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PubMed2005

[Study on apoE gene polymorphism and subclasses of serum high density lipoprotein in type IV hyperlipidemia].

OBJECTIVE: The aim of the study was to investigate apolipoprotein(apo) E polymorphism and its relationship with serum lipids and apolipoprotein, serum high density lipoprotein(HDL) subclasses in patients with type IV hyperlipidemia. METHODS: apoE genotype was assayed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The subclasses of serum HDL in 103 patients with type IV hyperlipidemia and 146 normolipidemic subjects were determined by two-dimensional gel electrophoresis in conjunction with immunodetection method. RESULTS: The apoE3/3 genotype frequency and allele epsilon 3 frequency were both the highest in the frequency distribution profiles of the type IV hyperlipidemia group and the control group. In type IV hyperlipidemia group, the genotype of apoE2 had higher serum HDL-C,apoE, HDL(2a) apoE/apoCIII ratio but lower TG/HDL-C,apoCIII, HDL(3c) levels when compared with the genotype of apoE(3) (P<0.05). In control group, the genotype of apoE(2) had higher serum TG, apoE levels and apoE/aopCIII ratio but lower HDL (3a) level when compared with the genotype of apoE(3) (P<0.05). CONCLUSION: An association of allele epsilon 2 of apoE gene with the maturation of HDL in type IV hyperlipidemia was noted in the study.

Adult↗
PubMed1996

[Reproducibility of fasting serum cholesterol and triglycerides in ambulatory patients with mixed hyperlipidemia].

Intraindividual variability of serum lipid concentrations in normal volunteers and in patients with hyperlipidemia is substantial. The aim of this study was to investigate prospectively the reproducibility of fasting serum triglyceride and total cholesterol concentrations in primary health care patients with combined hyperlipidemia, i.e. under conditions of daily medical practice. Secondary forms of hyperlipidemia were excluded. 19 general medical outpatients with primary combined hyperlipidemia were studied. Serum total cholesterol and triglyceride concentrations were measured after an overnight fast at 08.00 h 4 times at weekly intervals. To study the influence of alcohol intake on serum lipid concentrations, total cholesterol and triglycerides were measured without alcohol influence and 12 hours after consumption of a mean of 100 g alcohol in the evening. In 19 patients (10 males, 9 females, mean age 55 years, body mass index 27.9 +/- 4.4 kg/m2), mean +/- SD of serum triglycerides was 3.97 +/- 1.8 mmol/l and of total cholesterol 7.9 +/- 1.8 mmol/l. The combined intraindividual and interassay coefficient of variation was 18.7 +/- 8.2% for triglycerides and 5.1 +/- 2.5% for total cholesterol. Fasting serum triglycerides (3.5 +/- 1.1 vs. 3.7 +/- 1.4 mmol/l) and total cholesterol (7.6 +/- 1.4 vs. 7.8 +/- 1.0 mmol/l) did not significantly change 12 hours after acute alcohol consumption. Patients with primary combined hyperlipidemia in a primary health care setting show small intraindividual variations of overnight fasted serum triglyceride and total cholesterol concentrations. Moderate alcohol consumption 12 hours before blood sampling does not significantly affect triglyceride and cholesterol values.

Adult↗
PubMed2002

Genetic factors play an important role in the pathogenesis of hyperlipidemia post-transplantation.

BACKGROUND: Our purpose was to identify factors associated with hyperlipidemia post-transplantation in a Hispanic population. METHODS: From 1985 to 1999, a kidney graft survival longer than 3 months occurred in 293 cases at the Instituto Nacional de la Nutrición. Most of the patients living in Mexico City were included (n = 83). The evaluation included a questionnaire, blood samples, and assessment of body composition and dietary habits. As many as possible first-degree relatives were studied. RESULTS: Women had higher values of cholesterol (236 +/- 51 versus 215 +/-41; P < 0.05), low-density lipoprotein cholesterol (147 +/- 42 versus 131 +/- 34; P = 0.05), high-density lipoprotein cholesterol (57.3 +/- 14 versus 47.9 +/- 14; P = 0.002) and high-density lipoprotein-2 cholesterol. Isolated hypercholesterolemia was the most common lipid abnormality (40.9%), followed by mixed hyperlipidemia. Lipoprotein (a) greater than 30 mg/dL was found in 13 cases. Familial combined hyperlipidemia (FCHL) in the patient's relatives was a marker for dyslipidemia (odds ratio, 7.04; 95% confidence interval, 1.2 to 59.7). These cases had a worse lipid profile. Cyclosporine-treated FCHL patients had higher lipid levels compared with the non-FCHL, cyclosporine-treated patients. The effects of cyclosporine on the lipid levels were lower, but significant, after the exclusion of the FCHL cases. CONCLUSION: Post-transplant dyslipidemia is determined by genetic and environmental factors. FCHL in the patient's relatives was associated with post-transplant hyperlipidemia; an additive effect with cyclosporine was found. The evaluation of the lipid profile of relatives may be useful for the assessment of the risk of post-transplant dyslipidemia.

