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PubMed1996

Hypertriglyceridemia, but not hypercholesterolemia, is associated with the alterations of fibrinolytic system.

Derangements of the blood coagulation-fibrinolytic system are thought to be associated with the development of cardiovascular disease. Previous studies have identified the alterations in patients with advanced atherosclerosis, however, studies on subjects without apparent cardiovascular complications are scarce. To evaluate the potential risk of thrombosis, we examined the serum lipid levels and fibrinolytic parameters in 54 subjects of different types of primary hyperlipoproteinemia (HL) and 18 normolipidemic controls. Plasma tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) antigen levels were significantly higher in type IV HL than in the controls. Serum triglyceride concentrations were correlated with t-PA (r = 0.537, p < 0.01) and PAI-1 (r = 0.249, p < 0.05) antigen levels, while serum cholesterol levels did not. The current study demonstrated that hypertriglyceridemia, but not hypercholesterolemia, is associated with the alterations of fibrinolytic system.

Adult↗
PubMed1993

An apolipoprotein CIII haplotype protective against hypertriglyceridemia is specified by promoter and 3' untranslated region polymorphisms.

Five DNA polymorphisms were detected in the promoter of the apolipoprotein CIII gene of a type III hyperlipidemic subject with severe hypertriglyceridemia (HTG). The polymorphic sites were C-641-->A, G-630--> A, T-625-->deletion, C-482-->T, and T-455-->C, with the previously reported base at each site designated allele 1 and the variant base designated allele 2. The sites were in strong linkage disequilibrium with each other and with a polymorphic Sst I site in the apolipoprotein CIII 3' untranslated region whose presence (S2 allele) has previously been shown to be associated with HTG. The distribution of haplotypes of the form -625 -482 Sst I among 78 normolipidemic adults and 79 adults with severe HTG was estimated by maximum likelihood analysis. The 211 haplotype was estimated to be 3.8-fold more common in normal subjects than in HTG subjects (estimated proportions, 0.186 and 0.049, respectively). This haplotype was associated with reduced HTG risk (relative risk, 0.28; P = 0.005) when compared with other haplotypes lacking the Sst I site (S1 allele). The 222 haplotype was estimated to be present on 48 of the 54 S2-containing chromosomes observed and was associated with increased risk for HTG (relative risk, 3.14; P < 0.0025). These results support the existence of apolipoprotein CIII promoter/Sst I haplotypes conferring either protection against or susceptibility to severe HTG.

Alleles↗
PubMed1998

Overexpression and accumulation of apolipoprotein E as a cause of hypertriglyceridemia.

The molecular mechanisms of hypertriglyceridemia (HTG), a common lipid metabolic disorder in humans, often of genetic origin, are not well understood. In studying the effect of apolipoprotein (apo) E on the metabolism of triglyceride-rich lipoproteins, we found that expressing high plasma levels of human apoE3 in transgenic mice lacking endogenous mouse apoE caused HTG. These transgenic animals had 3-fold higher plasma triglyceride levels, higher very low density lipoproteins (VLDL), and lower high density lipoproteins than did nontransgenics. Removing one or both low density lipoprotein receptor alleles in the apoE3-overexpressing mice caused severe HTG (8-11-fold over nontransgenics) and increased VLDL and decreased low and high density lipoproteins, and apoE3-enriched VLDL were markedly depleted in apoC-II. At least two mechanisms could explain HTG associated with apoE3 overexpression: stimulated VLDL triglyceride production and impaired VLDL lipolysis. The apoE3 mice with HTG had a 50% increase in hepatic VLDL triglyceride production. Furthermore, overexpression of apoE (E2, E3, or E4) in cultured hepatocytes (McA-RH7777 cells) correlated positively with secretion of VLDL into the medium. However, apoE3 overexpression-associated HTG was only partially explained by VLDL overproduction, as lipoprotein lipase-mediated VLDL lipolysis was also decreased 20-86% depending on apoE3 levels, most likely by displacing or masking apoC-II on the particles. In human subjects, HTG correlated positively with increased VLDL triglyceride and plasma and VLDL apoE levels. However, plasma and VLDL apoE correlated negatively with VLDL apoC-II levels and lipoprotein lipase-mediated VLDL lipolysis. Thus, optimal expression of apoE is crucial for normal metabolism of triglyceride-rich lipoproteins, and overexpression and/or accumulation of apoE may contribute to HTG by stimulating VLDL triglyceride production and by impairing VLDL lipolysis. The apoE3-overexpressing mice will be useful for studying the pathophysiology of this disorder.

