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

It is becoming increasingly clear that the intrinsic properties of both the heart and vasculature exhibit dramatic oscillations over the course of the day. Diurnal variations in the responsiveness of the cardiovascular system to environmental stimuli are mediated by a complex interplay between extracellular (i.e., neurohumoral factors) and intracellular (i.e., circadian clock) influences. The intracellular circadian clock is composed of a series of transcriptional modulators that together allow the cell to perceive the time of day, thereby enabling preparation for an anticipated stimulus. These molecular timepieces have been characterized recently within both vascular smooth muscle cells and cardiomyocytes, giving rise to a multitude of hypotheses relating to the potential role(s) of the circadian clock as a modulator of physiological and pathophysiological cardiovascular events. For example, evidence strongly supports the hypothesis that the circadian clock within the heart modulates myocardial metabolism, which in turn facilitates anticipation of diurnal variations in workload, substrate availability, and/or the energy supply-to-demand ratio. The purpose of this review is therefore to summarize our current understanding of the molecular events governing diurnal variations in the intrinsic properties of the heart, with special emphasis on the intramyocardial circadian clock. Whether impairment of this molecular mechanism contributes toward cardiovascular disease associated with hypertension, diabetes mellitus, shift work, sleep apnea, and/or obesity will be discussed.
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PMID:The circadian clock within the heart: potential influence on myocardial gene expression, metabolism, and function. 1637 89

The concept of sleep apnea as a risk factor for primary stroke derives mainly from evidence implicating sleep-disordered breathing (SDB) in the causation or aggravation of systemic hypertension and heart disease. Evidence of an association between SDB and sustained systemic hypertension is available from several large studies, though the exact mechanism involved is unknown. Another study found a 37% increase in risk of developing cardiovascular disease among middle-aged men attending a sleep clinic. The same study also found that treatment of SDB reduced the cardiovascular risk. Other mechanisms less well studied linking SDB with cerebrovascular risk include reduction in cerebral blood flow, altered cerebral autoregulation, impaired endothelial function, and accelerated proinflammatory states.
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PMID:Sleep apnea and stroke. 1640 Feb 98

This article boldly challenges the dynamic psychiatrist to engage directly and vigorously into a matter that many would prefer to regard somewhat passively. That passivity is no longer acceptable. The metabolic syndrome has become a central medical concern because of the epidemic of obesity. It causes cardiovascular disease, diabetes, some cancers, sleep apnea, sexual dysfunction, and infertility. Obesity leads to depression, anxiety, and osteoarthritis. Some atypical antipsychotic medicines contribute to the metabolic syndrome, but the epidemic is widespread independent of atypicals. Practical steps by psychiatrists to monitor metabolic parameters are not as simple as they appear to be. Yet this is an area of clinical practice that cannot be ignored. Psychodynamic therapists need to awaken to the health of patients because the metabolic syndrome is more life-threatening than self-mutilation and many other self-destructive behaviors. The article discusses countertransference and transference issues stirred up when physicians begin to take responsibility for the total health of their patients. Freud oriented us to focus on both sides of the mind body relationship. Recent research on obesity, hypertension, diabetes, sleep, anxiety,depression, exercise and dyslipidemia is reviewed from the viewpoint of how it impinges on the office practice of a dynamic psychiatrist.
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PMID:A psychodynamic approach to screening for the metabolic syndrome. 1701 91

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

Adrenomedullin (AM) is a potent endothelial-derived vasodilator secreted under the influence of various stimuli such as hypoxia, shear stress and cytokines. As all of these stimuli might be active under the conditions of obstructive sleep apnoea (OSA), we hypothesized that vascular AM production is increased in these patients. The study included 41 consecutive OSA patients and 28 control subjects without sleep-disordered breathing who were recruited from a pool of patients hospitalized for other reasons. Both groups were matched for anthropometric and comorbid factors. In all patients, i.e. OSA and controls, peripheral venous blood samples were taken at 07:00 hours after diagnostic polysomnography. In subsets of OSA patients, this was repeated after two nights of continuous positive airway pressure (CPAP) therapy (n = 28) and after several months of constant CPAP use (n = 11). The controls and the untreated OSA patients did not have serial blood sampling. In all blood samples, plasma AM levels were measured by an enzyme immunoassay kit. At baseline, the OSA patients had markedly elevated AM concentrations when compared to the controls. There were no differences between normo- and hypertensive OSA patients. After two nights of CPAP therapy, AM levels significantly decreased. Patients on long-term CPAP treatment showed complete normalization of plasma AM concentrations. In conclusion, this pilot study suggests that circulating AM is increased in untreated OSA irrespective of coexistent arterial hypertension and declines after CPAP therapy. AM upregulation might be considered as an adaptive mechanism to counteract the emergence of OSA-related cardiovascular disease.
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PMID:Circulating adrenomedullin in obstructive sleep apnoea. 1649 7

Obstructive sleep apnea is a common disorder characterized by repetitive collapse of the pharyngeal airway during sleep. The disorder results primarily from an anatomically small upper airway in conjunction with pharyngeal dilator muscles that can compensate for the anatomic deficiency awake, but not asleep. Ventilatory control instability and a low arousal threshold may contribute to the disorder as well. The consequences of sleep apnea fall into two domains: (1) neurocognitive dysfunction (sleepiness and decreased quality of life) resulting from sleep fragmentation and (2) cardiovascular disease (hypertension, stroke, myocardial infarction, and heart failure) likely resulting from the intermittent hypoxia. The disorder is generally diagnosed in the sleep laboratory over the course of a night, although alternative approaches in the home are also utilized. A number of treatment options are available. Continuous positive airway pressure remains the most consistently effective approach, although oral appliances (generally mandibular-advancing devices) and a number of surgical procedures have some demonstrated efficacy. Thus, therapy must be individualized to the patient's desires and the severity of the apnea.
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PMID:Sleep apnea. 1649 60

