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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 34 severely obese men with a history of heavy snoring and excessive daytime sleepiness indicative of obstructive sleep apnoea syndrome (OSAS) were studied prospectively. Their mean age was 46 years, and mean body mass index was 41.6 kg m-2. During a 4-year follow-up, 15% (5/34) of these subjects died (three cases of acute myocardial infarction and two cases of pulmonary oedema), all of them suddenly and unexpectedly, outside hospital. On autopsy the degree of atherosclerosis was found to be moderate in all cases. In 68% (15/22) of the men a pathological apnoea index (mean value 46 +/- 20) confirmed the OSAS diagnosis. Exercise tests and neurological examinations did not reveal any other causes of daytime sleepiness. Mean blood pressure at rest and during exercise was normal, and mean serum lipid and blood glucose levels were normal. Spirometry revealed intrapulmonary restrictive changes that could not be attributed to the heavy thoracic wall. Compliance was reduced to about 50% of reference values, and the mean pCO2 level (5.8 kPa) was close to the upper reference limit. Blood tests suggested that high alcohol consumption may be an important factor contributing to OSAS. These results demonstrate that morbidly obese men with a history of OSAS have a high risk of sudden cardiovascular death, despite the absence of other conventional risk factors.
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PMID:The sleep apnoea syndrome in obesity: risk of sudden death. 186 65

We transplanted autologous adrenal medullary tissue into the caudate nucleus of 3 patients with advanced Parkinson's disease. The 1st patient, a 59-year-old man with parkinsonian symptoms for 15 years, had mild improvement in his motor functioning after the operation. However, his postoperative course was characterized by prolonged drowsiness and complex visual hallucinations. The patient died suddenly 8 months after the transplant, and an autopsy revealed coronary atherosclerosis. Examination of the graft site showed necrotic adrenal medullary tissue surrounded by inflammatory cells. The 2nd patient, a 50-year-old man with a 21-year history of parkinsonian symptoms, improved the most after the procedure. The 3rd patient, a 43-year-old man with 12 years of parkinsonian symptoms, had mild improvement in his motor functioning. CSF homovanillic acid increased postoperatively in the 3 patients, but then returned to preoperative levels in all except the 2nd patient. The anatomic, neurochemical, and physiologic basis for the modest clinical improvement shown in these patients is not yet understood.
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PMID:Clinical, biochemical, and neuropathologic findings following transplantation of adrenal medulla to the caudate nucleus for treatment of Parkinson's disease. 233 Jan 21

Obstructive sleep apnoea (OSA) is a very prevalent disorder particularly amongst middle-aged, obese men, although its existence in women as well as in lean individuals is increasingly recognized. Despite the early recognition of the strong association between OSA and obesity, and OSA and cardiovascular problems, sleep apnoea has been treated as a 'local abnormality' of the respiratory track rather than as a 'systemic illness'. In 1997, we first reported that the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor-alpha (TNF alpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. Also, we reported a positive correlation between IL-6 or TNF alpha plasma levels and the body mass index (BMI). In subsequent studies, we showed that IL-6, TNF alpha, leptin and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnoea. The association of OSA with insulin resistance and diabetes type 2 has been confirmed since then in several epidemiological and clinical studies. Furthermore, our findings that women with polycystic ovary syndrome (PCOS, a condition associated with hyperandrogenism and insulin resistance) were much more likely than controls to have sleep disordered breathing (SDB) and daytime sleepiness support the pathogenetic role of insulin resistance in OSA. Other findings that support the view that sleep apnoea and sleepiness may be manifestations of a serious metabolic disorder, namely the Metabolic or Visceral Obesity Syndrome, include: obesity without sleep apnoea is associated with daytime sleepiness; PCOS and diabetes type 2 are independently associated with EDS after controlling for SDB, obesity and age; and increased prevalence of sleep apnoea in postmenopausal women, with hormonal replacement therapy associated with a significantly reduced risk for OSA. In conclusion, accumulating evidence provides support to our model of the bi-directional, feedforward, pernicious association between sleep apnoea, sleepiness, inflammation and insulin resistance, all promoting atherosclerosis and cardiovascular disease.
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PMID:Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. 1282 41

