Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with heterozygous familial hypercholesterolaemia (FH) have a substantially increased risk of atherosclerosis due to very high plasma levels of cholesterol. Recent evidence has shown that coronary heart disease in these patients may regress with lipid-lowering therapy. In this study the efficacy and safety of simvastatin, an inhibitor of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A, was investigated in 30 patients with FH over a period of one year. Substantial reductions in the plasma concentrations of total cholesterol (-28%), low-density lipoprotein (LDL) cholesterol (-32%), intermediate-density lipoprotein (IDL) cholesterol and apolipoprotein (apo) B (-33%) were achieved with 20 mg/day of simvastatin; there were no significant changes in triglycerides high-density lipoprotein cholesterol or apo A. In contrast to previous studies, 40 mg/day of simvastatin did not result in a further statistically significant fall in LDL cholesterol, IDL cholesterol or apo B in the group as a whole. The drug was well tolerated and no adverse clinical or laboratory events were recorded. In particular, no ophthalmological, hepatic or renal disorders were observed and there were no sleep disturbances. We conclude that simvastatin is an efficacious and safe drug to treat patients with heterozygous FH and that rarely will the dose need to be increased above 20 mg/day.
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PMID:One year experience in the treatment of familial hypercholesterolaemia with simvastatin. 143 57

Clinical and polygraphical (EEG, EOG, EMG, ECG, REG) studies of nocturnal sleep and of the hemodynamics were carried out in 60 patients with dyscirculatory encephalopathy induced by hypertension and atherosclerosis. The findings obtained demonstrate that the clinical picture in these patients is always characterized by sleep disturbances which decrease the level of their diurnal wakefulness and their capacity for work. Hemodynamic disturbances responsible for sleep disorders are in turn maintained by the latter which leads to the formation of the vicious circle. This is also supported by the fact that compromized cerebral circulation causes changes in the activity of the structures involved both in sleep-wakefulness function and the regulation of the cerebral and systemic hemodynamics. Hence, deviations in the nocturnal sleep pattern attended with pronounced alterations in the cerebral hemodynamics may contribute to the development of acute disorders of the cerebral circulation. The authors recommend correcting not only the disrupted structure of sleep but also the cerebral circulation with relation to he sleep-wakefulness cycle.
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PMID:[Nocturnal sleep and cerebral hemodynamics in different sleep stages and cycles among patients with early manifestations of cerebral circulatory insufficiency]. 650 76

Four clusters of psychosocial risk factors for coronary heart disease (CHD) are reviewed. Socio-economic disadvantage acts through a number of influences to increase CHD risk. In advanced industrialized nations those in the lower social strata now have much higher CHD risk than persons in middle and upper social classes. Sustained disturbing emotions represent a second cluster. Anxiety, depression and other indices of neuroticism have frequently been found in association with angina pectoris and cardiac death, though not with myocardial infarction (MI). However, sleep disturbances are associated with angina, cardiac death and MI. The Type A behaviour pattern results from an interaction between a self-activating individual and an environment which rewards hurried and competitive activity. Despite a small number of negative findings, the Type A pattern has been shown in cross-sectional, retrospective and prospective studies by many research teams to be associated with a variety of manifestations of CHD. A fourth, and more recently recognized cluster of psychosocial risk factors, may be grouped together under the general heading of "overload". Many investigations have now shown, for example, that excessive workload is a powerful predictor of CHD risk. It is suggested that all four clusters share the common property of exposing the individual, either chronically, or in frequently recurring episodes, to excessive psychological demands. They appear to exert their pathogenic influence through long-term mechanisms such as atherosclerosis or plaque formation, rather than by precipitating sudden coronary events.
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PMID:Psychosocial risk factors for coronary heart disease. 698 1

The successful use of renal replacement therapy has resulted in longer survival and a population of older patients with chronic kidney disease (CKD) that includes patients with other significant preexisting illnesses. In this review, we analyze the short-term and long-term outcomes associated to persisting hypogonadism in CKD patients. The short-term manifestations, commonly observed in normal postmenopausal women, are either a rare complaint of women with CKD or are frequently attributed to the uremic state. These symptoms include hot flashes, sleep disturbances and depression, sexual dysfunction, vaginal dryness and atrophy, urinary incontinence, and skin aging and wrinkling. The long-term outcomes of hypogonadism have potentially devastating effects on bone, cardiovascular system, and cognitive function, which could significantly alter the quality of life and survival of women with stage 5 CKD (CKD-5). Postmenopausal osteoporosis has been recognized as an important entity associated with renal osteodystrophy, and efforts have begun to tackle the reduced bone-mineral density (BMD) and increased fracture rate seen in this population. Similarly, cardiovascular disease represents the major cause of death in the CKD-5 population, with a 10 to 20 times greater mortality than in the general population. The accumulating evidence for a possible link between osteoporosis and atherosclerosis is discussed, as well as new directions in the understanding of postmenopausal osteoporosis in the context of renal bone disease, under the guidance of the Global Bone and Mineral Initiative endorsed by the Kidney Disease: Improving Global Outcomes initiative. Nephrologists must face gynecological issues with their women patients and design interdisciplinary clinical studies that include strategies that utilize well-tested and newer drug regimens in the management of osteoporosis, cardiovascular disease, and other postmenopausal manifestations in CKD-5 patients.
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PMID:Outcomes associated with hypogonadism in women with chronic kidney disease. 1549 73