Adult↗
PubMed1995

Nutrient quality of fat- and cholesterol-modified diets of children with hyperlipidemia.

OBJECTIVE: To assess the nutritional adequacy of low-fat, low-saturated fat, low-cholesterol-modified diets of children with hyperlipidemia. DESIGN: Case comparison study. SETTING: Tertiary care ambulatory pediatric atherosclerosis prevention center. PATIENTS AND OTHER PARTICIPANTS: White middle-class suburban children. Subjects were 54 consecutive children with hyperlipidemia (26 boys) with a mean (+/- SD) age of 10.8 +/- 3.4 years. Controls were 44 healthy children (19 boys) aged 10.8 +/- 0.9 years recruited from a local elementary school. INTERVENTION: The subjects received individual nutrition counseling on a National Cholesterol Education Program Step I Diet from a registered dietitian. MAIN OUTCOME MEASURE: The 3-day written food records were analyzed by a registered dietitian using the Minnesota Nutrient Data System. Outcome measures were intakes of energy, fat-soluble vitamins, and minerals as a percentage of the Recommended Dietary Allowance. The means between cases and controls were compared by Student's t test. RESULTS: There was no significant difference in consumption of energy, minerals, or vitamins D and E between the groups. The control group's diet contained significantly greater amounts of fat, saturated fat, and cholesterol. The children with hyperlipidemia consumed significantly more vitamin A (P < .005). CONCLUSION: The nutrient quality of fat- and cholesterol-modified diets of children who have received nutritional counseling compares favorably with the nutrient quality of controls on an unrestricted diet. Therefore, pediatricians can prescribe with confidence a Step I Diet for children with hyperlipidemia and adolescents when nutritional counseling is available.

Adolescent↗
PubMed1997

Hyperlipidemia in liver transplant recipients: prevalence and risk factors.

Hyperlipidemia is common in transplant patients. Although a causal relationship to the use of cyclosporine is accepted, additional risk factors are as yet unidentified. Eighty-five liver transplant recipients treated with standard triple immunosuppression with a survival of at least 6 months were evaluated. Pretransplantation and posttransplantation variables were analyzed as predictive factors of posttransplantation hyperlipidemia. Serum cholesterol and triglyceride levels were considered elevated if they were > 250 mg/dL and > 150 mg/dL, respectively. Before and after transplantation, hyperlipidemia occurred in 8% (95% confidence interval [CI], 3% to 16%) and 66% (95% CI, 55% to 76%), respectively. After transplantation, 47% (95% CI, 36% to 58%) of the patients had isolated high triglyceride levels, 12% (95% CI, 6% to 21%) had both elevated cholesterol and triglyceride levels, and 7% (95% CI, 3% to 15%) had isolated elevated cholesterol levels. Hypertriglyceridemia occurred early after transplantation (67% by first month) and persisted nearly unchanged throughout the first year. In contrast, cholesterol levels increased with time (5%, 13%, and 27% at 1, 3, and 6 months, respectively). In univariate analysis, factors predictive of hypercholesterolemia included female sex, pretransplantation cholestatic liver disease, pretransplantation cholesterol levels > 141 mg/dL, and > 3 methylprednisolone "boluses." In multivariate analysis, only a pretransplantation cholesterol level of > 141 mg/dL (odds ratio [OR], 5.5; 95% CI, 1.4 to 21) was an independent risk factor. Risk factors associated with hypertriglyceridemia included pretransplantation hepatocellular liver disease (OR, 6.8; 95% CI, 1.2 to 40) and posttransplantation renal dysfunction (OR, 5.4; 95% CI, 1.9 to 15.4). Hyperlipidemia is a frequent finding in liver transplant recipients, and hypertriglyceridemia is the most common abnormality. Hypertriglyceridemia can be predicted on the basis of pretransplant hepatocellular disease and posttransplant renal dysfunction. Pretransplant serum cholesterol level is an independent risk factor for posttransplant hypercholesterolemia.