Obesity is epidemic in the modern world. It is becoming increasingly clear that obesity is a major cause of cardiovascular disease, diabetes, and renal disease, as well as a host of other comorbidities. There are at present no generally effective long-term medical therapies for obesity. Surgical therapy for morbid obesity is not only effective in producing long-term weight loss but is also effective in ameliorating or resolving several of the most significant complications of obesity, including diabetes, hypertension, dyslipidemia, sleep apnea, gastroesophageal reflux disease, degenerative joint disease, venous stasis, pseudotumor cerebri, nonalcoholic steatohepatitis, urinary incontinence, fertility problems, and others. The degree of benefit and the rates of morbidity and mortality of the various surgical procedures vary according to the procedure.
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PMID:The effect of obesity surgery on obesity comorbidity. 1661 33

Obesity has been described as an epidemic because of the rapid increase in the number of overweight and obese individuals over the past 20 yr. This increasing prevalence of obesity is a worldwide phenomenon affecting both children and adults. The metabolic syndrome is a constellation of central adiposity, impaired fasting glucose, elevated blood pressure, and dyslipidemia (high triglyceride and low HDL cholesterol). When three of these five criteria are present, the risk of cardiovascular disease and diabetes is increased 1.5- to 2-fold. As body weight, expressed as the BMI, rises, there are a number of other diseases that are associated with it. First, life span is shortened and the risk of sudden death increases. Second, the risk of diabetes, gall bladder disease, hypertension, heart disease, osteoarthritis, sleep apnea, and certain forms of cancer also increase.
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PMID:Epidemiology, trends, and morbidities of obesity and the metabolic syndrome. 1662 98

An increased incidence of cardiovascular disease has previously been reported in middle-aged males during a follow-up period of 7 yrs. The aim of the present study was to address the incidence of coronary artery disease (CAD) in a larger sample without any heart disease at baseline. The population comprised 308 snorers (245 males and 63 females) with a mean +/- sd age of 49.0 +/- 9.9 yrs in 1991. Data were collected via the Swedish Hospital Discharge Register, National Cause of Death Registry, clinical charts and questionnaires. Over 7 yrs, CAD was observed in 17 (16.2%) of 105 patients with obstructive sleep apnoea (OSA; overnight (6 h) oxygen desaturations > or =30 events) compared with 11 (5.4%) of 203 snorers without OSA. OSA diagnosis at baseline was associated with an increased risk of development of CAD in a multivariate model. In the OSA group, CAD was confirmed in 16 (24.6%) of 65 incompletely treated patients compared with one (3.9%) of 26 efficiently treated subjects. Efficient treatment of OSA reduced this risk. It is concluded that middle-aged sleep apnoeics are at high risk of developing coronary artery disease if they are not treated efficiently, which should be considered in cardiovascular disease prevention models.
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PMID:Increased incidence of coronary artery disease in sleep apnoea: a long-term follow-up. 1664 Nov 20

Polycystic ovary syndrome (PCOS) is a syndrome, which can be defined as a group of recognisable patterns of symptoms or abnormalities that indicate a particular medical situation. The current definition of PCOS requires the presence of two of the following three conditions: (i) oligo- and/or anovulation; (ii) clinical and/or biochemical signs of hyperandrogenism; and (iii) polycystic ovaries--and the exclusion of other aetiologies. It is generally accepted that the prevalence of PCOS is approximately 5-10%, and that of polycystic ovaries alone is 21-23%. Other features of PCOS are obesity, insulin resistance, impaired glucose tolerance and type 2 diabetes mellitus, dyslipidaemia, cardiovascular disease, obstructive sleep apnoea and infertility. An approach to a patient with possible PCOS should be directed towards making a diagnosis and screening for associated endocrine abnormalities. Therapeutic interventions are directed towards addressing the needs of the patient at present and towards preventing long-term complications of the syndrome. Body mass index, which is a primary mediator in the relationship between PCOS and health-related quality of life in obese PCOS adolescents, may play a similar role in other PCOS patients. Any intervention directed at reducing central obesity will not only improve quality of life but also correct hyperinsulinism and improve fertility and lipid and androgen profiles. It is also the only currently available intervention that can have a lifelong impact on reducing possible long-term complications of the syndrome. Lifestyle modification is the cardinal intervention. Pharmacological treatments are available for specific indications. Infertility can be treated with clomifene (clomiphene citrate), metformin, gonadotropins or surgery to the ovaries. Cyproterone (alone or in combination with ethinylestradiol) and spironolactone are the main drugs used in the treatment of hirsutism. Other drugs that can be considered include flutamide, ketoconazole and finasteride. Women with PCOS require ongoing surveillance to detect impaired glucose tolerance, hyperlipidaemia, endometrial hyperplasia and consequent complications. Obese women, in particular, require regular glucose tolerance testing because of the potential for rapid progression from normal to impaired glucose tolerance and diabetes. The focus of this article is the epidemiology, diagnosis and management of this common endocrine disorder. Diagnostic and co-morbid features are discussed separately to facilitate understanding of PCOS. Symptom-directed strategies, as well as short- and long-term goals of treatment, are outlined.
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PMID:Diagnosis and management of polycystic ovary syndrome: a practical guide. 1674 5


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