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

Immunological factors seem to play an important role in the pathogenesis of atherosclerosis, which is a multifactorial chronic disease. It was demonstrated on animals that antibodies, immune complexes and cells may be the reason why the immunological damage in the vascular wall appears and may lead in consequence to the development of atherosclerotic changes. Immunological mechanisms of atherosclerosis are discussed.
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PMID:[The role of immunological factors in the pathogenesis of arteriosclerosis]. 194 91

CAD results from atherosclerosis, a chronic disease process that has its origin in childhood. Children and adolescents can be at higher risk for CAD by virtue of being from families with premature CAD or familial dyslipoproteinemias. The plasma lipid and lipoprotein levels result from a number of complex metabolic processes that are under the control of genetic and environmental (e.g., diet) influences. The normal ranges of plasma lipids and lipoproteins in children are known, and children and adolescents with dyslipoproteinemia are ordinarily defined as those having levels of plasma total, LDL, or triglyceride above the 95th percentile or with a low HDL cholesterol below the 5th percentile. Children of a parent with documented dyslipoproteinemia or with family history of premature CAD may be screened in the fasting state any time after 2 years of age. Following the exclusion of secondary causes of dyslipoproteinemia, the diagnosis of primary dyslipoproteinemia can be made. Lipoprotein patterns are not diagnostic for a given genotype. Efforts to determine further the biochemical defects responsible for a given phenotype have led to the investigation of gene coding for the apolipoproteins, the key enzymes in the lipoproteins pathways (LPL, HDL, and LCAT) and the receptors that process lipoproteins, such as the LDL receptor and the chylomicron remnant receptor. From a practical standpoint, the diagnosis of the kind of dyslipoproteinemia in a child will depend upon the nature and severity of the dyslipoproteinemia, both in the child (or adolescent) and in parents and siblings. Marked increases in plasma total and LDL cholesterol in the child and in at least one of the parents often reflect the presence of familial hypercholesterolemia, an inherited dominant condition due to a defect in the LDL receptor gene. The triglyceride levels are often normal. If the child has a different dyslipoproteinemia pattern from siblings and parents, then the diagnosis of familial combined hyperlipidemia or hyperapobetalipoproteinemia should be considered. Most children with mild or borderline elevations in total and LDL cholesterol will have polygenic hypercholesterolemia. Triglyceride problems in children and adolescents are relatively uncommon, particularly the more severe hypertriglyceridemia such as that found in lipoprotein lipase and apoC-II deficiency, dysbetalipoproteinemia, and type V hyperlipoproteinemia. High levels of Lp(a) lipoprotein, in isolation or in combination with other dyslipoproteinemia, accelerate risk for CAD. Low levels of HDL cholesterol in the absence of other abnormalities suggest the diagnosis of hypoalphalipoproteinemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diagnosis and management of familial dyslipoproteinemia in children and adolescents. 225 50

In a human, the cells function adequately to the needs of the organism, and to their own needs. Consequently, adequate cell function is comprised of the organism-oriented, and cell-oriented functions. It is suggested that an independent stage in the pathogenesis of a chronic disease exists which so far has not been considered. This is the disturbance of the cell-oriented function of the cells involved. This initial stage may last for years and decades, whereas function of the organ remains preserved. Organism-oriented cellular function appears to become involved in the pathologic process long after the disease has actually started. At this time the cells themselves are severely impaired, and as a result a disease acquires its progressive, irreversible course. Pathogenesis of atherosclerosis is considered as an example of the above-mentioned developments.
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PMID:General mechanism of chronic diseases. 364 72

Although several risk factors for heart disease including high blood pressure, diabetes mellitus, and lipid and lipoprotein abnormalities are associated with overweight, overweight is not consistently associated with coronary heart disease risk. Some prospective studies of white men (life insurance cohorts, airline pilots, cancer study volunteers, and the Framingham population) have shown a positive linear relationship of weight to coronary heart disease. Other epidemiologic studies show a negative association, no association, a U-shaped relationship, or a threshold effect. The inconsistencies do not appear to be explained by differences in the definition or distribution of obesity, duration of follow-up, or risk factor distribution. Neither misclassification bias nor confounding by cigarette smoking or chronic disease appears to explain the inconsistencies. No known protective effect of obesity could explain these divergent findings. Inconsistent results with regard to the nature, strength, and linearity of the association between obesity and atherosclerosis do not support the hypothesis that obesity causes atherosclerosis, despite its biological plausibility.
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PMID:Obesity, atherosclerosis, and coronary artery disease. 390 65

Cigarette smoking is the largest single preventable cause of illness and premature death in the United States. It is the major single cause of cancer mortality in the United States and is a causal factor for coronary heart disease and arteriosclerotic peripheral vascular disease; is associated with increased risk of coronary atherosclerosis; and is the most important cause of chronic obstructive lung disease. Cigarette smoking increases the risk of bladder, pancreatic, and renal cancer, and peptic ulcer disease. Maternal cigarette smoking during pregnancy causes: retarded fetal growth; an increased risk for spontaneous abortion, fetal death, and neonatal death; and, possibly, slight impairment of growth and development during early childhood. Cigarette smoking acts synergistically with oral contraceptives to increases the risk for coronary heart disease and some forms of cerebrovascular disease; with alcohol to increase the risk of cancer of the larynx, oral cavity, and esophagus; with asbestos and some other occupationally encountered substances to increase the likelihood of cancer of the lung and larynx; and with other coronary risk factors such as hypercholesteremia to enhance cardiovascular risk. Smoking is the major identifiable cause of residential fire deaths and injuries as well as a contributor to accidental injuries. Cigarette smokers have a 70 percent higher overall death rate than nonsmokers, and tobacco is associated with an estimate in excess of 300,000 premature deaths a year. It is estimated that smoking contributes to as many as 225,000 deaths from coronary heart disease, the major cause of death among men and women in the United States; more than 100,000 deaths from cancers; and more than 20,000 deaths from chronic obstructive lung disease. Another 10 million Americans currently suffer from debilitating chronic disease caused by smoking. But substantial progress has been made since the release of the first Surgeon General's Report in 1964. More than 30 million smokers have quit since 1964 and the proportion of adult smokers has declined from about 42 percent in 1965 to approximately one-third today. Adult per capita consumption of cigarettes declined temporarily in 1953, 1954, 1964 and 1968-70, and the rate of decline has accelerated since 1977. Teenage smoking, particularly among adolescent girls, appears to be declining.
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PMID:Health promotion: Smoking control. 641 11

