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Results for “HYPERLIPEMIA”

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At least 19 recordsLinked to original sources

PubMed1995

[Possible relationship between overweightness and prevalence of hyperlipemia in the children of patients with heterozygote familial hypercholesterolemia and combined familial hyperlipemia].

BACKGROUND: Heterozygote familial hypercholesterolemia and combined familial hyperlipemia are associated to a greater risk of coronary disease. Combined familial hyperlipemia has classically been indicated to manifest after the second decade in life. The aim of this study was to establish whether a systematic search would demonstrate the existence of combined familial hyperlipemia earlier and analyze whether the antropometric parameters related with the overweightedness accompany the appearance of the lipid disorders of this disease found at an early age. PATIENTS AND METHODS: Different lipid parameters were studied in 89 subjects under the age of 18 who were children of patients with heterozygote familial hypercholesterolemia and combined familial hyperlipemia. Likewise the weight, height and waist/hip quotient were evaluated. Hyperlipemia was considered as the presence of cholesterol/LDL and/or triglicerides greater than the 95 percentile for age and sex. RESULTS: Hyperlipemia was observed in 51% and 40% of the children of patients with heterozygote familial hypercholesterolemia and combined familial hyperlipemia, respectively. The body mass index and the waist/hip quotient of the latter children significantly correlated with the cholesterol-HDL values and the LDL/HDL quotient. CONCLUSIONS: The patients with known combined familial hyperlipemia have a high percentage of children with hyperlipemia during infancy. These data suggest a possible association between obesity in the appearance of hyperlipemia in the children of patients with combined familial hyperlipemia at this age.

Adolescent↗

PubMed2000

Effect of omega-3 fatty acids and simvastatin on hemostatic risk factors and postprandial hyperlipemia in patients with combined hyperlipemia.

Patients with combined hyperlipemia have lipid abnormalities associated with an increased tendency to develop atherosclerosis and thrombosis. This tendency may be accelerated during postprandial hyperlipemia. In the present double-blind parallel study, 41 patients with combined hyperlipemia and serum triacylglycerols between 2.0 and 15.0 mmol/L and serum total cholesterol >5.3 mmol/L at the end of a 3-month dietary run-in period were treated with simvastatin at 20 mg/d for at least 10 weeks; patients were then randomized into 2 groups receiving simvastatin+omega-3 fatty acids at 3.36 g/d or placebo (corn oil) for an additional 5 weeks. Hemostatic variables that have been associated with increased thrombotic tendency were evaluated with subjects in the fasting state and during postprandial hyperlipemia before and after combined treatment. Supplementation of omega-3 fatty acid reduced tissue factor pathway inhibitor antigen (P<0.05) in the fasting state, reduced the degree of postprandial hyperlipemia (P<0.005), and reduced activated factor VII concentration appearing during postprandial hyperlipemia. In conclusion, omega-3 fatty acids given in addition to simvastatin to patients with combined hyperlipemia reduced the free tissue factor pathway inhibitor fraction in the fasting state and inhibited the activation of factor VII occurring during postprandial lipemia, thus representing a potential beneficial effect on the hemostatic risk profile in this patient group.

Adult↗

PubMed2000

Relationship between apolipoprotein E polymorphism, postprandial hyperlipemia and hemostatic variables in patients with combined hyperlipemia.

BACKGROUND AND AIM: Combined hyperlipemia is a common lipid abnormality associated with coronary heart disease (CHD). Aim of this study was to investigate the relationship between this abnormality and hemostatic risk factors related to thrombosis. METHODS AND RESULTS: Forty-one patients were examined in the fasting state and during postprandial hyperlipemia. They had high levels of factor VIIc in the fasting state. During postprandial hyperlipemia a highly significant (p < 0.001) increase of activated factor (VIIa) occurred. This activation was not correlated to the increase in free fatty acids, but to the degree of postprandial hypertriglyceridemia. The absolute postprandial triglyceridemia was highest in subjects with the apolipoprotein (apo) E2 allele. Tissue factor pathway inhibitor activity (TFPIa) was correlated to LDL cholesterol and apo B concentrations and was highest in subjects with genotypes containing the E4 allele. CONCLUSIONS: Subjects with combined hyperlipemia may have an increased thrombotic risk related to activation of factor VII during postprandial hyperlipemia. Subjects with genotypes including the apoE4 allele may have a high lipid risk profile associated with high levels of LDL cholesterol.

