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PubMed2007

Effect of rosuvastatin 5-20mg on triglycerides and other lipid parameters in Japanese patients with hypertriglyceridemia.

To evaluate the potential dose effect of rosuvastatin on triglyceride (TG) levels in Japanese hypertriglyceridemic patients, we randomized 154 patients with TG levels of >or=200 and <800 mg/dL to 8 weeks of treatment with rosuvastatin 5, 10 or 20mg once daily; bezafibrate 200mg twice daily; or placebo. Compared with placebo, TG was reduced by 30.1% with rosuvastatin 5mg, 30.1% with 10mg and 32.3% with 20mg (all p<or=0.0001), with no evidence of a dose effect. Changes in TG were evident after 2 weeks of treatment and maintained thereafter. In a benchmark comparison, rosuvastatin across its dose range reduced TG by 29.1-31.1% from baseline versus 45.4% for bezafibrate. Compared with bezafibrate, rosuvastatin was superior with respect to changes in non-high-density lipoprotein cholesterol (non-HDL-C, -36.8 to -44.3% for rosuvastatin versus -2.0% for bezafibrate), low-density lipoprotein cholesterol (-31.9 to -41.0% versus +29.3%), total cholesterol (-27.1 to -33.3% versus +2.1%), although smaller improvements in HDL-C (12.4-16.7% versus 19.6%) were observed. Rosuvastatin also produced superior dose-related decreases in median high-sensitivity C-reactive protein (22.9-38.5%). Treatment was well tolerated in both rosuvastatin and bezafibrate patients, with clinically important increases in alanine aminotransferase being rare, no adverse effect on renal function being observed and no cases of myopathy or rhabdomyolysis being reported. The current study does not suggest a dose-related effect of rosuvastatin in lowering TG in hypertriglyceridemic Japanese patients, although dose-related improvements in other elements of the atherogenic lipid profile were observed.

Apolipoproteins↗
PubMed2007

Effect of bezafibrate therapy on atherosclerotic aortic plaques detected by MRI in dyslipidemic patients with hypertriglyceridemia.

Fibrates reduce triglycerides (TG) and increase HDL-cholesterol levels, but there was no report showing plaque regression by fibrates. Using MRI, we investigated the effects of bezafibrate on aortic plaques in 22 dyslipidemic patients. All patients were asked to receive 400mg bezafibrate, but 8 who declined to have bezafibrate became the control group. Changes in vessel wall area (VWA) and lumen area (LA) from baseline to 1-year were evaluated. Bezafibrate reduced TG (-55%) and increased HDL-cholesterol levels (+29%). Bezafibrate reduced HDL size and increased LDL size. In thoracic plaques, bezafibrate reduced VWA (-6%, P<0.001) with no LA change, but VWA slightly progressed without bezafibrate (+5%). In abdominal plaques, bezafibrate reduced VWA (-8%, P<0.001) with LA increase (+3%, P<0.02), but VWA progressed without bezafibrate (+6%). VWA changes in thoracic and abdominal plaques correlated with TG reduction and HDL-cholesterol increase. Notably, VWA change in only abdominal plaques correlated with HDL size reduction and LDL size increase. Thus, bezafibrate induced plaque regression in thoracic and abdominal aortas with marked TG reduction and HDL-cholesterol increase, but the processes of plaque regression and vascular remodeling may differ between thoracic and abdominal aortas. However, because our study was not a controlled, randomized trial, further study is needed.

Aged↗
PubMed2006

A novel experimental model of acute hypertriglyceridemia induced by schisandrin B.

Mice were intragastrically treated with single doses (0.05-0.8 g/kg) of schisandrin B (a dibenzocyclooctadiene derivative isolated from the fruit of Schisandra chinensis). Twenty-four hours after schisandrin B administration, the serum triglyceride level was increased by 10-235% in a dose-dependent manner. However, the serum low density lipoprotein cholesterol level was significantly decreased by 28% at a dose of 0.8 g/kg. When given once daily (0.01-0.2 g/kg) for 4 days, schisandrin B also dose-dependently elevated the serum triglyceride level (17-134%). Kinetics parameters estimated by Scott's plot analysis of schisandrin B-induced changes in serum and hepatic triglyceride levels were determined: serum-E(max) (maximal effect)=6 mmol/L (384% increase, P<0.001); K(D) (affinity)=0.59 mmol/kg; pD(2) (an index of affinity)=6.62; liver-E(max)=21 micromol/g (68% increase, P<0.001); K(D)=0.37 mmol/kg; pD(2)=6.83. The efficacy of schisandrin B in increasing the triglyceride level was 5.6-fold higher in serum than in liver tissue. Fenofibrate (0.2g/kg) treatment, when in combination with schisandrin B (0.2g/kg), for 4 days significantly reduced the schisandrin B-induced increase in serum triglyceride level (by 81%, P<0.001). Hepatic triglyceride level was also decreased (by 100%, P<0.001) by co-treatment with fenofibrate. Our results suggest that schisandrin B treatment can be used to establish a mouse model of acute hypertrigylceridemia.