Adult↗
PubMed2000

Differential expression of lipoprotein lipase gene in tissues of the rat model with visceral obesity and postprandial hyperlipidemia.

Postprandial hyperlipidemia is frequently accompanied with intra-abdominal visceral accumulation in human subjects. We have found that the decreased lipoprotein lipase (LPL) mass and activity is negatively associated with the amount of visceral fat accumulation. Here, we studied the postprandial hyperlipidemia using the OLETF rat, a model with visceral obesity, in order to clarify the molecular mechanism causing postprandial hyperlipidemia accompanied with visceral obesity. At the same age of 32 weeks, the OLETF rats showed obviously higher plasma leptin, total cholesterol, triglyceride, and HDL-cholesterol levels than the control LETO rats, although the plasma glucose level was not significantly different. Fat-loading test revealed the delayed metabolism of exogenous fat in the OLETF rats compared to the LETO rats, similar to human subjects with visceral obesity. In the obese rats, plasma levels of LPL mass and activities were 60 and 49% of control rats. The expression of LPL gene was decreased in subcutaneous adipose tissues and skeletal muscle of OLETF rats to 40 and 52% compared to those of LETO rats. In OLETF rats, plasma tumor necrosis factor-alpha (TNF-alpha) and insulin levels were increased to 2.0- and 2.3-folds compared to those in control rats. Furthermore, plasma insulin and TNF-alpha levels in OLETF rats were negatively correlated with the expression levels of LPL gene in subcutaneous fat and muscle. These results indicate that decreased LPL mass and activity in the animal model with visceral obesity is possibly caused by decreased expression of LPL gene in tissues mediated by the increased levels of insulin and TNF-alpha. The different expression of LPL gene in tissues associated with the increased levels of insulin and TNF-alpha possibly elucidate the underlying mechanisms involving the postprandial hyperlipidemia observed in visceral obesity.

Adipose Tissue↗
PubMed1977

The characteristics of human plasma lipoprotein metabolism: influence of low caloric diet on hyperlipidemia.

We have classified hyperlipidemia into three groups according to different levels of VLDL-TG, and postulated the effect of low calorie-diets on plasma TCh are as follows: 1) Low calorie-diets are effective on VLDL-TG in every type of hyperlipidemia, except hyperlipidemia with VLDL-TG under 180 mg/100ml; 2) There was a reciprocal relation between the decreased amount of plasma TCh and the change VLDL-TG induced by the diet; 3) Catabolism of VLDL was accelerated by an increased esterification of VLDL-FC; 4) In the the group with VLDL-TG less than or equal to 180 mg/100ml, the LDC showed a high level of TCh: protein ration, and in the group with VLDL-TG greater than or equal to 260 mg/100ml, there was to be low level of TG: protein ratio in VLDL: 5) In hyperlipidemia with plasma TCh unchanged by the diet LDL-TCh increased significantly without any increase in LDL protein and LDL-TG.

Apolipoproteins↗
PubMed1996

Vitamin E inhibits fish oil-induced hyperlipidemia and tissue lipid peroxidation in hamsters.

Previous research has linked hyperlipidemia with increased serum concentrations of lipid peroxidation products; however, a specific association between diet-induced oxidative stress and hyperlipidemia has not been studied. In the present study, the relationship between tissue lipid peroxidation and hyperlipidemia induced by ingestion of fish oil was examined. In Experiment 1, male Golden Syrian hamsters were fed semipurified diets composed of 1.6 wt% safflower oil plus 15.0 wt% of either butterfat (BF), safflower oil (SAFF), or high-cholesterol menhaden oil [MHO(H-CHOL)] semipurified diets for 27 d. The cholesterol contents of the diets were adjusted to 0.088%. The MHO(H-CHOL)-fed hamsters exhibited higher serum concentrations of total cholesterol, triglycerides, apolipoprotein B, and lipid peroxides when compared to the BF and SAFF diet groups. In a further study (Experiment 2), hamsters were fed for 27 d three dietary treatments: (i) MHO(H-CHOL) with no vitamin E content; (ii) a low-cholesterol menhaden oil containing high concentrations of vitamin E (2.5 mg tocopherol/g oil or dietary concentrations of 375 mg/kg) [MHO(L-CHOL) + E]; and (iii) the MHO(L-CHOL + E) with added cholesterol (595 mg/kg) [MHO(L-CHOL) + CHOL + E] to match the cholesterol content of the MHO(H-CHOL). The MHO(L-CHOL) + E and MHO(L-CHOL) + CHOL + E diet groups showed lower concentrations of serum cholesterol, triglycerides, and hepatic lipid peroxides than the MHO(H-CHOL)-treated group. Moreover, in contrast to the hypercholesterolemia caused by the MHO(H-CHOL) feeding, the MHO(L-CHOL)+ E and MHO(L-CHOL) + CHOL + E diets did not show a serum cholesterol-elevating action. This study supports the hypothesis that oxidative stress in the Syrian hamster could play a causal role in dietary-induced hyperlipidemia which can be inhibited by high vitamin E intake.