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
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PMID:Cytokine dysregulation, inflammation and well-being. 1616 5

Sleep is an important modulator of cardiovascular function, both in physiological conditions and in disease states. In individuals without a primary sleep disorder, sleep may exert significant effects on the autonomic nervous system, systemic hemodynamics, cardiac function, endothelial function, and coagulation. Some of these influences can be directly linked to specific modulatory effects of sleep stages per se; others result from the natural circadian rhythm of various physiological processes. There is a temporal association between physiological sleep and occurrence of vascular events, cardiac arrhythmias, and sudden death. Epidemiological and pathophysiological studies also indicate that there may be a causal link between primary sleep abnormalities (sleep curtailment, shift work, and sleep-disordered breathing) and cardiovascular and metabolic disease, such as hypertension, atherosclerosis, stroke, heart failure, cardiac arrhythmias, sudden death, obesity, and the metabolic syndrome. Finally, sleep disturbances may occur as a result of several medical conditions (including obesity, chronic heart failure, and menopause) and may therefore contribute to cardiovascular morbidity associated with these conditions. Further understanding of specific pathophysiological pathways linking sleep disorders to cardiovascular disease is important for developing therapeutic strategies and may have important implications for cardiovascular chronotherapeutics.
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PMID:Sleep and cardiovascular disease. 1630 Oct 95

Sleep is an essential part of our daily living, and sleep disturbances may intervene with the biological and physiological processes in human body leading to the development of metabolic dysfunction. Short sleep duration and poor sleep quality have adverse effects on metabolism and hormonal processes, contributing to increased cardiovascular risk. Obstructive sleep apnoea is a chronic condition characterized by repetitive upper airway collapse during sleep, causing intermittent hypoxaemia, recurrent arousals and sleep fragmentation. Sleep disturbances can increase sympathetic activity, provoke systemic inflammation and oxidative stress, and impair vascular endothelial function. Obstructive sleep apnoea is increasingly recognized to be an independent cardiovascular risk factor. There is intense research interest in the association between obstructive sleep apnoea and the metabolic syndrome - the constellation of inter-related metabolic derangements including central obesity, hypertension, insulin resistance and dyslipidaemia, which appears to directly promote the development of atherosclerosis. The underlying pathophysiologic pathways or mechanistic links between obstructive sleep apnoea and metabolic syndrome have not been well delineated. This article reviews the current knowledge of the relationship between sleep disturbances, sleep-disordered breathing and the metabolic syndrome in adults.
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PMID:Sleep & the metabolic syndrome. 2030 46

In developing countries, shift work represents a considerable contingent workforce. Recently, studies have shown that overweight and obesity are more prevalent in shift workers than day workers. In addition, shift work has been associated with a higher propensity for the development of many metabolic disorders, such as insulin resistance, diabetes, dislipidemias and metabolic syndrome. Recent data have pointed that decrease of the sleep time, desynchronization of circadian rhythm and alteration of environmental aspects are the main factors related to such problems. Shortened or disturbed sleep is among the most common health-related effects of shift work. The plausible physiological and biological mechanisms are related to the activation of the autonomic nervous system, inflammation, changes in lipid and glucose metabolism, and related changes in the risk for atherosclerosis, metabolic syndrome, and type II diabetes. The present review will discuss the impact of shift work on obesity and metabolic disorders and how disruption of sleep and circadian misalignment may contribute to these metabolic dysfunctions.
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PMID:Metabolic impact of shift work. 2231 92

Many aspects of human health and disease display daily rhythmicity. The brain's suprachiasmic nucleus, which interprets recurring external stimuli, and autonomous molecular networks in peripheral cells together, set our biological circadian clock. Disrupted or misaligned circadian rhythms promote multiple pathologies including chronic inflammatory and metabolic diseases such as atherosclerosis. Here, we discuss studies suggesting that circadian fluctuations in the vessel wall and in the circulation contribute to atherogenesis. Data from humans and mice indicate that an impaired molecular clock, disturbed sleep, and shifting light-dark patterns influence leukocyte and lipid supply in the circulation and alter cellular behavior in atherosclerotic lesions. We propose that a better understanding of both local and systemic circadian rhythms in atherosclerosis will enhance clinical management, treatment, and public health policy.
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PMID:Circadian Influence on Metabolism and Inflammation in Atherosclerosis. 2734 Feb 72

Circadian rhythm is an internal biological clock which initiates and monitors various physiological processes with a fixed time-related schedule. The master circadian pacemaker is located in the suprachiasmatic nucleus in the hypothalamus. The circadian clock undergoes significant changes throughout the life span, at both the physiological and molecular levels. This cyclical physiological process, which is very complex and multifactorial, may be associated with metabolic alterations, atherosclerosis, impaired cognition, mood disturbances and even development of cancer. Sex differences do exist, and the well-known sleep disturbances associated with menopause are a good example. Circadian rhythm was detected in the daily pattern of hot flushes, with a peak in the afternoons. Endogenous secretion of melatonin decreases with aging across genders, and, among women, menopause is associated with a significant reduction of melatonin levels, affecting sleep. Although it might seem that hot flushes and melatonin secretion are likely related, there are not enough data to support such a hypothesis.
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PMID:Circadian rhythm and menopause. 2784 37


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