Animals↗
PubMed2006

Effects of raloxifene on lipid and lipoprotein levels in postmenopausal osteoporotic women with and without hypertriglyceridemia.

This post hoc analysis reports the effects of raloxifene on lipids and lipoproteins in 2659 women with either normal (< or =150 mg/dL) or high (>150 mg/dL) triglyceride levels from a substudy of the Multiple Outcomes of Raloxifene Evaluation (MORE) trial. In both triglyceride subgroups, raloxifene significantly improved low-density lipoprotein cholesterol, total cholesterol, non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein B, apolipoprotein A-I, and fibrinogen compared with placebo (P < .05). After raloxifene treatment, women with high triglycerides experienced an equal or more robust reduction in cholesterol, lipoprotein parameters, and ratios of total cholesterol to HDL-C and non-HDL-C to HDL-C than was observed in women with normal triglycerides (P < .05). Mean levels of low-density lipoprotein cholesterol and apolipoprotein B were reduced by 16.5% and 15.8%, respectively, in women with high triglycerides, and by 12.7% and 11.3%, respectively, in women with normal triglycerides. These findings further substantiate that raloxifene improves concentrations of both cholesterol and beta-lipoprotein. The subgroup of women with high triglycerides, who have elevated cardiovascular risk, appear to derive at least equal, if not greater, overall effect on lipid and lipoprotein lowering with raloxifene.

Aged↗
PubMed2006

Associations between hypertriglyceridemia, dietary fat intake, oxidative stress, and endothelial activation in men.

OBJECTIVE: We examined the associations between intake of different types of dietary fat and plasma levels of oxidative stress and endothelial activation markers in men. METHODS: For that purpose, a complete physical and metabolic profile was assessed. Dietary habits of subjects were determined with a 3-d food record. We also measured fasting plasma 8-iso-prostaglandin F2alpha and oxidized low-density lipoprotein concentrations and soluble forms of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin. All these measurements were performed with commercial enzyme-linked immunosorbent assay kits and standards. RESULTS: We found that a high total dietary fat intake was associated with high plasma sICAM-1 (r = 0.40, P < 0.005), sVCAM-1 (r = 0.31, P < 0.05), and E-selectin (r = 0.28, P < 0.05) levels. We also found that in men matched for plasma triacylglycerol levels, those consuming a diet rich in total fat (>105 g/d, n = 21) were characterized by higher circulating levels of sICAM-1 (P < 0.05) and E-selectin (P < 0.05) compared with triacylglycerol-matched individuals with a low total dietary fat intake (<105 g/d, n = 21). However, no significant difference was noted in plasma oxidized low-density lipoprotein levels between groups. Further, we conducted multivariate analyses and found that saturated fatty acid intake was the only dietary variable after inclusion of other dietary variables that contributed to circulating sICAM-1 (P < 0.05) and sVCAM-1 (P < 0.05). CONCLUSION: Our study suggests that high dietary fat consumption is associated with endothelial activation in men and that this detrimental effect is likely attributable to the saturated fatty acid content of the diet.

Adult↗
PubMed2002

Contribution of abdominal obesity and hypertriglyceridemia to impaired fasting glucose and coronary artery disease.

Multiple logistic regression models were used in a cross-sectional study to determine the relation of fasting glycemia to angiographically assessed coronary artery disease (CAD) in 569 men (aged 18 to 69 years) who were stratified according to fasting blood glucose concentrations (<6.1 mmol/L, and 6.1 to 6.9 mmol/L or 110 to 124 mg/dl), waist circumference (<90 vs >or=90 cm), and fasting triglyceridemia (<2.0 vs >or=2.0 mmol/L or <177 vs >or=177 mg/dl). For this purpose, nondiabetic impaired fasting glucose was defined as from 6.1 to 6.9 mmol/L (110 to 124 mg/dl) compared with 250 normoglycemic controls (fasting glycemia <6.1 mmol/L or <124 mg/dl) without history of CAD. In the absence of "hypertriglyceridemic waist," impaired fasting glucose was not predictive of CAD. However, the risk of CAD was markedly higher among subjects characterized by both the hypertriglyceridemic waist phenotype and the presence of impaired fasting glucose (odds ratio 8.5, 95% confidence intervals 3.5 to 20.4; p <0.05) compared with the normoglycemic group with low waist circumferences and triglyceride levels. Thus, the results of the present study emphasizes the importance of other underlying metabolic abnormalities, such as abdominal obesity and related atherogenic dyslipidemia, in the modulation of the CAD risk associated with hyperglycemia.

