.01). We found 197 patients with CRP-values below the cut-off of 0.5 mg/dl (group 1) and 54 patients with no active infection but CRP>0.5 mg/dl (group 2). Severity of SDB was significantly higher in group 2 (p = 0.01). SDB has a high prevalence in CAD patients and seems to be associated with chronic inflammation, which may be linked to CAD progression and/or acute coronary events.
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PMID:Sleep apnea is common in patients with coronary artery disease. 2069 65