Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the relations of gender and lipoproteins to subclasses of high density lipoproteins (HDLs) in a cross-sectional sample of moderately overweight men (n = 116) and women (n = 78). The absorbance of protein-stained polyacrylamide gradient gels was used as an index of mass concentrations of HDL at intervals of 0.01 nm across the entire HDL particle size range (7.2-12 nm). At least five HDL subclasses have been identified by their particle sizes: HDL3c (7.2-7.8 nm), HDL3b (7.8-8.2 nm), HDL3a (8.2-8.8 nm), HDL2a (8.8-9.7 nm), and HDL2b (9.7-12 nm). Men had significantly higher HDL3b and significantly lower HDL2a and HDL2b than did women. Correlations of HDL subclasses with concentrations of other lipoprotein variables were generally as strong for gradient gel electrophoresis as for analytical ultracentrifugation measurements of HDL particle distributions. In both sexes, high levels of HDL3b were associated with coronary heart disease risk factors, including high concentrations of triglycerides, apolipoprotein B, small low density lipoproteins, intermediate density lipoproteins, and very low density lipoproteins and low concentrations of HDL2 cholesterol and HDL2 mass. Plasma concentrations of HDL3 cholesterol were unrelated to protein-stained HDL3b levels. HDL3 cholesterol concentrations also did not exhibit the sex difference or the relations with lipoprotein concentrations that characterized HDL3b. Thus, low HDL3b levels may contribute in part to the low heart disease risk in men and women who have high HDL cholesterol. Measurements of HDL3 cholesterol may not identify clinically important relations involving HDL3b.
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PMID:Associations of lipoproteins and apolipoproteins with gradient gel electrophoresis estimates of high density lipoprotein subfractions in men and women. 154 92

The correlations between lipid and lipoprotein measurements and other risk factors of coronary artery disease were evaluated in 101 men undergoing coronary angiography. Clinically significant disease was present in 75 patients, whereas 24 had no observable lesions and 2 had minimal lesions. Comparisons of individual lipid and lipoprotein levels were nearly all significantly different between patients with and patients without clinically significant disease; however, no single variable could predict the presence of disease among patients. Logistic regression analysis identified five factors: apolipoprotein A-I, apolipoprotein B, diabetes, age, and family history of heart disease, which account for most of the differences between the two patient groups. These results could have important implications for the evaluation and management of patients suspected of having coronary atherosclerosis.
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PMID:Correlates of atherosclerosis in coronary arteries of patients undergoing angiographic evaluation. 211 60

Several recent reports have examined whether there is a correlation between the presence of some minor alleles of the highly polymorphic apolipoprotein B gene and atherosclerosis and premature heart disease. The present study extends this investigation. A high-resolution method was used to study the allele frequencies of a hypervariable minisatellite region close to the apolipoprotein B gene in 110 patients with severe coronary disease and in 117 normal controls. Alleles containing 38, 44, 46, or 48 hypervariable elements showed an association with coronary heart disease. These alleles were also associated with elevated serum levels of total cholesterol and apolipoprotein B among patients and with elevated serum levels of total triglycerides among controls. The hypervariable region showed strong linkage disequilibrium with a polymorphic EcoRI site in exon 29 and was in linkage equilibrium with a polymorphic MspI site in exon 26. Two patients carried a base change at codon 3500 that results in an arginine-to-glutamine substitution; the base change was linked in both instances to the allele with 48 hypervariable elements.
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PMID:Hypervariability in a minisatellite 3' of the apolipoprotein B gene in patients with coronary heart disease compared with normal controls. 235 70