Alanine Transaminase↗
PubMed1995

Reduction of hyperlipidemia in hepatoma-bearing rats by dietary fish oil.

The effect of dietary fish oil on serum lipid levels was studied by comparing it with dietary corn oil in Donryu rats subcutaneously implanted with an ascites hepatoma cell line (AH109A). The hepatoma-bearing rats exhibited hyperlipidemia characterized by a rise in both serum cholesterol and triglyceride levels. Increased cholesterogenesis in the host liver and decreased steroid excretion into feces are suggested to be responsible for the hepatoma-induced hypercholesterolemia, and increased fatty acid mobilization from peripheral adipose tissues and decreased triglyceride clearance from the blood circulation are considered causes for the hepatoma-induced hypertriglyceridemia. Dietary fish oil reduced the hyperlipidemia in these animals, suppressed the hepatoma-induced increase in hepatic cholesterogenesis and fatty acid mobilization from adipose tissue. Dietary fish oil also tended to increase fatty acid oxidation in the liver. Such diverse effects of fish oil may lead to the reduction of the hepatoma-induced hyperlipidemia. These results suggest that studies on dietary fish oil may be warranted in patients with cancer-related hyperlipidemia.

Animals↗
PubMed2005

In vivo hypolipidemic effects and safety of low dosage Monascus powder in a hamster model of hyperlipidemia.

Monascus or more commonly known as red mold rice is fermented rice on which Monascus purpureus has been grown. It has been a traditional Chinese food additive for thousands of years in China. Secondary metabolite product of Monascus, monacolin K, has been proven that it could be used as an antihypercholesterolemic agent. In this study, M. purpureus NTU568 mutated and selected from a monacolin K productivity strain-M. purpureus HM105 produced high quantities of monacolin K at a level of 9,500 mg kg(-1). This research focused on the effect of adding red mold rice powder of M. purpureus NTU568 to a hamster diet on total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol (LDL-C). In the results, the oral administration of Monascus powder in hyperlipidemia hamster was indeed proven to decrease TC, TG, and LDL-C levels. Plasma TC levels in hamster fed with Monascus powder at one-fold dosage [10.78 mg (day 100 g bw)(-1)] for 4 and 8 weeks were significantly lower (31.2 and 22.0%, respectively) than that in hyperlipidemia hamster. Plasma TG (30.1 and 17.9%) and LDL-C levels (36.0 and 20.7%) were also significantly lowered by feeding Monascus powder at one-fold dosage for 4 and 8 weeks compared to hyperlipidemia hamster. In addition, examinations of liver TC and TG levels of hyperlipidemia hamster were also performed and showed similar effects on lipid-lowering action by oral administration of Monascus powder. Since citrinin is a mycotoxin that possesses nephrotoxic and hepatoxic effects, it has a negative impact on the safety of red mold rice for people. This study examined the liver somatic index [plasma glutamyl oxaloacetic transaminase (GOT) and glutamyl pyruvic transaminase (GPT) levels] and liver biopsy to investigate whether Monascus powder induced damage in liver. It was found that the plasma GOT and GPT levels were not significantly increased by feeding Monascus powder. There was no difference in the results of the liver biopsy between the Monascus powder-treated groups and the control group.

Animals↗
PubMed1999

Joint effects of HMG-CoA reductase inhibitors and eicosapentaenoic acids on serum lipid profile and plasma fatty acid concentrations in patients with hyperlipidemia.

