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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The three forms of origin of the atherosclerotic plaque of adults, that is, the fatty streaks, gelatinous elevations, and microthrombi, all occur in arteries of normal infants and children. Some of these may become arrested or regress, but many progress to the prominent lesions that precipitate various clinical catastrophies. The aim of modern medicine is to modify or eliminate many of the factors known to advance the atherosclerotic process and thus decrease the incidence of this disease, which ranks highest on the list of causes of morbidity and mortality in the Western world. Of these factors, some may be controlled by dietary means (low salt; low total fat and cholesterol; appropriate ratios of saturated to mono- and polyunsaturated fatty acids; high content of complex carbohydrates and fiber); controlling hypertension, diabetes, and obesity; abstaining from cigarette smoking; and vigorous physical activities. Because patterns of life-style are determined in childhood and adolescence, and because it is only during that period of life that measures to prevent progression of atherosclerosis may be predictably effective, it becomes increasingly apparent that atherosclerosis is, indeed, a pediatric problem.
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PMID:The genesis of atherosclerosis in pediatric age-group. 217 19

Two thousand four hundred schoolchildren ages 9, 12, and 15 years were randomly selected to participate in the Health and Fitness Survey of Australian Schoolchildren in 1985. Data on blood lipids, aerobic fitness, blood pressure, and obesity were obtained through physical measurement. Information on socioeconomic status and ethnic origin was collected via questionnaire. Serum total cholesterol and low and high-density lipoprotein cholesterol were lowest in the oldest age group. Girls had significantly higher serum lipid levels, the difference being greatest at 15 years. However, comparison of the total cholesterol/high-density lipoprotein cholesterol ratio showed a trend in the direction of decreasing risk with increasing age for girls, with the reverse being found in boys. Fifteen-year-old girls were also the fattest and least fit of all the children, but had significantly lower systolic and diastolic blood pressures than their male peers. Children of Asian ethnic origin had significantly lower systolic and diastolic blood pressures and a significantly higher mean high-density lipoprotein cholesterol and were less likely to be overweight compared with other ethnic groups. Children from Mediterranean/Middle-East countries were significantly fatter and had a higher mean diastolic blood pressure than the other ethnic groups. These differences were detectable at age 9 years. Children from lower socioeconomic backgrounds were fatter and had a significantly lower mean high-density lipoprotein cholesterol and higher mean serum triglyceride levels. As with ethnic origin, these differences were detectable at age 9 years. The results demonstrate that age, sex, ethnic origin, and socioeconomic status can be used as variables to describe mean differences in the levels of cardiovascular risk factors in the national population of children. As some elevations in risk factors appear to be present in the youngest age group and these levels correlate with fatty streak and fibrous plaque formation in young adulthood, preventive programs should aim at intervention prior to puberty.
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PMID:Differences in modifiable cardiovascular disease risk factors in Australian schoolchildren: the results of a nationwide survey. 237 91

Rat pituitary cells were evaluated in the reverse hemolytic plaque assay for calcitonin (CT) secretion. The secretion of CT could be demonstrated by the formation of hemolytic plaques around single pituitary cells when a specific CT antibody was used. Approximately 0.1 percent of the cells secreted CT in the basal state. Phorbol stimulated CT secretion by up to 25-fold. The diameter of the hemolytic plaques around pituitary cells from genetically obese (Zucker) rats was significantly greater than normal rats (24 versus 37 microns). This study demonstrates that pituitary cells secrete CT and that the secretion may be regulated by pharmacological agents (phorbol) and physiological signals (obesity).
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PMID:Pituitary cells secrete calcitonin in the reverse hemolytic plaque assay. 330 93