Abdomen↗
PubMed1996

Hypertriglyceridemia and elevated lipoprotein(a) are risk factors for major coronary events in middle-aged men.

Cardiovascular risk factors were analyzed in 4,849 male participants, aged 40 to 65 years, in an 8-year follow-up of the Münster Heart Study (Prospective Cardiovascular Münster Study; PROCAM). One hundred eighty-one definite nonfatal myocardial infarctions, 49 fatal myocardial infarctions, and 28 sudden cardiac deaths were observed. Multiple logistic function analysis confirmed that age, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, cigarette smoking, diabetes mellitus, angina pectoris, and family history of myocardial infarction were important cardiovascular risk factors. Interestingly, this analysis revealed a significant and independent association between serum levels of triglycerides and the incidence of major coronary events. The relation between lipoprotein(a) [Lp(a)] levels and the occurrence of major coronary events was analyzed in a subgroup of 878 men. Thirty-three probands with major coronary events had significantly higher geometric mean levels of Lp(a) than 828 men who did not experience major coronary events (0.09 vs 0.05 g/L; p <0.011). Thus, in addition to established risk for factors, serum levels of triglycerides and Lp(a) are sensitive indicators of increased risk major coronary events.

Adult↗
PubMed1998

Hypertriglyceridemia as a cardiovascular risk factor.

To determine the relation between plasma triglyceride levels and the risk of incident cardiovascular disease, the semiquantitative techniques of meta-analysis were applied to 17 population-based prospective studies of triglyceride and cardiovascular disease. Sixteen of these studies represented 2,445 events among 46,413 Caucasian men followed for an average period of 8.4 years, and 5 studies represented 439 events among 10,864 Caucasian women followed for an average period of 11.4 years. Univariate relative risk (RR) estimates for incident cardiovascular disease associated with a 1-mmol/L increase in triglyceride was 1.07-1.98 in men, with a summary RR of 1.32 (95% confidence interval [CI]: 1.26-1.39), indicating a 32% increase in disease risk associated with increased triglyceride. In the studies involving women, individual RR estimates for triglyceride were 1.69-2.05, with a summary RR of 1.76 (95% CI: 1.50-2.07), indicating a 76% increase in disease risk associated with increased triglyceride. After adjustment for high-density lipoprotein cholesterol and other risk factors, these risks were decreased to 14% in men and 37% in women but remained statistically significant. Three recent prospective epidemiologic studies have also shown that plasma triglyceride and low-density lipoprotein particle size predict subsequent coronary artery disease in Caucasian populations. Taken together, these studies demonstrate the importance of triglyceride levels as a risk factor for cardiovascular disease.

Cardiovascular Diseases↗
PubMed1999

Hypertriglyceridemia, insulin resistance, and the metabolic syndrome.

The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk of cardiovascular disease events. Insulin resistance may lie at the heart of the metabolic syndrome. Elevated serum triglycerides commonly associate with insulin resistance and represent a valuable clinical marker of the metabolic syndrome. Abdominal obesity is a clinical marker for insulin resistance. The metabolic syndrome manifests 4 categories of abnormality: atherogenic dyslipidemia (elevated triglycerides, increased small low-density lipoproteins, and decreased high-density lipoproteins), increased blood pressure, elevated plasma glucose, and a prothrombotic state. Various therapeutic approaches for the patient with the metabolic syndrome should be implemented to decrease the risk of cardiovascular disease events. These interventions include decreasing obesity, increasing physical activity, and managing dyslipidemia; the latter may require the use of pharmacotherapy with cholesterol-lowering and triglyceride-lowering drugs.

Exercise↗
PubMed1999

Role of fibrates in the management of hypertriglyceridemia.

Elevated plasma triglyceride levels are increasingly recognized as a risk factor for cardiovascular disease. Fibric acid derivatives (fibrates) substantially decrease triglyceride levels and have been demonstrated to decrease clinical cardiovascular events in some trials. Ongoing research will elucidate the molecular mechanisms by which fibrates modify lipoprotein metabolism, clarify their use in combination with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins), and determine their role in the prevention of cardiovascular events.

Anticholesteremic Agents↗