We are studying the genetic factors underlying the common forms of heart disease by identifying genes that affect normal variations in plasma lipid, lipoprotein, and apolipoprotein concentrations in baboons. For these studies we are using cloned human gene probes to identify restriction fragment length polymorphisms (RFLPs) at loci encoding the proteins of cholesterol metabolism. In this report we present the identification and mapping of a polymorphic Ava II cleavage site in intron 17 of the baboon low density lipoprotein (LDL) receptor gene. We determined genotypes for this RFLP on a population of 253 pedigreed baboons and assessed the effect of LDL receptor RFLP genotypes on serum concentrations of LDL cholesterol (LDL-C) and apolipoprotein B (apo B). These measures were obtained for each baboon on each of two diets: a low cholesterol, low fat (basal) diet and a high cholesterol, high saturated fat (atherogenic) diet. Statistical analysis detected a significant association between LDL receptor genotype and serum LDL-C and apo B concentrations on both diets. Homozygotes for the rarer allele had lower serum concentrations of LDL-C and apo B than did homozygotes for the common allele, and with the exception of apo B levels on the basal diet, intermediate levels were observed in heterozygotes. The LDL receptor RFLP accounted for approximately 3% to 7% of the variation in serum LDL-C and apo B concentrations on both diets.
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PMID:Identification of LDL receptor gene marker associated with altered levels of LDL cholesterol and apolipoprotein B in baboons. 257 32

A randomized controlled trial was conducted to examine the effects of coffee (as commonly drunk in Britain) on blood pressure and plasma lipids in healthy subjects. Fifty-four subjects followed three regimens successively, the order being randomized according to a Latin square design: five or more cups of coffee daily for 4 weeks; five or more cups of decaffeinated coffee daily for 4 weeks but no ordinary coffee; no coffee for 4 weeks. Coffee appeared to cause a small rise (of 3 mm Hg) in recumbent systolic blood pressure; this effect was less than, and obscured by, changes induced by posture and mild stress. No consistent changes attributable to coffee were found in diastolic blood pressure or pulse rate. Small changes in the expected directions occurred in plasma high density lipoprotein (HDL) cholesterol and apolipoprotein AI (decrease), and in total cholesterol, non-HDL cholesterol and apolipoprotein B (increase), but none of these were statistically significant. The effect of coffee on risk of heart disease in Britain is probably small.
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PMID:Coffee, blood pressure and plasma lipids: a randomized controlled trial. 268 Apr 75

Clinical experience of diagnostic and interventional procedures, including cardiac surgery, indicates a greater prevalence of coronary heart disease in white men than in other race-gender groups. Studies of children and young adults in the Bogalusa Heart Study have provided evidence that might account for this race-gender contrast. A variety of anthropometric and metabolic parameters influencing serum lipid and lipoprotein levels places white boys and young white men selectively at high risk for the development of atherosclerotic coronary artery disease. Obesity and greater central body fat, subtle aberrations in carbohydrate-lipid metabolic relations and variability in sex hormone profiles appear to underlie a trend to adverse lipoprotein changes in white men. A lower high-density lipoprotein cholesterol level and apolipoprotein A-l at puberty and a dramatic increase of low-density lipoprotein cholesterol are seen in young white men; such adverse changes identify them to be at greater risk. It is noteworthy that children whose fathers had myocardial infarction tend to be white. These children also have relatively high ratios of apolipoprotein B/apolipoprotein A-l and apolipoprotein B/low-density lipoprotein cholesterol. Studies of risk factors in children emphasize their importance in the early natural history of coronary artery disease. These findings show the need for beginning prevention of adult heart disease in childhood.
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PMID:Insight into a bad omen for white men: coronary artery disease--the Bogalusa Heart Study. 275 97

According to the Adult Treatment Panel of the National Cholesterol Education Program, age is a major risk factor for heart disease. To assess the relation between age and LDL oxidizability, we studied copper-mediated LDL oxidation in 13 healthy elderly subjects (> 59 years) and 13 sex-matched healthy young controls (< 30 years). Total and LDL-cholesterol concentrations were increased in elderly subjects. The time course of copper-mediated LDL oxidation showed no significant differences between the two groups as assessed by formation of conjugated dienes, lipid peroxides, and apolipoprotein B fluorescence. Kinetics of LDL oxidation as quantified by lag time, oxidation rate, and maximal oxidation were not significantly different between the elderly and young groups. Although the concentrations of 16:0, 18:0, 18:1, 18:3, and 20:4 and total polyunsaturated fatty acids were significantly higher in the elderly group, LDL fatty acid concentrations were similar in both groups. Lipid-standardized alpha-tocopherol, beta-carotene, and ascorbate concentrations were not significantly different between the two groups. The findings of the present study suggest that in the healthy elderly, LDL oxidation may not be a crucial mediator for atherogenesis.
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PMID:Effect of aging on susceptibility of low-density lipoproteins to oxidation. 758 53