Animals↗
PubMed2001

Severe hypercholesterolemia, hypertriglyceridemia, and atherosclerosis in mice lacking both leptin and the low density lipoprotein receptor.

Leptin-deficient mice (ob/ob) are an excellent murine model for obesity, insulin resistance, and diabetes, all of which are components of a multiple risk factor syndrome that, along with hypercholesterolemia, precipitates a potential high risk for atherosclerosis. In the current study, we show an unexpectedly severe hyperlipidemia in ob/ob mice on a background of low density lipoprotein receptor (LDLR) deficiency (-/-). Doubly mutant mice (LDLR-/-;ob/ob) exhibited striking elevations in both total plasma cholesterol (TC) and triglyceride (TG) levels (1715 +/- 87 and 1016 +/- 172 mg/dl, respectively), at age 3-4 months, resulting in extensive atherosclerotic lesions throughout the aorta by 6 months. Lipoprotein analyses revealed the elevated TC and TG levels to be due to a large increase in an apoB-containing broad-beta remnant lipoprotein fraction. While fasting, diet restriction, and low level leptin treatment significantly lowered TG levels, they caused only slight changes in TC levels. Hepatic cholesterol and triglyceride contents as well as mRNA levels of cholesterologenic and lipogenic enzymes suggest that leptin deficiency increased hepatic triglyceride production but did not change cholesterol production in ob/ob mice regardless of their LDLR genotype. These data provide evidence that the hypertriglyceridemia and hypercholesterolemia in the doubly mutant mice are caused by distinct mechanisms and point to the possibility that leptin might have some impact on plasma cholesterol metabolism, possibly through an LDLR-independent pathway. This model will be an excellent tool for future studies on the relationship between impaired fuel metabolism, increased plasma remnant lipoproteins, diabetes, and atherosclerosis.

Animals↗
PubMed2001

Caveolin-1-deficient mice are lean, resistant to diet-induced obesity, and show hypertriglyceridemia with adipocyte abnormalities.

Caveolae organelles and caveolin-1 protein expression are most abundant in adipocytes and endothelial cells. Our initial report on mice lacking caveolin-1 (Cav-1) demonstrated a loss of caveolae and perturbations in endothelial cell function. More recently, however, observation of the Cav-1-deficient cohorts into old age revealed significantly lower body weights, as compared with wild-type controls. These results suggest that Cav-1 null mice may have problems with lipid metabolism and/or adipocyte functioning. To test this hypothesis directly, we placed a cohort of wild-type and Cav-1 null mice on a high fat diet. Interestingly, despite being hyperphagic, Cav-1 null mice show overt resistance to diet-induced obesity. As predicted, adipocytes from Cav-1 null null mice lack caveolae membranes. Early on, a lack of caveolin-1 selectively affects only the female mammary gland fat pad and results in a near complete ablation of the hypo-dermal fat layer. There are also indications of generalized adipose tissue pathology. With increasing age, a systemic decompensation in lipid accumulation occurs resulting in dramatically smaller fat pads, histologically reduced adipocyte cell diameter, and a poorly differentiated/hypercellular white adipose parenchyma. To gain mechanistic insights into this phenotype, we show that, although serum insulin, glucose, and cholesterol levels are entirely normal, Cav-1 null mice have severely elevated triglyceride and free fatty acid levels, especially in the post-prandial state. However, this build-up of triglyceride-rich chylomicrons/very low density lipoproteins is not due to perturbed lipoprotein lipase activity, a major culprit of isolated hypertriglyceridemia. The lean body phenotype and metabolic defects observed in Cav-1 null mice are consistent with the previously proposed functions of caveolin-1 and caveolae in adipocytes. Our results show for the first time a clear role for caveolins in systemic lipid homeostasis in vivo and place caveolin-1/caveolae as major factors in hyperlipidemias and obesity.

Adipocytes↗
PubMed2003

Hypertriglyceridemia in lecithin-cholesterol acyltransferase-deficient mice is associated with hepatic overproduction of triglycerides, increased lipogenesis, and improved glucose tolerance.

