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)

Several fibrinolytic variables, including plasminogen activator inhibitor activity, were studied before and after exercise in 67 normolipidaemic patients with coronary artery disease and in 25 hyperlipidaemic patients with coronary artery disease. Before exercise plasminogen activator inhibitor activity was higher in the patient groups than in a group of 10 healthy volunteers. For those who were normolipidaemic plasminogen activator inhibitor activity was greater in patients with angina pectoris who had had a myocardial infarction. The concentration of antigenic tissue-type plasminogen activator was similar in all the patients with coronary artery disease and higher than in the control group. After the exercise test fibrinolytic capacity was lower in the patients with angina pectoris and a previous history of myocardial infarction. After exercise both the released immunological tissue-type plasminogen activator and fibrinolytic capacity were lower in the hyperlipidaemic patients than in the normolipidaemic patients. The concentration of plasminogen activator inhibitor was also higher in the hyperlipidaemic patients. Patients with hyperlipidaemia IV had the highest plasminogen activator inhibitor activity. The increase in plasminogen activator inhibitor activity found in the patients was partially inhibited by antiserum against plasminogen activator inhibitor-1 in vitro. The formation of a complex of about 115,000 daltons between plasminogen activator inhibitor and purified tissue-type plasminogen activator was detected by a zymographic fibrin technique. These findings show that in patients with coronary artery disease fibrinolytic activity is impaired by an increase in plasminogen activator inhibitor. Impaired fibrinolysis may be related to the clinical evolution of coronary artery disease in these patients.
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PMID:Plasminogen activator inhibitor activity and other fibrinolytic variables in patients with coronary artery disease. 313 63

There is abundant evidence that dietary omega 3 fatty acids effect a favorable change in lipoprotein profiles of normolipidemic individuals. However, there is relatively little information available on the lipoprotein responses of hyperlipidemic individuals at risk for premature coronary artery disease. We studied a group of subjects with familial combined hyperlipidemia (FCHL), as well as a group of normal controls, on three rigidly controlled diets differing primarily in their fatty acid composition. The normal subjects demonstrated significant reductions in total cholesterol, low density lipoprotein (LDL) cholesterol, and total apolipoprotein B (apo B) levels on both an omega 3 (salmon) and omega 6 (safflower) fatty acid-enriched diet when these were compared with a basal diet high in saturated fat. The primary difference in response to the polyunsaturated diets was the potent triglyceride-lowering effect of the salmon diet. The FCHL subjects demonstrated a response to the safflower diet similar to that observed in normals and also manifested a marked triglyceride lowering with the salmon diet. However, total cholesterol and total apo B levels were not lowered by the salmon diet, and LDL cholesterol and apo B levels exhibited an upward trend. Thus, individuals with FCHL, a common disorder associated with premature coronary artery disease, do not appear to have a favorable lipoprotein response to diets enriched in omega 3 fatty acids.
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PMID:The effects of omega 3 and omega 6 fatty acid-enriched diets on plasma lipoproteins and apoproteins in familial combined hyperlipidemia. 318 85

The apo E locus contributes to determining the variation in plasma cholesterol levels of healthy and diseased populations. It also influences the expression of hyperlipidemia and appears to modulate the susceptibility to atherosclerosis in a complex multifactorial interaction. There is evidence that the presence of apo E2 is protective, whereas that of apo E4 predisposes to coronary artery disease. The burden of proof, however, lies on future, well-designed clinical trials and prospective studies. The study of the biological significance of the apo E polymorphism in humans has emphasized the importance of gene-gene and gene-environment interactions in the pathogenesis of hyperlipidemia and atherosclerosis. The apo E polymorphism involves the coding region of the apo E gene and results in alterations of the gene product which, in turn, either directly or secondarily affect the metabolic fate of the lipoprotein particles. Rapid advances in knowledge over the last decade have provided a metabolic explanation for the observation of the opposite effects of the epsilon 4 and the epsilon 2 alleles on lipoprotein levels. Apo E2 has lower receptor binding affinity which results in delayed clearance of apo E2-bearing lipoprotein particles from plasma. Apo E4 is distributed differently from apo E3 between VLDL and HDL, is degraded more rapidly than apo E3, and may enhance the catabolism of E4-bearing particles, leading to other alterations in lipoprotein metabolism which result in elevated levels of LDL. In view of the significant opposite impacts of the epsilon 4 and the epsilon 2 alleles on plasma LDL cholesterol concentrations, it is evident that determination of the apo E phenotype will become a useful adjunct to the assessment of the cardiovascular risk profile of an individual. In addition, the relationship between the epsilon 2 allele and type III hyperlipoproteinemia provides a valuable model for the study of complex genetic interactions in the pathogenesis of hyperlipidemia. The further study of apo E and its interactions shows great promise for a deeper comprehension of the pathogenesis of atherosclerosis.
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PMID:Apolipoprotein E polymorphism and atherosclerosis. 327 11