Nutritional modulation of the immune response can be demonstrated both in nutritional deficiency and in obesity. A proportion of obese adolescents and adults showed a variable impairment of cell-mediated immune responses in vivo and in vitro and reduction of intracellular bacterial killing by polymorphonuclear leukocytes. Immunological changes correlated with subclinical deficiencies of iron and zinc, and therapy with these micronutrients for 4 weeks resulted in improvement in immunological responses. In genetically obese mice, the number of mononuclear cells and Thy 1.2-positive lymphocytes in the thymus and the spleen is less compared with that in lean controls. The plaque-forming antibody response is reduced. Natural killer cell activity is increased. Cytotoxic response of spleen cells of obese animals immunized in vivo was markedly lower than that of lean controls, whereas the same response after in vitro sensitization was normal. These data point to the importance of metabolic and nutritional factors in the pathogenesis of altered immunocompetence.
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PMID:Immune response in overnutrition. 726 Sep 49

The study of the fibrous lipid plaque formation in young subjects showed that the proliferation of the smooth muscle cells in the arterial wall intima was the primary process in the genesis of the atherosclerotic lesions. The hypoxic alterations and metabolic deterioration of the vascular wall occur at the sites of the proliferation of smooth muscle cells and focal hyperplasia. This results in the obesity of the smooth muscle cells and increased permeability for plasma proteins, which intensifies even more the focal intimal sclerosis. The necrosis and degradation of the smooth muscle cells "overloaded" with fat in the centre of the plaque result in the release of lipids into the extracellular space and in the formation of atheroma. Further progressing of atheroma occurs due to the involvement of the new "foamy" and smooth muscle cells, located in its periphery, but not due to the immediate lipid deposition from the arterial lumen.
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PMID:[Fibrous lipid plaque formation in young people]. 727 47

Cerebrovascular accidents are responsible for killing or disabling half a million Americans every year and are the third leading cause of death in this country. Finding cost-effective means of decreasing stroke mortality and morbidity is of great humanitarian and economic importance. Panoramic dental radiography was done on 19 white men who had a recent cerebrovascular accident and who were hospitalized at a Department of Veteran Affairs medical center. Inclusion criteria included clinical suspicion or imaging study evidence that the stroke arose from atheroembolic disease of the carotid artery bifurcation. Women were omitted from the study because of their paucity in the patient pool, and African-Americans and Asian-Americans were omitted because strokes in those groups usually develop as a result of disease of intracranial vessels. Carotid arterial calcifications appearing as a radiopaque nodular mass adjacent to the cervical vertebrae at or below intervertebral space C3-4 were noted in seven persons (37%). These patients had an average age of 65 years and demonstrated multiple risk factors (prior transient ischemic attacks, prior stroke, hypertension, obesity, tobacco and alcohol abuse, hyperlipidemia) associated with occurrence of a stroke. We concluded that some white men at risk for a cerebrovascular accident may be identified in the dentist's office by appropriate review of the panoramic dental radiograph and medical history. The presence of carotid artery calcifications demands an expeditious referral to an appropriate practitioner who can assist in the control of risk factors and arrange prophylactic surgical removal of the carotid arterial plaque, which are both safe and reliable methods of reducing the incidence of stroke.
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PMID:Prevalence of detectable carotid artery calcifications on panoramic radiographs of recent stroke victims. 806 36

The risks of cardiovascular disease associated with dyslipidemia differ in women and men, being more strongly associated with triglyceride/high-density lipoprotein in middle-aged women than in men. Although the incidence of heart disease is lower in women because they live longer, over a lifetime, cardiovascular disease in women is equal to that in men, with the greatest incidence after age 65 years. Major coronary events are rare among reproductive-age women who use oral contraceptives and are related to the concomitant effects of age, smoking, diabetes, hypertension, and obesity. Low estrogen-progestin dose oral contraceptives appear not to promote cardiovascular disease and can be used in women with controlled cholesterol elevations. Alternative contraceptive measures should be considered for patients with severe uncontrolled hypercholesterolemia or a lipid disorder that carries a high risk of coronary heart disease. In these conditions, thrombotic propensity associated with supraphysiologic doses of estrogen in oral contraceptives might accelerate coronary thrombosis should an arteriosclerotic plaque rupture. Treatment of hypercholesterolemia should follow the guidelines of the National Cholesterol Education Program and emphasize hygienic measures. Contraceptive selection in hyperlipidemic patients should reflect a balance between the risks--and their management--of developing cardiovascular disease versus the risks of pregnancy.
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PMID:Contraception and dyslipidemia. 851 44

