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

The relationship between overweight and cardiovascular disease was a matter of debate for many years. Recent studies have demonstrated that obesity defined as body mass index of 30 kg/m2 or higher is associated with an exponential increase of cardiovascular complications. This effect is largely mediated by the induction of established risk factors such as dyslipidemia, hypertension and type 2 diabetes mellitus. Recently, there is growing evidence that the occurrence of most complications of obesity depends not only on the degree of overweight but also on the pattern of body fat distribution. Many data suggest that the anatomical localization of body fat is more important for the risk of developing complications than the adipose tissue mass per se. An abdominal, upper-body type of fat distribution, which can be easily determined by the measurement of waist and hip circumferences (waist/hip ratio = WHR), is also a confirmed risk factor for metabolic disturbances, hypertension and atherosclerosis, independent of body weight. However, the clinical appearance of these disturbances is frequently associated with the development of obesity. This network of metabolic disorders and their vascular complications is termed "metabolic syndrome" or "syndrome X" (Table 2). Abdominal obesity is now known to be closely associated with the metabolic syndrome and is regarded to represent its readily recognizable phenotypic feature. The components of the metabolic syndrome are characterized by varying forms and degrees of insulin resistance. It is assumed that insulin resistance, defined as diminished biological response to the action of insulin, represents the primary defect or at least the common pathogenetic link between these disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal obesity and coronary heart disease. Pathophysiology and clinical significance]. 771 76

Insulin is frequently considered to be a risk factor for atherosclerosis (or for coronary and vascular disease). Furthermore, hyperinsulinaemia is claimed to be the primary cause underlying the other features which make up the insulin resistance syndrome. However, if proof of these assertions is based only on prospective studies, its value is limited. Only two studies, both carried out, surprisingly, in policemen, have shown convincingly that insulin was a coronary risk factor. In one of the studies, the Paris Prospective Study, the insulin-coronary disease correlation was shown to subside with increasing duration of follow-up. The other prospective studies have failed to evidence a correlation between insulinaemia and cardiovascular events, even with univariate analysis. One study even showed a negative correlation between insulinaemia and coronary complications. In view of the fact that insulinaemia has been shown repeatedly to be associated with classic cardiovascular risk factors--systolic hypertension, decrease in HDL cholesterol, increase in triglycerides, and abdominal obesity--it is highly surprising that univariate analysis has not been able to show the same correlation between insulin and cardiovascular complications. In fact, the combination of elevated insulinaemia and classic risk factors may result in protection against the deleterious effects of these factors. Another possibility would be that insulinaemia is associated with unknown protective factors. Both hypotheses would account for the existence of a correlation between insulin and current cardiovascular disease, as well as the absence of correlation between insulin and later onset of cardiovascular disease.
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PMID:[Why is insulin tied to the prevalence of cardiovascular diseases without being a risk factor for their incidence?]. 782 81

Hypertension and atherosclerosis are highly prevalent disorders which contribute substantially to the burden of premature morbidity and mortality at significant cost to the economy. Hypertension, abdominal obesity and risk factor clustering represent complex regulatory disorders which probably reflect an interaction of multiple genetic and environmental factors. Information has been summarised which indicates that fish oil, obtained either as a dietary supplement or by the consumption of more fish products, represents a relatively simple and comparatively inexpensive dietary intervention which may lower BP, especially in combination with a low salt diet, and favourably alter multiple risk factors in the cluster. This summary also indicates that multiple significant gaps in our knowledge about fish oil remain. Closing these gaps through further clinical and basic research may lead to greater acceptance and more appropriate therapeutic use of fish oil for health maintenance and disease prevention.
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PMID:Is there a role for dietary fish oil in the treatment of hypertension? 788 88

The relationship between obesity and prevalence of dyslipidemia is well known. Recent studies affirm that differences in fat distribution can be predictive for differences in the prevalence of metabolic disturbances and cardiovascular disease independently of the BMI, presently the most common index of obesity. In order to verify whether body fat distribution can be associated with a higher risk of atherosclerosis, we have evaluated in a group of obese women the eventual presence of endocrine and metabolic diseases. Assessing regional fat distribution, the waist/hip ratio has been shown to be more closely correlated with these diseases than BMI. We have studied two groups of 10 women, comparable for age and BMI: group A aged 45.8 +/- 6.9 years with a BMI of 35.6 +/- 2.8 kg/m2; group B aged 48.3 +/- 3.6 years with a BMI of 38.5 +/- 2.8 kg/m2. The women were divided according to the waist-hip ratio, which was calculated by measuring the circumference of the waist, namely the smallest circumference between the xiphoid and the umbilicus, and the circumference of the hips at the point of the maximum protuberance of the buttocks. The cut-off value for the waist/hip ratio was considered as 0.80 for the reason that this variable is the most accurate cut-off value for abdominal obesity: for group A 0.76 +/- 0.02; for group B 0.89 +/- 0.02 (p < 0.01). All the women were healthy. None of them was in therapy with any kind of drugs, nor was there any restriction to diet. Nobody was a smoker, neither did anyone drink alcoholic beverages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transverse study of obesity: distribution of adipose tissue and correlated pathology]. 823 18