Obstructive sleep apnea (OSA) is a common medical condition that occurs in approximately 5% to 15% of the population. The pathophysiology of OSA is characterized by repetitive occlusions of the posterior pharynx during sleep that obstruct the airway, followed by oxyhemoglobin desaturation, persistent inspiratory efforts against the occluded airway, and termination by arousal from sleep. Obstructive sleep apnea is associated with daytime sleepiness and fatigue, likely due to fragmented sleep from recurrent arousals. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA and that OSA is a risk factor for the development of hypertension. Recent studies show that OSA may be implicated in stroke and transient ischemic attacks. Obstructive sleep apnea appears to be associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with preexisting pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified to be important in the development of atherosclerosis. Obstructive sleep apnea is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, and plasminogen activator inhibitor, and reduced fibrinolytic activity. Obstructive sleep apnea has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.
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PMID:Obstructive sleep apnea and cardiovascular disease. 1530 32

Obstructive sleep apnea (OSA) occurs commonly in the U.S. population and is seen in both obese as well as non-obese individuals. OSA is a disease characterized by periodic upper airway collapse during sleep, which then results in either apnea, hypopnea, or both. The disorder leads to a variety of medical complications. Neuropsychiatric complications include daytime somnolence, cognitive dysfunction, and depression. Increased incidence of motor vehicle accidents has been documented in these patients and probably reflects disordered reflex mechanisms or excessive somnolence. More importantly, vascular disorders such as hypertension, stroke, congestive cardiac failure, arrhythmias, and atherosclerosis occur frequently in these patients. The lungs may be affected by pulmonary hypertension and worsening of asthma. Recent data from several laboratories demonstrate that obstructive sleep apnea is characterized by an inflammatory response. Cytokines are elaborated during the hypoxemic episodes leading to inflammatory responses as marked clinically by elevated C-reactive protein (CRP). As elevated CRP levels are considered markers of the acute phase response and characterize progression of vascular injury in coronary artery disease, it is likely that obstructive sleep apnea could lead to worsening of vasculopathy. Moreover, as inflammatory mechanisms regulate bronchial asthma, it is also likely that cytokines and superoxide radicals generated during hypoxemic episodes could exacerbate reactive airway disease. Patients with Cough, Obstructive sleep apnea, Rhinosinusitis, and Esophageal reflux clustered together can be categorized by the acronym, "CORE", syndrome. The purpose of this manuscript is to review the inflammatory responses that occur in patients with obstructive sleep apnea and relate them to the occurrence of cardiopulmonary disease.
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PMID:Obstructive sleep apnea, inflammation, and cardiopulmonary disease. 1535 23

Obstructive sleep apnea (OSA) is a prevalent disorder particularly among middle-aged, obese men, although its existence in women as well as in lean individuals is increasingly recognized. Despite the early recognition of the strong association between OSA and obesity, and OSA and cardiovascular problems, sleep apnea has been treated as a 'local abnormality' of the respiratory track rather than as a 'systemic illness.' In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. Also, we reported a positive correlation between IL-6 or TNFalpha plasma levels and the body-mass-index (BMI). In subsequent studies, we showed that IL-6, TNFalpha, and insulin levels were elevated in sleep apnea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnea. Furthermore, our findings that women with the polycystic ovary syndrome (PCOS) (a condition associated with hyperandrogenism and insulin resistance) were much more likely than controls to have sleep disordered breathing (SDB) and daytime sleepiness, suggests a pathogenetic role of insulin resistance in OSA. Other findings that support the view that sleep apnea and sleepiness in obese patients may be manifestations of the Metabolic Syndrome, include: obesity without sleep apnea is associated with daytime sleepiness; PCOS and diabetes type 2 are independently associated with EDS after controlling for SDB, obesity, and age; increased prevalence of sleep apnea in post-menopausal women, with hormonal replacement therapy associated with a significantly reduced risk for OSA; lack of effect of continuous positive airway pressure (CPAP) in obese patients with apnea on hypercytokinemia and insulin resistance indices; and that the prevalence of the metabolic syndrome in the US population from the Third National Health and Nutrition Examination Survey (1988-1994) parallels the prevalence of symptomatic sleep apnea in general random samples. Finally, the beneficial effect of a cytokine antagonist on EDS in obese, male apneics and that of exercise on SDB in a general random sample, supports the hypothesis that cytokines and insulin resistance are mediators of EDS and sleep apnea in humans. In conclusion, accumulating evidence provides support to our model of the bi-directional, feed forward, pernicious association between sleep apnea, sleepiness, inflammation, and insulin resistance, all promoting atherosclerosis and cardiovascular disease.
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PMID:Sleep apnea is a manifestation of the metabolic syndrome. 1589 51