Lecithin-cholesterol acyltransferase deficiency is frequently associated with hypertriglyceridemia (HTG) in animal models and humans. We investigated the mechanism of HTG in the ldlr-/- x lcat-/- (double knockout (dko)) mice using the ldlr-/- x lcat+/+ (knock-out (ko)) littermates as control. Mean fasting triglyceride (TG) levels in the dko mice were elevated 1.75-fold compared with their controls (p < 0.002). Both the very low density lipoprotein and the low density lipoprotein/intermediate density lipoprotein fractions separated by fast protein liquid chromatography were TG-enriched in the dko mice. In vitro lipolysis assay revealed that the dko mouse very low density lipoprotein (d < 1.019 g/ml) fraction separated by ultracentrifugation was a more efficient substrate for lipolysis by exogenous bovine lipoprotein lipase. Post-heparin lipoprotein lipase activity was reduced by 61% in the dko mice. Hepatic TG production rate, determined after intravenous Triton WR1339 injection, was increased 8-fold in the dko mice. Hepatic mRNA levels of sterol regulatory element binding protein-1 (srebp-1) and its target genes acetyl-CoA carboxylase-1 (acc-1), fatty acid synthase (fas), and stearoyl-CoA desaturase-1 (scd-1) were significantly elevated in the dko mice compared with the ko control. The hepatic mRNA levels of LXRalpha (lxralpha) and its target genes including angiopoietin-like protein 3 (angptl-3) in the dko mice were unchanged. Fasting glucose and insulin levels were reduced by 31 and 42%, respectively in the dko mice, in conjunction with a 49% reduction in hepatic pepck-1 mRNA (p = 0.014). Both the HTG and the improved fasting glucose phenotype seen in the dko mice are at least in part attributable to an up-regulation of the hepatic srebp-1c gene.

Acetyl-CoA Carboxylase↗
PubMed2000

Maternal hypertriglyceridemia during late pregnancy does not affect the increase in circulating triglycerides caused by the long-term consumption of a sucrose-rich diet by rats.

Feeding a sucrose-rich diet (SRD) during pregnancy enhances maternal hypertriglyceridemia. The goal of this study was to investigate whether this effect is modified when pregnancy is initiated in rats at different times during feeding of a SRD (63 g sucrose/100 g). One group of rats was fed the SRD; another group received the same diet except that the sucrose was replaced by an equal amount of cornstarch. At different times during the feeding of the diets, i.e., 5, 45 or 90 d, half of the rats were mated; after serial tail blood collections, rats were studied at d 20 of pregnancy. Virgin rats fed the same diets were always studied in parallel. Plasma triglycerides increased progressively in virgin rats fed the SRD from d 1 to 35, declined thereafter up to d 50, increased again to attain the highest level at d 65-70, partially declined at d 100 and increased again at d 110. During late pregnancy, rats fed the control diet (CD) always had greater plasma triglyceride concentrations than virgin rats, whereas triglyceride levels did not differ between pregnant and virgin rats fed the SRD. These intergroup differences were similar to those seen for plasma VLDL-triglycerides. The liver triglyceride concentration in virgin rats fed the SRD was always significantly higher than that of rats fed the CD, whereas it did not differ in pregnant rats fed the SRD for either 25 or 65 d from those fed the CD. However, in those fed the SRD for 110 d, values were higher than in either pregnant or virgin rats fed the CD. We propose that the known capability of the liver to enhance triglyceride secretion during pregnancy protects dams from developing a fatty liver when fed a SRD for short periods of time, although not for long-term treatments.

Analysis of Variance↗
PubMed2001

Long-term ingestion of dietary diacylglycerol lowers serum triacylglycerol in type II diabetic patients with hypertriglyceridemia.