The hypothesis that a causal relationship exists between insulin resistance and atherogenesis was first proposed over 23 years ago, and has given rise to a vast literature. Biological plausibility has been lent to the hypothesis by studies in which insulin has produced some effects in cell and tissue culture, and in vivo in arterial tissue, consistent with our understanding of the pathogenesis of atherosclerosis. Clinical studies demonstrating a complex interrelationship between insulin resistance-hyperinsulinaemia and established risk factors for CHD--hypertension, hypertriglyceridaemia, low HDL cholesterol levels and abdominal obesity--are reviewed. A review of the studies examining an independent association between hyperinsulinaemia and coronary heart disease is presented. Cross-sectional studies in both the general population and diabetes support the relationship; however, prospective studies in the general population provide limited and inconsistent support for this hypothesis and highlight the confounding effects of blood pressure, dyslipidaemia and obesity on the effects of hyperinsulinaemia. In subjects with NIDDM and impaired glucose tolerance, prospective studies have not shown a deleterious effect of insulin treatment per se, nor have they consistently shown a significantly increased risk for those with higher endogenous insulin levels. The therapeutic implications of the evidence to date are less complex and involve weight reduction by diet and exercise, the lowering of elevated blood pressure with metabolically neutral agents, the judicious use of lipid lowering drugs and, in diabetes, the use of insulin where clinically indicated.
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PMID:Relationship between insulin resistance and coronary heart disease in diabetes mellitus and the general population: a critical appraisal. 830 14

Despite numerous reports that abdominal obesity is related to disease risk, the study of body-fat distribution remains a largely empirical science. Elucidation of the pathophysiologic linkage between abdominal obesity and disease would be better served by generating hypotheses and testing them--the process of deductive science. Physiologists have proposed that adipose tissue of the intra-abdominal compartment (that drained by the portal vein) contributes strongly to atherosclerosis. If this is so, then the volume of the intra-abdominal fat depot might be better correlated with disease states than a less specific anthropometric index such as the waist-to-hip girth ratio. Alternative abdominal-obesity indices (e.g. sagittal abdominal diameter divided by thigh girth) could be tested in epidemiologic studies to improve our pathophysiologic understanding of how body-fat distribution is related to atherosclerosis and other diseases.
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PMID:Choosing an index for abdominal obesity: an opportunity for epidemiologic clarification. 189 Apr 38

Recent evidence suggests that non-insulin-dependent diabetes mellitus (NIDDM) and cardiovascular disease, rather than being related as underlying disease and complication, share common genetic and environmental antecedents, that is, they "spring from the same soil." Fetal and early-life nutritional deficiencies appear to predispose persons to both NIDDM and cardiovascular disease in later life. The insulin resistance syndrome, including abdominal obesity, may constitute the intermediate link between fetal and early-life nutritional deficiency and later disease. The insulin resistance syndrome includes insulin resistance, hyperinsulinemia, abdominal obesity, dyslipidemia with high triglyceride and low high-density lipoprotein cholesterol levels, and hypertension. Each element of the insulin resistance syndrome has been firmly established as a risk factor for development of diabetes. In addition, most of these elements are also well-recognized cardiovascular risk factors, although the weight of evidence now suggests that hyperinsulinemia itself is not. This last point is significant because of concern that aggressive insulinization of diabetic patients, which has been proved to reduce microvascular complications, might paradoxically increase the risk for large-vessel atherosclerosis. Available clinical trials suggest that this fear is unwarranted, but definitive trials are needed to resolve this important clinical question.
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PMID:Do non-insulin-dependent diabetes mellitus and cardiovascular disease share common antecedents? 855 1