During adolescence and the third decade of life a redistribution of bodily fat is occurring away from the extremities towards the trunk. During this time the process is occurring in both sexes although more rapidly in males than females, hence it is a masculinizing process. The process is seen in human populations from various ethnic and cultural backgrounds. Masculinizing characteristics like this one are predictors of chronic diseases such as diabetes and atherosclerosis late in life. The period from adolescence through young adulthood may be a sensitive time for the development of characteristics that predispose one to the chronic diseases of aging. Socioanthropological investigations of chronic disease related to human obesity may benefit by focusing on this developmental period.
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PMID:The changes with age of the anatomical distribution of fat. 698 Apr 68

An analysis of the effects of diabetes and generalized atherosclerosis on death due to ischemic heart disease or stroke was conducted using multiple cause mortality statistics. Specifically, all U.S. deaths in 1969 were classified into two groups on the basis of whether diabetes or generalized atherosclerosis was mentioned anywhere on the death certificate. Then race and sex specific analyses were made of ischemic heart disease deaths (or alternately of stroke deaths) using modified life table techniques for each group (one with the specified chronic disease and one without). Comparisons were made of mortality due to the acute circulatory events (ischemic heart disease or stroke) in the two groups to determine the implications of the chronic disease for the progression of the circulatory disease events. It was found, according to expectations, that diabetes and generalized atherosclerosis play very different roles in deaths due to stroke and ischemic heart disease.
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PMID:Mortality of the chronically impaired. 738 60

We examined the association of serum albumin concentration with diabetes mellitus and other cardiovascular risk factors, prevalent cardiovascular disease, and ultrasonographically assessed carotid artery intima-media thickness using data from 45- to 64-year-old adults in the Atherosclerosis Risk in Communities (ARIC) Study. The mean albumin concentration was 0.04 to 0.12 g/L lower in participants with diabetes and 0.02 to 0.06 g/L lower in those with cardiovascular disease, compared to participants without these conditions. However, lower serum albumin level was also correlated with most traditional risk factors and hemostatic variables. On adjustment for these, there was essentially no association between serum albumin and prevalent cardiovascular disease. Likewise, there was no association between albumin and carotid intima-media thickness (a marker of atherosclerosis). While hypoalbuminemia may be a marker for chronic disease and perhaps renal loss of albumin, it seems unlikely that it is an important cause of atherosclerosis.
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PMID:Low serum albumin. Association with diabetes mellitus and other cardiovascular risk factors but not with prevalent cardiovascular disease or carotid artery intima-media thickness. The Atherosclerosis Risk in Communities (ARIC) Study Investigators. 760 7

Non-insulin dependent diabetes mellitus (NIDDM) is an important cause of morbidity and mortality, both in developed as well as in developing countries. The eyes, kidneys, and cardiovascular and neurological systems are predominantly affected by this chronic disease, leading to loss of employment and sometimes life. The most common setting is uncontrolled glycaemia after dietary restriction, exercise and oral hypoglycaemic drug therapy. Insulin may be needed for treating NIDDM some time during the course of the disease. Insulin therapy results in improved beta-cell function, a decrease in the hepatic glucose output and an improvement of the lipoprotein profile. Some of these beneficial effects are due to nullification of 'glucose toxicity'. Objective evidence of a link between tight metabolic control and chronic complications of NIDDM is still not established, despite the results of recent trials. Many insulin regimes have been tried. Recently, attention has been focused on combination therapy with sulphonylureas and insulin, using long-acting insulin at bedtime only. This regime improves the glycaemic profile (due to a reduction of hepatic glucose output), using lower doses of insulin and sulphonylureas. However, experience with this regime suggests that it is only suitable for a subset of NIDDM patients. Adverse effects of insulin therapy include weight gain and hypoglycaemia, which can usually be easily managed. It is hyperinsulinaemia, with its complex array of adverse metabolic effects, that has recently concerned physicians. Acceleration of atherosclerosis, hypertension and worsening of the lipoprotein profile have been cited as possible adverse effects. The presence of such dysregulation is included in the recently described syndrome X.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin treatment in non-insulin dependent diabetes mellitus. 763 12

Oxygen-free radical reactions have been implicated in many chronic disease processes, including atherosclerotic cardiovascular disease. Recent studies of lipid metabolism have suggested that oxidative modification of low-density lipoprotein accelerates atherogenesis. Micronutrient antioxidants, including alpha-tocopherol and beta-carotene, however, can neutralize oxygen-free radicals and inhibit low-density lipoprotein oxidation. This review examines (1) the role of oxidized low-density lipoprotein in atherogenesis, (2) the association between nutritional antioxidant intake and atherosclerosis, and (3) observational and clinical trial data on the effect of antioxidants in reducing the risk of coronary heart disease. While evidence suggests that antioxidant supplements protect against coronary heart disease, definitive recommendations await results from ongoing randomized trials of primary and secondary prevention.
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PMID:Antioxidants and the prevention of coronary heart disease. 761 96


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