Dietary fats play a critical role in atherogenesis and thrombosis. Both the amount of fat consumed and its composition affect various events associated with coronary artery disease. Dietary unsaturated fatty acids appear to reduce the incidence of these events, in particular polyunsaturated fatty acids (PUFAs), which exert markedly different effects on risk factors related to heart disease. The omega-3 (n-3) PUFAs, at high levels of dietary intake, significantly reduce hyperlipidemia and the production of the prothrombotic substance thromboxane, and they enhance the production of the platelet-antiaggregatory substance prostacyclin. Data from clinical trials indicate a significant reduction of levels of very low density lipoprotein (VLDL). The n-3 PUFAs also depress hepatic fatty acid and triglyceride synthesis and VLDL secretion. The n-3 PUFAs of fish oils displace arachidonic acid from tissue phospholipids and concomitantly increase n-3 PUFA levels, which inhibit thromboxane synthesis. Most significantly, in human subjects the antiaggregatory prostacyclin PGI3 is also synthesized and the net effect is enhanced antiaggregatory/antiadhesive activity. In addition, the chemotactic platelet adhesion-promoting substance leukotriene B4 is suppressed. These composite effects reduce atherogenesis and thrombosis. Fish oil n-3 PUFAs may also reduce blood pressure and blood viscosity. Through the combined vasodilatory effects via prostacyclin (PGI2 and PGI3), fish oils may improve peripheral circulation and thereby facilitate VLDL removal. The n-3 PUFAs of fish oils, by altering membrane fluidity in a specific manner, alter the activities of membrane-bound enzymes and may change receptor activity, specificity and signal transduction. Overall, these data indicate a beneficial role for n-3 PUFAs as part of a dietary approach to minimizing coronary artery disease.
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PMID:Effects of polyunsaturated fatty acids on factors related to cardiovascular disease. 331 46

Plasma lipid abnormalities derive their importance from their association with coronary artery disease. Elevated cholesterol levels accentuate risk, and clinical trials have shown that reductions lead to a decline in coronary events. The major plasma lipids, cholesterol and triglyceride, circulate in association with specific proteins as lipid-protein or lipoprotein complexes. The proteins direct and regulate the metabolism of these complexes by interacting with tissue enzymes and receptors. The metabolic fate of circulating triglyceride is governed by the activity of the enzyme lipoprotein lipase, situated in adipose tissue and skeletal muscle. Cellular demand for cholesterol, on the other hand, is met by activation of a specific receptor which mediates the delivery of sterol-rich lipoproteins to lysosomal degradation in liver and peripheral tissues. In order to prevent excess cholesterol accumulation at the periphery, there is a system of reverse cholesterol transport which involves assimilation and trapping of the sterol in the plasma lipoproteins through the action of the enzyme lecithin:cholesterol acyltransferase. Thereafter, the cholesterol is delivered to the liver, the only organ capable of excreting it in significant amounts. Disturbances in these processes may produce gross changes in the plasma lipid profile, clearly recognizable as hyperlipidaemia. However, it is becoming increasingly clear that a number of inherited traits can subtly perturb the lipoprotein spectrum and increase coronary risk even in subjects whose plasma lipoprotein profile would be considered normal.
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PMID:Lipid transport through the plasma: the metabolic basis of hyperlipidaemia. 333 Apr 20

The National High Blood Pressure Education Program has released three Joint National Committee reports and a task force report on the detection, evaluation, and treatment of high blood pressure. Like its predecessors, the 1988 Joint National Committee report was developed using the consensus process; it is based on the latest scientific research and reflects the state of the art regarding hypertension management. This report updates findings of previous reports in several respects: it broadens the step-care approach to provide more flexibility for clinicians; encourages greater patient involvement in the treatment program; emphasizes a consideration of the quality of life in the management of patients; and addresses the cost of care. It also provides more emphasis on control of other risk factors for cardiovascular disease; includes a discussion of the new cholesterol guidelines; recommends a reduction in alcohol consumption; and discusses the use of calcium and fish oil supplementation. This document expands earlier reports on special populations, including blacks and other racial and ethnic minority groups, young and elderly patients, pregnant patients, surgical candidates, and hypertensive patients with cerebrovascular disease, coronary artery disease, left ventricular hypertrophy, congestive heart failure, peripheral vascular disease, renal disease, chronic obstructive pulmonary disease or bronchial asthma, gout, diabetes mellitus, and hyperlipidemia. The report also updates previous drug tables to include new drugs, revised recommended doses of some drugs, and drug interactions. Consideration of step-down therapy after blood pressure has been controlled is suggested. This report is intended as a guide for practicing physicians and other health professionals in their care of hypertensive patients and as a reference for those participating in the many community high blood pressure control programs throughout the country.
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PMID:The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. 256