Excessive deposition of visceral adipose tissue is known to predispose to cardiovascular diseases. Considerable epidemiological and experimental evidence suggests that many physiological factors are involved in the aetiology of premature atherosclerosis associated with visceral obesity. Insulin resistance is frequently associated with abdominal obesity, and probably plays an important role in the pathophysiology of hypertriglyceridaemia, low levels of plasma high-density lipoprotein (HDL)-cholesterol, hypertension and reduced fibrinolytic activity. Exercise training may counteract the aberrant metabolic profile associated with abdominal obesity both directly and as a consequence of body fat loss. Exercise may increase insulin sensitivity, favourably alter the plasma lipoprotein profile and improve fibrinolytic activity. Changes in the activity of insulin-sensitive glucose transporters and of skeletal muscle lipoprotein lipase are some of the possible explanations for the increased insulin sensitivity and improved blood lipid profile associated with regular exercise. This review presents physical training as a relevant nonpharmacological tool in the treatment of abdominal obesity and associated metabolic disorders. The impact of regular exercise on the different aspects of the insulin resistance syndrome is discussed. The roles of gender, age and the state of insulin resistance on the metabolic effect of physical training are also considered.
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PMID:Effects of exercise training on abdominal obesity and related metabolic complications. 877 9

Increased abdominal obesity has been related to lower insulin sensitivity (SI), independent of overall obesity, but it has been suggested that this relationship may be weaker in non-whites. In the Insulin Resistance and Atherosclerosis Study (IRAS), SI was estimated using a minimal model analysis of the frequently sampled intravenous glucose tolerance test in 1,625 men and women aged 40-69 years. Subjects included African-Americans, Hispanics, and non-Hispanic whites from Oakland and Los Angeles, CA, San Antonio, TX, and the San Luis Valley, CO. Minimum waist circumference was significantly (P = 0.0001) associated with SI after adjusting for age, sex, height, BMI, glucose tolerance status, ethnicity, and clinic. This relationship was significantly (P = 0.0001) stronger in subjects with normal glucose tolerance (NGT) (beta = -0.030, P = 0.0001) than in those with impaired glucose tolerance (IGT) (beta = -0.010, P = 0.02; NIDDM: beta = -0.013, P = 0.0001). There were no significant ethnic differences in effect size across the spectrum of glucose tolerance. Waist circumference was also positively related to fasting insulin, an indirect measure of insulin sensitivity, in NGT (P = 0.0001), IGT (P = 0.0003), and NIDDM (P = 0.0002). The waist-fasting insulin relationship was significantly weaker in African-Americans, relative to non-Hispanic whites, in NGT and IGT (tests of statistical interaction: P = 0.04 and P = 0.02, respectively). In general, these patterns were similar in models specifying waist-to-hip ratio (WHR), rather than waist circumference, as the independent variable. While some ethnic variability exists, a negative relationship between abdominal obesity and insulin sensitivity was confirmed for all three ethnic groups across the spectrum of glucose tolerance.
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PMID:Insulin sensitivity and abdominal obesity in African-American, Hispanic, and non-Hispanic white men and women. The Insulin Resistance and Atherosclerosis Study. 886 60

A variety of studies indicates that the process of atherosclerosis begins in childhood and progresses during adulthood. Chronic obesity, inadequate caloric intake, and hypertension and smoke, are associated with an increased cardiovascular disease. The aim of this study is to investigate if the presence of some risk factors during adolescence may involve in accelerated atherosclerosis disease. 50 subjects, median age 11 +/- 0.6 SD (27 females, and 23 males) are admitted to the study. After overnight fasting we have investigated: lipoproteina A (nephelometric test), glycemia and insulin baseline and after load 120', tryglycerides, cholesterolo, apolipoproteina A, B, plasma concentrations. In addition to general medical evaluation, anthropometric measurements of weight, height, blood pressure, BMI, overnight ratio were calculated according to Tanner's charts. The means anthropometric and metabolic values in different groups were compared. One group affected with abdominal obesity state (waist-hips ratio > 0.9), the second with mid obesity condition (waist-hip ratio < 0.9). Tryglycerides, cholesterolo, insulin plasma concentrations in both groups were considered similar. However in the first group higher levels of apolipoproteina A (means 102 + 10.2 SD) and lipoproteina A were demonstrated (P = 0.03 in males, P = 0.01 Statview for Mann Whitney test). Childhood is an important period for the development of the atherosclerosis such as the presence of obesity during this time has a very high likelihood of persisting into adulthood. The severity of obesity in adults is greater in those who were obese as adolescents. In accord with other authors we have not observed abnormal tryglicerides and cholesterolo plasma concentrations, which probably are found in adulthood obesity. We believe indeed the risk factors are different in obesity of childhood, atherosclerosis may be induced by high endogenous insulin secretion and abnormal uptake of lipoprotein. However the potential consequence of excessive insulin secretion could be due in part to insulin effects on recruitment of histiocytosis cells during the development of atheroma and through the modulation of hepatic production and peripheral uptake of lipoproteins.
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PMID:[Atherosclerosis in childhood: the role of obesity]. 934 Jun 7


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