Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk factors for coronary artery disease were present to a greater degree in children of men who had experienced premature myocardial infarction when compared to children of unaffected male parents. Levels of cholesterol and body weight, as well as family history of premature CAD, differed significantly between the groups of children. The chance of identifying a child with hyperlipidemia was three times greater if the father had premature CAD. Data regarding familial aggregation of risk factors for CAD are reviewed and their significance discussed.
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PMID:Risk factors for coronary artery disease in children of affected families. 118 18

None of more widely accepted theories of atherogenesis can explain all the more pertinent features of atherosclerosis: a) foam dell formation; b) endothelial cell stress/injury; c) protective effect of HDL; d) atherogenicity of triglyceride-rich lipoproteins; e) the vesicular nature of early lipid deposits in atherosclerosis, f) dissociation of diet risk from the risk due to elevation in plasma cholesterol; or g) correlation of postprandial lipemia with CAD risk. The data obtained from our studies provide a new theory of atherogenesis. This theory is that: a) lipolytic surface remnants of TG-rich lipoproteins may represent a major class of atherogenic lipoproteins which are exacerbated during postprandial hyperlipidemia; b) clearance of these surfaces remnants by HDL in vivo may be one important way that HDL prevents atherosclerosis; c) excess surface remnants may be linked to delayed clearance of potentially atherogenic core remnants, directly linked to atherogenicity via surface remnant-mediated cytotoxicity to cells of the artery wall and/or linked to the deposit of unesterified cholesterol-rich vesicles in early atherosclerosis. An appealing aspect of this hypothesis is that it can account for several unexplained features of atherosclerosis, such as anatomic differences in susceptibility to atherosclerosis in the vascular tree, the preference of early atherosclerosis in humans to the region of the coronary artery subjected to low hemodynamic shear stresses, and the vesicular nature of lipid deposits in early atherosclerosis.
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PMID:Cytotoxicity of remnants of triglyceride-rich lipoproteins: an atherogenic insult? 185 66

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

The problem of caring for patients undergoing reoperative coronary revascularization is one that cardiac anesthesiologists will face with increasing frequency. Many thousands of CABG procedures continue to be performed annually with ever-increasing survival rates. Consequently, the population at risk for reoperative CABG is growing, while surgical intervention necessarily follows apace. As one recent long-term, retrospective study showed, patients surviving 12 years after CABG have a reoperative rate of 17.3%. Physicians caring for these patients must recognize that they are not seeing patients with routine CAD, but with a different entity: coronary graft disease (CGD). These patients with CGD are different in many ways from those with native CAD, and these differences must be taken into account when planning for their perioperative care. Cardiologists have strived to check the growth of CGD by aggressive emphasis on modification of coronary risk factors such as tobacco use, hypertension, and hyperlipidemia. In addition, recent interest has been focused on a pharmacologic approach via the platelet-prostaglandin system. Surgeons have also attempted to reduce the incidence of CGD by recognition that significantly improved long-term patency rates can be achieved by the use of the internal thoracic artery as a bypass conduit. Consequently, an expanded role for this vessel in the form of free, sequential, and bilateral ITA grafting is currently being advocated as a surgical solution to the problem of CGD. In contrast, the anesthesiologist probably has little to add to the prevention of CGD, but may be able to contribute to a favorable outcome at reoperation. The medical variables and preoperative characteristics that make reoperative CABG patients different from those presenting for primary CABG should be recognized. A firm appreciation of the nature of graft disease, as well as the surgical intricacies required for correction, can only serve to improve the care offered during these often complex operations. Aggressive, invasive hemodynamic monitoring, constant vigilance for signs of early ischemia, and preparedness for prebypass hemorrhage and postbypass ventricular dysfunction should be made. Furthermore, if anesthesiologists are to contribute to an improved outcome in these patients, strategies must be developed to attenuate cerebral and myocardial damage resulting from hemorrhage and atheroembolic catastrophies that appear to be frequent complications in these challenging surgical patients.
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PMID:Reoperation for coronary artery bypass grafting: anesthetic challenge. 1717