We examined the effect of daily consumption of dietary diacylglycerol (DG) oil on serum lipid concentrations in patients with diabetes whose serum triacylglycerol (TG) levels were persistently increased despite continuous nutritional counseling at the outpatient clinic. Patients (n = 16) were divided into DG and control groups (n = 8 each). DG was incorporated (target dose 10 g/d) by substituting DG oil (80 g DG/100 g oil) for the ordinary TG cooking oil used at home for 12 wk. The control group continued consuming ordinary TG cooking oil. Dietary records indicated that there were no differences between groups in total energy intake or percentage of energy from fat. In the DG group, TG intake decreased from 26.8 +/- 9.3 to 15.7 +/- 8.9 g/d, whereas DG intake increased from 0.3 +/- 0.1 to 10.6 +/- 3.9 g/d. No differences between groups were observed in body weight, total fat intake or total oil consumption throughout the study period. In the DG group, serum TG levels decreased 39.4% from 2.51 +/- 0.75 mmol/L to 1.52 +/- 0.28 mmol/L. Serum glycohemoglobin A(1c) (HbA(1c)) concentration also decreased 9.7%. In contrast, there were no changes in these variables in the control group. Serum total and HDL cholesterol were not affected in either group. These results indicate that DG oil may be useful as an adjunct to the standard diet therapy of fat restriction in the management of diabetics with hypertriglyceridemia.

Blood Glucose↗
PubMed2004

Individual serum triglyceride responses to high-fat and low-fat diets differ in men with modest and severe hypertriglyceridemia.

It is not yet clear whether a low-fat or a high-fat diet is more suitable for the treatment of hypertriglyceridemia. Therefore, we conducted a dietary study with nonobese hypertriglyceridemic men using a randomized crossover design. After a 2-wk acclimation period, the subjects were randomly assigned to 2 groups. One group consumed a low-fat (29% of energy) diet for 3 wk, followed first by a 2-wk washout period, then a 3-wk high-fat (40% of energy) diet period. The second group consumed the low- and high-fat diets in reverse order. Both diets were isocaloric, rich in monounsaturated fatty acids (MUFAs) and long-chain (n-3)-PUFAs, and contained no alcohol. Absolute amounts of long-chain (n-3)-PUFAs and fiber were similar, as were the fatty acid and carbohydrate compositions. Serum triglyceride concentrations in fasting subjects decreased during the high-fat diet period by 34% (95% CI = -19 to -46%, P = 0.001), and during the low-fat diet period by 31% (95% CI = -0.5 to -51.8%, P = 0.048). Triglyceride concentrations did not differ between the low- and high-fat diet periods. However, the high-fat diet lowered triglyceride concentrations more effectively in all subjects with a baseline triglyceride concentration < 4.5 mmol/L, whereas the low-fat diet lowered triglyceride levels more effectively in half of the subjects with a baseline value > 4.5 mmol/L. Based on these findings, we recommend a high-fat triglyceride-lowering diet for patients with only slightly elevated serum triglyceride concentrations (<4.5 mmol/L). However, a lower-fat diet is more suitable for some subjects with more distinctly elevated triglyceride concentrations.

Adult↗
PubMed2006

Fish oil increases bile acid synthesis in male patients with hypertriglyceridemia.

Fibrates are drugs of choice in patients with hypertriglyceridemia (HTG), but may increase the risk for gallstones by decreasing bile acid synthesis. Fish oil might be a therapeutic alternative, but its effect on bile acid metabolism in humans is unknown. We compared the effects of triglyceride-lowering therapy by fish oil or bezafibrate on cholesterol synthesis and bile acid metabolism in HTG. Cholesterol synthesis, bile acid pool sizes, and synthesis rates were compared between 9 male HTG patients and 10 normolipidemic controls matched for age, sex, and BMI. Effects of bezafibrate or fish oil were studied only in HTG patients in a randomized crossover trial. Patients had 14-fold higher serum triglyceride concentrations and greater cholesterol synthesis, as indicated by a 107% higher ratio of serum lathosterol to cholesterol (P < 0.01) than controls. The groups did not differ in bile acid metabolism. Both bezafibrate and fish oil reduced serum TG concentration (-68 and -51% vs. baseline, respectively). Compared with baseline, bezafibrate therapy was associated with reduced cholesterol synthesis (-25%, P = 0.009) without changes in bile acid synthesis rate and pool size. In contrast, fish oil increased bile acid synthesis (+31% vs. baseline, P = 0.07 and +53% vs. bezafibrate, P = 0.02) and altered bile acid distribution, as reflected by an increased ratio of the cholic acid (CA) synthesis rate to the chenodeoxycholic acid (CDCA) synthesis rate (+35% vs baseline, P = 0.05 and + 32% vs bezafibrate, P = 0.07) without effects on bile acid pool size or cholesterol synthesis. In conclusion, cholesterol synthesis is greater in HTG patients than in controls, whereas bile acid synthesis does not differ. Bezafibrate and fish oil have similar triglyceride-lowering capacities, but distinct effects on cholesterol synthesis. Bile acid synthesis is increased by fish oil, but not by bezafibrate therapy.