HMG-CoA reductase inhibitors reduce serum total cholesterol concentrations and the risk of coronary heart disease in patients with hypercholesterolemia. Recently, it has been reported that patients with combined hyperlipidemia are also at risk of coronary heart disease. However, HMG-CoA reductase inhibitor therapy alone does not sufficiently reduce serum triglyceride concentrations. Epidemiological and clinical evidence has shown that fish oil can lower plasma lipid levels, especially triglycerides. Consequently, we investigated the effects of the combination of HMG-CoA reductase inhibitors and eicosapentaenoic acid, a major component of fish oil, on hyperlipidemia. We administered 900-1,800 mg/day of the ethyl ester of eicosapentaenoic acid to patients with hyperlipidemia who had been treated with HMG-CoA reductase inhibitors for 30 +/- 6 months (means +/- SE). Serum total cholesterol and triglyceride concentrations were significantly decreased 3 months after the administration of eicosapentaenoic acid (from 5.63 +/- 0.23 mmol/l to 5.02 +/- 0.20 mmol/l, P < 0.05; from 2.07 +/- 0.41 mmol/l to 1.08 +/- 0.17 mmol/l, P < 0.01, respectively). Serum high-density lipoprotein-cholesterol concentrations were significantly increased after the treatment (from 1.23 +/- 0.12 mmol/l to 1.34 +/- 0.13 mmol/l, P < 0.05). Plasma eicosapentaenoic acid concentrations and the ratio to arachidonic acid in plasma were also significantly increased 3 months after the treatment (from 101.9 +/- 8.1 mg/l to 181.8 +/- 23.9 mg/l, P < 0.001; from 0.640 +/- 0.075 to 1.211 +/- 0.170, P < 0.001, respectively). These results suggested that the combination therapy of HMG-CoA reductase inhibitors and eicosapentaenoic acid was effective for patients with hyperlipidemia.

Aged↗
PubMed1988

The Prospective Cardiovascular Münster (PROCAM) study: prevalence of hyperlipidemia in persons with hypertension and/or diabetes mellitus and the relationship to coronary heart disease.

The ongoing Prospective Cardiovascular Münster (PROCAM) study was initiated in 1979. The objectives of this trial were to determine the prevalence of coronary heart disease (CHD) risk factors in the German population, improve the prediction and early detection of CHD, and derive recommendations for the primary prevention of vascular disease from the trial results. Of male PROCAM trial participants, ages 40 to 65 years, who had been free of myocardial infarction or stroke at the time of entry and had been followed up for 4 years, longitudinal data analysis shows that hypertension, diabetes mellitus, and hyperlipidemia are independent risk factors for CHD. The concomitant occurrence of these factors leads to a cumulative increase in CHD risk. Hyperlipidemia is a more significant risk factor for CHD than hypertension or diabetes mellitus. Ongoing data from 4043 men and 1333 women, ages 50 to 65 years, show that more than 50% of all diabetics are hypertensive. Cholesterol is slightly increased in male hypertensives and diabetics of either sex, whereas low-density lipoprotein cholesterol is slightly raised in male hypertensives and female diabetics only. The serum triglyceride concentrations are higher for hypertensives and markedly higher for diabetics of both sexes. High-density lipoprotein cholesterol concentrations are decreased in hypertensives, especially in hypertensive women, and even more so in diabetics. The European Consensus Conference for primary prevention of CHD has classified hyperlipidemia into five groups (A to E). For hypertensives, the proportion of patients in group D (cholesterol between 200 and 300 mg/dl and triglyceride levels between 200 and 500 mg/dl) is 20.4% for men and 6.2% for women, about twice as high as those in the control groups. The occurrence of combined (group D) or massive hyperlipidemia (group E: cholesterol greater than 300 mg/dl and/or triglycerides greater than 500 mg/dl) is prevalent in more than 30% of all diabetics: two to three times more frequently than in nondiabetic patients. When concomitant hypertension is included, this prevalence increases to more than 40% for diabetic men. Among those patients endangered by three risk factors, approximately 40% of all men and 60% of all women have the particularly atherogenic combination that includes lowered high-density lipoprotein cholesterol.

Adult↗
PubMed1991

Hyperlipidemia in hypertension: causes and prevention.