To determine the relationship between Type A behavior pattern and angiographically documented coronary atherosclerosis (CAD), we analyzed risk factor, behavioral, and angiographic data collected on 2,289 patients undergoing diagnostic coronary angiography at Duke University Medical Center between 1974 and 1980. Multivariable analyses using ordinal logistic regression techniques showed that Type A behavior as assessed by the structured interview (SI) is significantly associated with CAD severity after age, sex, hyperlipidemia, smoking, hypertension, and their various significant interactions were controlled for. This relationship, however, is dependent upon age. Among patients aged 45 or younger, Type A's had more severe CAD than did Type B's; among patients aged 46-54, CAD severity was similar between Type A's and B's; and among patients 55 and older, there was a trend toward more severe CAD among Type B's than among Type A's. These Type A-CAD relationships did not appear to be the result of various factors relating to the selection of patients for angiography. Type A behavior as assessed by the Jenkins Activity Survey was unrelated to CAD severity. These findings suggest that SI-determined Type A behavior is associated with more severe CAD among younger patients referred for diagnostic coronary angiography. The reversal of the Type A-CAD relationship among older patients may be due to survival effects. Inadequate sample sizes, use of assessment tools other than the SI, and failure to consider the Type A by age interaction could account for failures to find a Type A-CAD relationship in other studies. We conclude that the present findings are consistent with the hypothesis that Type A behavior is involved in the pathogenesis of CAD, but only in younger age groups. The Type A effect in the present data is small relative to that of both smoking and hyperlipidemia, however, and future research should focus more specifically on the hostility and anger components of Type A behavior, particularly in younger samples.
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PMID:Type A behavior and angiographically documented coronary atherosclerosis in a sample of 2,289 patients. 337 4

The recently completed NHLBI sponsored multicenter double-blind Coronary Heart Disease Prevention Trial has provided the long sought-after proof that hyperlipidemia is a major CAD risk factor and that the incidence of CHD and its complications can be favorable modified by control of hyperlipidemia with appropriate diet-drug therapy. This nationwide study confirms and validates the earlier reports on the feasibility to stabilize or to promote regression of atherosclerotic arterial lesions through hyperlipidemia control. Current investigations suggest that in most instances, simple differentiation of hyperlipidemias into hypercholesterolemia and hypertriglyceridemia (major components of low-density and very low-density lipoprotein) can supply adequate information for clinical practice. In difficult-to-control hyperlipidemias, the application of lipoprotein analysis may provide insight of the underlying genetic-metabolic abnormality for selection of more specific therapeutic modality. Before considering hypolipemic therapy, secondary hyperlipidemias should be excluded. In those cases, treatment should be directed to the primary disease(s) for the solution of the hyperlipemic problem. Life-long dietary modification is the key step to treatment of all types of hyperlipidemias, and especially the primary hyperlipidemias. In this latter group, both the patient and the family should be educated on the principles and the importance of dietary modification to boost compliance. In familial hyperlipidemias, a specifically effective hypolipemic drug, or a combination of drugs with minimal or no long-term toxic and side effects, should be prescribed to augment the therapeutic diet to lower the elevated plasma lipid levels and stabilize them at normal range. Early detection and control of atherosclerosis-prone hyperlipidemias in children and young adults should be vigorously promoted to improve cardiovascular health of the population and to reduce the escalation of health care expenses.
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PMID:When and how to treat hyperlipidemia. 387 80

Twenty-five patients with precocious coronary heart disease (CHD) (aged forty years or less) and 82 first-degree relatives were studied for lipid profile. Eighty-eight age- and sex-matched controls were also studied. The mean serum cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, and total cholesterol/high density lipoprotein cholesterol of patients and their first-degree relatives were significantly higher as compared with normal controls. High density lipoprotein cholesterol values were found to be almost identical in the patient group, their first-degree relatives, and normal controls. Hyperlipidemia was found in 68% of patients with CAD, of their first-degree relatives, and 24% of controls. Almost all lipid fractions in relatives of hyperlipidemic patients paralleled those of the patients suffering from CHD. Of 25 families studied, 16 had hyperlipidemia. In conclusion, it can be stated that there is a statistically significant hyperlipidemia in young patients with CHD that has a significant familial clustering, thus delineating a group of high-risk individuals (first-degree relatives of young coronary patients) for possible primary prevention of CHD. This familial clustering could be due to genetic or environmental factors; however, the relative contribution of these two factors requires further investigation.
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PMID:Lipid profile in the first-degree relatives of patients with precocious coronary heart disease in Rohtak area (Northern India). 781 60