Dietary cholesterol in infancy may alter cholesterol metabolism and the propensity to develop atherosclerosis. This study examined the effects of a 1% cholesterol diet (HC) vs. a no-cholesterol diet (NC) during the first 2 mo of life on pigs selectively bred for leanness or obesity. Three lean and three obese pigs received the no-cholesterol diet, and four lean and four obese pigs received the 1% cholesterol diet from d 1. Lean and obese pigs fed the no-cholesterol diet showed no increase in serum lipid concentrations, nor did they develop atherosclerosis. Obese pigs fed the 1% cholesterol diet developed significantly higher serum total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) at 35 d than lean pigs fed the 1% cholesterol diet. By d 55, only HDL-C remained significantly higher in the obese pigs, resulting in a higher (P < 0.1) TC/HDL-C ratio in the lean pigs. Atherosclerotic plaque formation in the aorta was more extensive in the lean pigs. Cholesterol synthesis measured in vivo and at termination was equally suppressed in lean and obese pigs fed the 1% cholesterol compared with pigs fed the no-cholesterol diet. We conclude that genetic differences in the response of these lean and obese pigs to a high cholesterol diet render obese pigs less susceptible to atherosclerosis despite higher serum TC concentrations. The persistent elevation of HDL-C in obese pigs is the most likely mechanism of protection.
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PMID:Obese pigs fed a high cholesterol diet from birth to 2 months are less susceptible than lean pigs to atherosclerosis. 863 32

Cerebral infarction (CI) is still a leading cause of death in Japan. Thus, the management of risk factors for CI as primary prevention is one of the most important tasks in multiphasic health testing and services. To determine whether carotid intima-media thickness (IMT) is a risk for CI, ultrasonographically assessed carotid IMT was compared between normal subjects (N) and subjects with asymptomatic CI (ACI) in 243 subjects who underwent human brain dry dock. ACI was found in 68 people (28.0%). Age, body mass index, and mean blood pressure were higher in ACI than in N. Also, atherogenic index was higher in ACI than in N. Carotid IMT was significantly thicker in ACI than in N. Furthermore, incidence of atherogenic plaque in ACI was significantly higher than that in N. In conclusion, not only aging, obesity, blood pressure, and plasma lipids, but also carotid IMT may be a risk for ACI.
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PMID:Ultrasonographically assessed carotid intima-media thickness and risk for asymptomatic cerebral infarction. 955 5

The high atherogenic potential of the insulin resistance syndrome can be only partly explained by the association of "classical" risk factors of atherosclerosis which are considered part of it, i.e. impaired carbohydrate tolerance/diabetes mellitus type II, dyslipidaemia, hypertension and obesity. Impaired fibrinolysis due to excessive production of the plasminogen activator inhibitor-1 (PAI-1) are further risk factors which participate in the process of atherogenesis from the beginning of formation of the atheromatous plaque to the thrombotic occlusion of the vascular lumen. The authors present a group of 25 patients with different grades of glucose resistance, evaluated by theinsulin response to a glucose load. The insulin resistant group (n = 15) differed significantly from the non-resistant one (n = 10) as regards body weight and the central type of obesity (< 0.01 and 0.001 resp.) insulin level on fasting and after a load (< 0.0001 and 0.001 resp.), triglyceride levels (< 0.01), the incidence of diabetes or impaired carbohydrate tolerance (66.7 vs. 20%) and hypertension (53.3 vs. 20%), but also as regards the PAI-1 activity (.0001). As regards blood sugar levels, total and HDL cholesterol the groups did not differ. The authors investigated also the relationship between PAI-1 activity and different components of the insulin resistance syndrome in the whole group. The closest correlation was found between the PAI-1 activity and the general insulinaemic response to a glucose load (< 0.001) and between PAI-1 and triglycerides (< 0.001). Based on the presented results it may be stated that hypofibnrinolysis as a result of excessive production of PAI.1 is part of the insulin resistance syndrome and potentiates its high atherogenic risk.
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PMID:[The insulin resistance syndrome and fibrinolysis disorders]. 960 68


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