Hyperlipidemia is prevalent in hypertension, but the cause of this association is unknown. Treatment of hypertension with thiazide diuretics accentuates the hyperlipidemia, perhaps by causing potassium or sodium depletion. To assess the role of hypokalemia in thiazide hyperlipidemia, I measured lipid concentrations while using a spironolactone-thiazide regimen to prevent potassium wastage during the treatment of hypertension. Blood pressure decreased substantially, but hyperlipidemia occurred despite the maintenance of normal serum potassium. To test a role of sodium balance, I measured lipid levels during periods of sodium feeding and placebo therapy. Cholesterol levels decreased during sodium administration. Carrying this information to therapy, I participated in a multicenter comparison of enalapril and indapamide therapy in resistant hypertension. Both regimens caused minor metabolic effects, but indapamide provided superior antihypertensive potency. This evidence suggests that sodium feeding improves lipid metabolism, but sodium diuresis enhances an antihypertensive effect. Low-dose therapy combining a diuretic, such as indapamide, with a nondiuretic agent promises to improve metabolic tolerance and maximize hypertension control. This strategy optimally lowers overall cardiovascular risk.

Benzothiadiazines↗
PubMed1993

Genetic markers in the apo AI-CIII-AIV gene cluster for combined hyperlipidemia, hypertriglyceridemia, and predisposition to atherosclerosis.

The aim of the present study was to search for genetic determinants of combined hyperlipidemia and hypertriglyceridemia, and to evaluate whether such determinants might be associated with predisposition to atherosclerosis. Four DNA polymorphisms in the apo AI-CIII-AIV gene cluster (G to A mutation at position -75 basepairs in the apo AI promoter, XmnI, PstI and SstI) were studied in relation to combined hyperlipidemia, hypertriglyceridemia, lipoprotein levels, atherosclerosis and age in 221 Danish men. The frequency of the rare allele of the XmnI polymorphism, the X+ allele, was higher in individuals below 55 years of age with combined hyperlipidemia than in individuals with normal lipid levels (0.31 vs. 0.14; P = 0.05). The rare allele of the SstI polymorphism, the S+ allele, was more frequent in hypertriglyceridemic individuals compared with normotriglyceridemic individuals (0.16 vs. 0.09; P < 0.05) and on analysis of variance the combined S-S+ and S+S+ genotypes were also associated with the highest triglyceride levels. Furthermore, the frequency of the S+ allele decreased significantly as a function of age in nonatherosclerotic subjects (from 0.15 to 0.10 to 0.02 in 48-, 63- and 85-year-olds, respectively; 48- versus 85-year-olds, P = 0.03). These results suggest that genetic variation in the apo AI-CIII-AIV gene complex is associated with combined hyperlipidemia and hypertriglyceridemia and may have an impact on longevity and/or predisposition to atherosclerosis.

Aged↗
PubMed1981

Genetic transmission of isoapolipoprotein E phenotypes in a large kindred: relationship to dysbetalipoproteinemia and hyperlipidemia.

The largest reported kindred of a proband with type III hyperlipoproteinemia was investigated by assessment of lipid and lipoprotein levels and very low density lipoprotein (VLDL) isoapolipoprotein E distributions in all accessible family members (56% of the 124 living blood relatives and 59% of the 37 spouses). The results confirm in this kindred a trimodal distribution of apoE3/E2 ratios, and segregation analysis of 16 informative matings classified according to E3/E2 ratio demonstrated classical Mendelian inheritance of the autosomal codominant type: the E3/E2 ratio is determined by two alleles, apoE3d and apoE3n, which produce three phenotypes apoE3-D, apoE3-ND, and apoE3-N, corresponding to the low, intermediate, and high modes, respectively. Vertical transmission of the apoE3-D phenotype occurred in two branches of the second generation. In both instances this represented pseudodominance; i.e., products of heterozygous (apoE3-ND) x homozygous (apoE3-D) matings. Hyperlipidemia (defined as a low density lipoprotein cholesterol and/or plasma triglyceride level exceeding the respective age-, sex-, and sex-steroid-specific 95th percentiles derived from Lipid Research Clinics population studies) was present in 15 blood relatives in multiple lipoprotein patterns, consistent with the presence of familial combined hyperlipidemia in this kindred. Eight of nine members with the apoE3-D phenotype had either type III hyperlipoproteinemia or, in the absence of hyperlipidemia, beta-VLDL and at least marginally cholesterol-rich VLDL (VLDL-cholesterol/plasma triglyceride greater than 0.25) (defined as dysbetalipoproteinemia). The ninth such member, the only child with this phenotype, was normal. beta-VLDL and marginally cholesterol-rich VLDL was seen in but one of six hyperlipidemic family members of phenotype apoE3-ND, in none of seven hyperlipidemic blood relatives of phenotype apoE3-N, in no normolipidemic family members of phenotype apoE3-ND or apoE3-N, and in no spouses (three of whom were hyperlipidemic and nine of phenotype apoE3-ND). Thus, among adult members of the O'D kindred the apo3-D phenotype was nearly specifically associated with dysbetalipoproteinemia or, when hyperlipidemia was present, type III hyperlipoproteinemia.