This article has focused on the appropriate indications for lipid-lowering drugs in adult patients with different lipoprotein disorders, which we have divided into primary hypercholesterolemia, combined hyperlipidemia,and hypertriglyceridemia. The mechanism of action, efficacy, and safety profile of the major drugs have been reviewed, and based on this information, we have presented our views on the appropriate drugs of first choice and appropriate second-choice agents for treatment of adult patients with different dyslipidemias. The rationale for the use of hypolipidemic drugs is strongest in patients with hyperlipidemia who concurrently have evidence for coronary or peripheral vascular disease, in whom the goal of secondary prevention is to retard further progression of atherosclerosis and potentially induce some regression, whereas in selected high-risk patients without evidence of atherosclerosis, the goals of therapy are to prevent the premature development of CAD or, in patients with severe hypertriglyceridemia, prevent the adverse sequelae of hepatomegaly, splenomegaly, and potentially pancreatitis. We have focused on the use of hypolipidemic drugs in adult patients, and the guidelines discussed are not appropriate for use in children with hyperlipidemia, in whom drug therapy should be undertaken selectively and in consultation with a lipid specialist. Many areas of controversy in the use of lipid-lowering drugs remain to be addressed by future studies; these include the use of lipid-lowering drugs in patients with secondary causes of hyperlipidemia (e.g., the nephrotic syndrome), the use of lipid-lowering drugs in women, and recommendations for drug therapy in older patients.
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PMID:Drug treatment of dyslipoproteinemia. 828 33

The unesterified fatty acid patterns in plasma of predialytic (PHD) and hemodialysis (HD) patients were determined. The HD patients were divided into three groups: (1) HD without cardiovascular disease (HD-norm); (2) HD with cardiomyopathy (HD-CAD), and (3) HD with hyperlipidemia (HD-hyp). The relative abundance of saturated fatty acids (SFAs) was greater in the plasma of HD-norm and HD-CAD patients (73.3 and 70.0%, respectively) than that in controls (62.6%), and the relative abundance of monounsaturated fatty acids (MUFAs) was significantly greater in the plasma of HD-hyp patients than that in controls (38.9 vs. 21.6%, p < 0.01). In all HD patients the relative concentration of polyunsaturated fatty acids (PUFAs) was lower than in controls. There were no significant differences in the fatty acid patterns of PHD patients. In conclusion, the relative abundance of SFAs and MUFAs in plasma of HD patients is associated with their concomitant lipid disorders and cardiomyopathy, while the low relative abundance of PUFAs was common in all HD patients.
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PMID:Relative abundance of some free fatty acids in plasma of uremic patients: relationship between fatty acids, lipid parameters, and diseases. 943 63

The aim of the present cross-sectional angiographic study was to examine if there is a relationship between the severity of CAD and postprandial lipemia in patients with type 2 diabetes mellitus. Special emphasis was directed to determining the contribution of apolipoprotein B-48 (apoB-48)-containing and B-100 (apoB-100)-containing triglyceride-rich particles to the magnitude of postprandial lipemia and degree of CAD. The role of apolipoprotein E (apoE) phenotype as a modulator of postprandial lipemia was also evaluated. The severity of CAD was determined by a quantitative coronary angiography and the subjects were classified into two groups based on the presence (severe CAD) or absence (mild CAD) of at least 50% stenosis in a major coronary vessel. The study population consisted of 43 subjects (31 men and 12 women) with fair glycemic control and comparable fasting lipids and body mass index. Postprandial responses of TG, apoB-48 and apoB-100 in lipoprotein subfractions (chylomicrons, VLDL1, VLDL2 and IDL) were determined after a fat load. Type 2 diabetic patients exhibited the classical dyslipidemia of the insulin resistance syndrome and delayed clearance of both hepatic and intestinal particles. Fasting or postprandial lipid or lipoprotein measurements, including apoB-48 and apoB-100 concentrations, did not differ between the groups. The presence or absence of apoE-4 allele did not significantly influence postprandial lipemia. The severity of the most significant coronary stenosis in angiography correlated with plasma and with chylomicron area under curve (AUC) for TG (n=27) and chylomicron AUC for apoB-48 (n=20). The strongest correlate of maximal stenosis was area under incremental curve (AUIC) for apoB-100 in IDL fraction (r=0.548, P=0. 012, n=20). In conclusion, postprandial apoB-48 and apoB-100 metabolism in triglyceride rich lipoproteins is distorted in type 2 diabetic patients, even in those with only mild CAD. The data suggest that postprandial change in small remnant particle numbers may contribute to the severity of CAD in type 2 diabetes.
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PMID:Postprandial metabolism of apolipoprotein B-48- and B-100-containing particles in type 2 diabetes mellitus: relations to angiographically verified severity of coronary artery disease. 1078 48


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