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

Sleep-disordered breathing (SDB) is more probably the cause rather than the consequence of stroke because: apneas are essentially obstructive rather than central, the frequency of SDB is not different between transient ischemic attack and cerebral infarction; and previous excessive daytime sleepiness is significantly more frequent among stroke patients with SDB than those without. The presence of SDB in stroke patients could lead to a poor outcome. Pathophysiological relationships between strokes and SDB are multiple. Experimental and clinical studies have shown that both short- and long-term factors may play a role in increasing the susceptibility to stroke in patients with obstructive sleep apnea syndrome. The former include changes in cerebral hemodynamics, hematologic alterations, and cardiocirculatory dysfunctions that typically and repeatedly occur during apnea episodes and also may persist during wakefulness. Regarding long-term factors, some changes in the anatomical characteristics of carotid arteries wall have been recognized in SDB patients. This finding seems to suggest that the link between SDB and cerebrovascular disease might be explained, at least in part, by an increase in the progression of the atherosclerosis process involving cerebral vessels. There are several practical implications from the demonstrated significant role of sleep apnea in increasing the predisposition to developing stroke. Specific investigation is fundamental in the presence of a clinical suspect of SDB, especially in patients with history of transient ischemic attacks and stroke. Specific treatment of SDB may reduce the possibility of further cerebrovascular disturbances.
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PMID:Cerebrovascular diseases and sleep-disordered breathing. 1683 28

Excessive daytime sleepiness and sleep disorders, including sleep apnea syndrome, restless legs syndrome, and periodic limb movement disorder, occur with increased frequency in patients with end-stage renal disease (ESRD). The detection and management of sleep disorders in ESRD patients is often challenging but may have significant clinical benefits. Some of the poor quality of life in ESRD may be attributed to the presence of concomitant sleep disorders, yet the classical symptoms of sleep disorders (poor concentration, daytime sleepiness, and insomnia) are often ascribed to the uremic syndrome itself. Conventional risk factors and screening tools used in the diagnosis of sleep disorders seem to have limited applicability in dialysis patients implicating the unique pathophysiology of sleep disorders in ESRD. Emerging evidence suggests that sleep apnea may contribute to the augmented cardiovascular event rates and to the accelerated development of atherosclerosis in ESRD. Whether treatment of sleep disorders in ESRD patients can affect the high morbidity and mortality of ESRD patients has yet to be elucidated. To date, conventional renal replacement therapies do not appear to have a significant impact on the treatment of sleep disorders in ESRD. The promising therapeutic effects of optimal uremia control in the forms of nocturnal hemodialysis and renal transplantation on sleep disorders require further mechanistic and clinical studies.
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PMID:Sleep disorders in end-stage renal disease: 'Markers of inadequate dialysis'? 1696 88

This study was performed to determine whether there is a protective association between participation in vigorous or vigorous/moderately vigorous physical activity and the prevalence of sleep-disordered breathing (SDB). Polysomnographic and questionnaire data from the baseline examination of 4,275 participants in the Sleep Heart Health Study (SHHS) were analyzed in relation to information on amount of physical activity and other potentially relevant factors collected from five SHHS parent cohorts (Atherosclerosis Risk in Communities Study, Cardiovascular Health Study, Framingham Heart Study, Strong Heart Study, and Tucson Epidemiologic Study of Airways Obstructive Diseases). Logistic regression models were fitted to determine if amount and strenuousness of physical activity was associated with the presence of SDB. At least 3 h per week of vigorous physical activity reduced the odds of SDB, defined as a respiratory disturbance index (RDI) of at least 15 apneas/hypopneas per hour (Adjusted OR, 0.68; 95%CI, 0.51-0.91). A qualitatively similar but slightly weaker association was observed when SDB was defined as a RDI > or = 10 per hour (Adjusted OR, 0.81; 95%CI, 0.64-1.02). These findings remained after adjustment for sleepiness and restricting analyses to participants with good health. Three or more hours of moderately vigorous or vigorous physical activity also appeared to confer some protection against SDB, but these associations were weaker. Gender- and obesity-stratified analyses suggested that the protective association between physical activity and SDB occurred primarily in men and those who were obese. A program of regular vigorous physical activity of at least 3 h per week may be a useful adjunctive treatment modality for SDB, but this association needs confirmation with a prospective clinical trial.
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PMID:Association of physical activity with sleep-disordered breathing. 1722 Dec 74


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