Elevated levels of serum cholesterol are a major risk factor for coronary artery disease, yet few studies have investigated the extent to which practicing physicians recognize and treat their patients with hyperlipidemia. A retrospective chart review was performed on 93 patients who had documented cholesterol levels greater than or equal to 6.20 mmol/L (240 mg/dL) in an outpatient setting to determine the degree of recognition and treatment of hypercholesterolemia. Hypercholesterolemia was diagnosed in 66 percent of patients, dietary recommendations were made in 46 percent, and lipid-lowering medication was prescribed in only 6 percent. Lipid profiles or high-density lipoprotein levels were determined in 22 percent, and thiazide diuretics were being prescribed for 32 percent. There was a trend toward greater recognition and treatment in patients with cholesterol levels greater than 7.75 mmol/L (300 mg/dL) and in patients less than 70 years of age. These results suggest that physician recognition of hypercholesterolemia is greater when compared with previous studies, but more aggressive diagnosis and intervention are needed. Greater utilization of lipid-profile analysis in hypercholesterolemic patients should also be encouraged.
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PMID:Recognition and treatment of hypercholesterolemia in a family practice center. 336 15

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

Although the importance of the profunda femoris artery in maintenance of lower extremity integrity was recognized in the earliest days of modern vascular surgery, disappointment with the performance of primary profundaplasty has emerged fully only in recent years. During the 10 year period from 1977 to 1987, only 17 patients were subjected to this procedure at Northwestern Memorial Hospital. The nine men and eight women averaged 65.6 years in age and exhibited the usual precursors of arterial insufficiency: a history of smoking in 12 patients (71 percent), clinical coronary artery disease in 8 patients (47 percent), hypertension in 7 patients, diabetes mellitus in 6 patients, hyperlipidemia in 2 patients, and uremia in 1 patient. Four patients exhibited hemodynamic improvement after profundaplasty (ankle-brachial index increase of greater than 0.15). Four required amputation postoperatively, and a fifth exhibited hemodynamic failure 9 months postoperatively and required amputation. Two patients required subsequent femoral-to-peroneal bypass to improve distal arterial perfusion. One patient died after the procedure, for a 5.9 percent mortality rate. Thus, the fact that profundaplasty has proved disappointing in the treatment of severe arterial insufficiency deserves emphasis at this time.
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PMID:The demise of primary profundaplasty. 340 Aug 10

There is much evidence that altered lipid metabolism contributes to the development of coronary artery disease (CAD). It is generally accepted that there is a direct association between the extent of CAD and total plasma cholesterol, as well as an inverse association between the extent of CAD and plasma HDL-cholesterol. No general agreement exists about the atherogenetic potential of plasma triglycerides and of triglyceride-rich lipoproteins. Since lipoprotein lipase (LPL) is the key-enzyme in the catabolism of triglyceride-rich lipoproteins (chylomicrons and very low-density lipoproteins), we examine the relationship between triglyceride-rich lipoproteins and LPL in vitro and in vivo. The concentrations of the main lipoprotein density classes, namely very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3, are measured by rate zonal ultracentrifugation. The preparation of VLDL, IDL, LDL, HDL2, and HDL3 is performed by sequential ultracentrifugation. The activity of LPL is measured radioenzymatically in a glycerol-based triolein emulsion. It can be demonstrated in vitro that VLDL, IDL, and HDL2 from normal plasma are able to increase LPL-activity in contrast to VLDL, IDL, and HDL2 from hyperlipemic plasma. This difference seems to be caused by an altered composition of apolipoproteins in hyperlipemic lipoproteins. An artificial acidosis in three healthy subjects shows in contrast to alkalotic and neutral blood-pH a significant decrease of LPL-activity. This result seems to be of some interest, since diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show secondary hyperlipemias caused by a deficit of LPL-activity. It can be shown in 15 male patients who produce a secondary type-V hyperlipemia during severe abuse of alcohol, that LPL-activity is decreased significantly as compared to 15 healthy controls. During sober phases, this alcohol-induced hyperlipemia and the impairment of LPL-activity disappears completely. In an other group of 8 male patients, who are not producing severe secondary hyperlipemia during approximately the identical alcohol intake, LPL-activity is also significantly decreased, but the activity of hepatic lipase is significantly increased. This increase of the activity of hepatic lipase seems to protect these patients from the development of secondary type-V hyperlipemia. In 89 male patients with angiographically assessed CAD a very strong inverse association between the activity of LPL and the extent of CAD is found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic decrease in lipoprotein lipase activity in relation to the development of hyperlipemias and their significance for coronary heart disease]. 345 43


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