Adult↗

PubMed2001

Effects of atorvastatin and omega-3 fatty acids on LDL subfractions and postprandial hyperlipemia in patients with combined hyperlipemia.

BACKGROUND AND AIM: The aim of the present study was to see whether a moderate dose of omega-3 fatty acids (FA) potentiates the beneficial effects of statins on the high risk for coronary heart disease (CHD) in patients with combined hyperlipemia. METHODS AND RESULTS: In the present double-blind parallel study, 42 patients with combined hyperlipemia with serum triglycerides 2-15 mmol/L-1 and serum total cholesterol > 5.3 mmol/L-1 at the end of a three-month dietary run-in period were treated with 10 mg/d atorvastatin for 10 or more weeks. During the last 5 weeks they were randomized into two groups that received either 1.68 g/d omega-3 FA as ethylesters of eicosapentaenoic (45%) and docosahexaenoic acids (39%), or placebo (corn oil). As expected, atorvastatin significantly reduced serum total LDL-cholesterol (LDL-C), triglycerides and apolipoproteins B, E, CII and CIII, whereas HDL-cholesterol (HDL-C) was increased. Addition of omega-3 FA further increased HDL-C (p < 0.03), and reduced systolic blood pressure (< 0.03), while the small dense LDL-particles (LDL III) (p < 0.05) and postprandial hypertriglyceridemia (p < 0.01) were reduced compared with the baseline, though there were no significant differences to the placebo group. This may be related to the large individual variation in these parameters and the small number of patients. No significant effects on basic or postheparin activities of lipoprotein lipase or hepatic lipase were observed after atorvastatin with or without addition of omega-3 FA. CONCLUSIONS: This study indicates that addition of a low dose of omega-3 FA may further improve the risk profile for CHD in patients with combined hyperlipemia treated with atorvastatin. The effect is related to reduction of postprandial hyperlipemia and redistribution of LDL subfractions.

Adult↗

PubMed2006

Effect of gap junction uncoupler heptanol on resistance arteries reactivity in experimental models of diabetes, hyperlipemia and hyperlipemia-diabetes.

The understanding of the involvement of the gap junctions (GJ) in the vascular reactivity is an ongoing effort. In this study we questioned on impact of pathologies such as diabetes, hyperlipemia, and simultaneous hyperlipemia-diabetes on GJ involvement in the contractile/relaxant response of the mesenteric resistance arteries. To this purpose, four groups of Golden Syrian hamsters were used: (i) diabetics (D), injected by streptozotocin, (ii) hyperlipemics (H), fed the standard chow of the species supplemented with 3% cholesterol and 15% butter, (iii) simultaneously hyperlipemic-diabetics (HD), and (iv) controls (C), age-matched normal healthy animals. At 24 weeks after the beginning of the experiment, the vascular reactivity of the resistance arteries was measured by the myograph technique in the presence/absence of 1 mM Heptanol (Hep) and of vasoconstrictors and vasodilators. The results showed that: (i) in pathological conditions 1 mM Hep significantly impaired the constrictor response of the hamster resistance arteries to both 10(-5) M NA (noradrenaline, agonist of alpha(1)-adrenoceptors) and 64.1 mM K+ (potassium ion, the major intracellular cation). The impairment occur in the group range: HD < H < D < C being the highest at the simultaneous insult of hyperlipemia and diabetes; (ii) independently of the pathological condition, 1 mM Hep abolishes both endothelium-dependent and independent relaxation of the hamster resistance arteries. At 1 mM Hep we noticed a reversible effect on endothelium-dependent relaxation that may be partially restored (in normal) in the presence of L-arginine. It is hoped that these results may contribute to understanding of the involvement of GJ in vascular pathology/dysfunction.

Acetylcholine↗

PubMed1955