Significant risk factors for premature coronary heart disease include: (1) family history, (2) elevated low density lipoprotein (LDL) cholesterol level > or = 160 mg/dl, l, (3) decreased high density lipoprotein (HDL) cholesterol level < 35 mg/dl, l, (4) cigarette smoking, (5) high blood pressure and (6) diabetes mellitus. All of these risk factors are common in patients with premature heart disease. Common familial lipid disorders associated with premature heart disease include familial lipoprotein(a) excess, familial dyslipidemia (elevated triglycerides and decreased HDL cholesterol), familial combined hyperlipidemia (elevations of LDL cholesterol and triglycerides, and often decreased HDL cholesterol), familial hypoapobetalipoproteinemia (elevated apolipoprotein B levels), familial hypoalphalipoproteinemia (low HDL cholesterol levels), and familial hypercholesterolemia (elevated LDL cholesterol levels). All these disorders have been characterized using age and gender specific 90th and 10th percentile values from the normal population. The diagnosis and potential management of these disorders is reviewed.
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PMID:Familial lipoprotein disorders and premature coronary artery disease. 780 28

An increase in factor VII was found to be a risk factor for ischemic heart disease. The present study was designed to test the hypothesis that this increase in factor VII is part of a general increase in vitamin K-dependent clotting factors. Initially, a prospective analysis of factor VII antigen and prothrombin activity was performed in two groups of young subjects without symptoms who differed in their risk of ischemic heart disease based on a history (or lack thereof) of premature heart disease in a first-degree relative. A statistically significant increase in prothrombin activity and factor VII antigen was found in the high-risk group of subjects when compared with the low-risk group. In a second series of subjects, factor IX and X activity assays were also performed, and all four of the vitamin K-dependent clotting factors were found to be significantly higher in high-risk subjects when compared with low-risk subjects. A second goal of the study was to explore whether correlations between factor VII and cholesterol and triglycerides might be due to binding of factor VII with apolipoprotein B. Although a significant correlation of factor VII antigen with apolipoprotein B (rho = 0.523, p < 0.025) was found in our high-risk group of subjects, the correlation between factor VII and triglycerides (rho = 0.641, p < 0.005) was even stronger statistically, suggesting a probable interaction of factor VII with very-low-density lipoproteins in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin K-dependent clotting factors are elevated in young adults who have close relatives with ischemic heart disease. 824 91

A pedigree of a large family with high prevalence of heart disease is subjected to association and sib-pair linkage analysis to investigate the role of 5 candidate genes in the regulation of lipoprotein metabolism and the development of coronary artery disease. At the 5% nominal significance level, the apolipoprotein B locus (APOB) was found to be linked to high-density lipoprotein cholesterol level (HDL-C), low-density lipoprotein cholesterol level (LDL-C), the ratio HDL-C/LDL-C, and apolipoprotein AI level times this ratio (apoAI x LDL-C/HDL-C). APOB (PvuII) was strongly associated with apolipoprotein B levels (apoB) (P = 0.006) and the VNTR region of the APOB locus showed highly significant association between allele 7 and low triglyceride levels (P = 0.004). No significant linkage results were found with cholesterol ester transfer protein (CETP). At the 1% nominal significance level, CETP [TaqI(B)] showed significant association with LDL-C, apoB, and HDL-C/LDL-C. There was significant linkage of lipoprotein lipase (LPL) with very-low-density lipoprotein cholesterol and the ratio apoAI/HDL-C, and strong association results between LPL (HindIII) and triglyceride levels (P = 0.005). At the 5% nominal significance level, haptoglobin (HPA) was associated with HDL-C, HDL-C/LDL-C, apoAI/HDL-C and apoAI x LDL-C/HDL-C. The apolipoprotein AI locus did not show any significant linkages or associations. The study thus indicated that genetic variation of APOB, LPL, CETP, and lecithin cholesterol acyl transferase (which is linked to HPA and CETP) may play an important role in the regulation of lipoprotein metabolism and could contribute to the risk of coronary artery disease.
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PMID:Genetic contributions to quantitative lipoprotein traits associated with coronary artery disease: analysis of a large pedigree from the Bogalusa Heart Study. 827 86


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