Adolescent↗
PubMed1982

The role of platelet hyperfunction in thrombus formation in hyperlipidemia.

The mechanism of thrombus formation in hyperlipidemia was studied. Attempts at artificial creation of an arterial thrombus in control rabbits stenosing the femoral artery by ligature were not successful unless ellagic acid was administered by injection. However, in rabbits with hyperlipidemia, mere creation of stenosis in the femoral artery resulted in a high percentage of thrombus formation. In rabbits with hyperlipidemia, both thromboxane (Tx) A2 biosynthesis in platelets and prostacyclin (PGI2) biosynthesis in the aorta were increased and these changes were noted at the level of cyclooxygenase in the arachidonic acid metabolic pathway. Therefore, these results suggest that thrombi are likely to be formed in hyperlipidemia and that such thrombus formation is due largely to platelet hyperfunction.

Animals↗
PubMed1993

Hypertension, hyperlipidemia, and renal damage.

Experimental studies have demonstrated that a number of factors participate in the progression of renal disease. Systemic and glomerular hypertension have been shown to be critical factors in renal injury. Hyperlipidemia that frequently coexists with renal disease also has been suggested as an important participatory factor in nephron damage. Interestingly, both hypertension and hyperlipidemia seem to evoke glomerular growth, a factor that has also been postulated to be involved in glomerular and tubular destruction. Recently, experimental and clinical data suggest that an important interaction occurs between hyperlipidemia and hypertension. Not only do they frequently coexist, but hypertension dramatically exaggerates hyperlipidemic injury, and hyperlipidemia alters systemic and glomerular vascular production of vasoactive substances which maintain basal vascular tone. Thus, these recent observations underscore the interactive potential of the various risk factors that participate in progression of renal disease. They also suggest that multiple interventional strategies may be needed to optimally prevent progressive nephron loss.

Animals↗
PubMed2006

Relation of preprocedural statin therapy to in-hospital procedural complications following percutaneous coronary interventions in patients with hyperlipidemia.

We investigated whether the observed protective effect of hyperlipidemia is stronger in patients who take statins and, if so, whether that effect is likely due to patient characteristics associated with statin use. In-hospital complications and long-term outcomes of patients with hyperlipidemia (cholesterol level > or = 240 mg/dl) undergoing percutaneous coronary interventions (PCI) on statins (group Ia, n = 2,052) and not on statins (group Ib, n = 1,650) were compared with 726 patients with lower cholesterol levels (group II). Despite a higher prevalence of co-morbidities and worse angiographic characteristics in patients with hyperlipidemia, patients in group Ia had significantly lower in-hospital mortality (0% vs 2% in the other 2 groups, p < 0.001), a lower increase in the postprocedure creatine kinase-MB fraction (14% vs 27% in group Ib and 28% in group II, p < 0.001), and fewer PCI complications (15% vs 30% in groups Ib and II, p < 0.001). After adjustment, patients in group Ia had a significant decrease in complications (odds ratio 0.72, 95% confidence interval 0.65 to 0.92, p = 0.009). In contrast, those in group Ib had outcomes similar to those of patients with lower cholesterol. After application of propensity analysis to adjust for the likelihood of receiving statins based on clinical, angiographic, and procedural characteristics, group Ia had fewer in-hospital complications (odds ratio 0.75, 95% confidence interval 0.62 to 0.90, p = 0.002) and lower in-hospital mortality (odds ratio 0.32, 95% confidence interval 0.12 to 0.84, p = 0.021). After successful PCI, overall survival after dismissal and survival free of myocardial infarction and target vessel revascularization were similar. In conclusion, hyperlipidemia per se is not associated with lower in-hospital complications after PCI. The benefit is largely limited to patients on statin treatment.

Aged↗