Bezafibrate↗
PubMed1995

Improvement of fibrinolysis and plasma lipoprotein levels induced by gemfibrozil in hypertriglyceridemia.

A randomized double-blind study was carried out with gemfibrozil (600 mg b.i.d.) vs placebo in 20 patients (twelve males and eight females, age 52 +/- 3 years, BMI 24.2 +/- 0.4) suffering from primary hypertriglyceridemia (Fredrickson's type IV). Each group was treated for a 12 week period with gemfibrozil (n = 10) or placebo (n = 10) patients) in a double-blind fashion. Total cholesterol, HDL-cholesterol (HDL-C) and its subfractions (HDL2-C and HDL3-C), blood glucose, Apolipoproteins A1 and B, fibrinogen, plasminogen, factor VII, t-PA:Ag and PAI activity pre- and post-venous occlusion (VO) were determined. In the gemfibrozil-treated group a significant decrease of total cholesterol and triglycerides and a significant increase of HDL-C and HDL2-C were found. During gemfibrozil treatment a significant reduction of factor VII, fibrinogen and plasminogen levels was also observed. After 12 weeks of treatment in the gemfibrozil group the release of t-PA:Ag in response to venous occlusion was significantly higher and plasma PAI activity was significantly lower than in placebo group. Moreover positive correlations between HDL cholesterol and t-PA:Ag post-VO (r = 0.56, P < 0.01) and between HDL2-C cholesterol and t-PA:Ag post-VO (r = 0.59, P < 0.01) and a negative correlation between triglycerides and t-PA:Ag post-VO (r = -0.65, P < 0.01) were found. The data obtained suggest that gemfibrozil, in addition to the well established lipid-regulating effect, appears to have a positive role in the regulation of reverse cholesterol transport and fibrinolytic system.

Apolipoprotein A-I↗
PubMed2001

Alterations in the extrinsic pathway in hypertriglyceridemia do not cause a 'procoagulant state': effects of bezafibrate therapy.

Hypertriglyceridemia (HTG) is an independent risk factor for cardiovascular disease (CVD). Hemostatic variables [factor VII antigen (FVIIag), factor VII coagulant activity (FVIIc), activated factor VII (FVIIa), free and endothelial-associated (EC) tissue factor pathway inhibitor (TFPI) antigen, pre- and post-heparin total TFPI activity, EC-TFPI activity, prothrombin fragment 1 + 2 (F1 + 2), fibrinogen and D-dimer] were compared between 18 HTG patients and 20 controls to investigate whether HTG is associated with alterations in the extrinsic pathway and whether such alterations create a procoagulant state, as expressed by F1 + 2 and D-dimer levels. In addition, the effects of bezafibrate therapy (6 weeks, 400 mg/day) on these variables were studied in 18 HTG patients in a double-blind, placebo-controlled, cross-over study. FVIIag, FVIIc, free TFPI and fibrinogen were significantly higher in HTG patients (by 44, 30, 45 and 31%, respectively; all P < 0.02), while FVIIa, EC-TFPIag and activity, total TFPI activities, F1 + 2 and D-dimer levels were similar in patients and controls. Bezafibrate reduced serum TG and fibrinogen levels (by 62 and 20%, respectively; both P < 0.001), whereas the other hemostatic variables were unaffected. In conclusion, the observed alterations in the extrinsic pathway in HTG are not associated with a procoagulant state. In contrast, the presence of elevated fibrinogen levels in HTG might enhance the risk for CVD. Bezafibrate therapy improved the adverse lipid profile and decreased fibrinogen levels in HTG patients.

Adult↗
PubMed1997

Exercise training, postprandial hypertriglyceridemia, and LDL subfraction distribution.

The purpose of this study was to examine differences in postprandial hypertriglyceridemia (PP-HTG) and low density lipoprotein (LDL) subfraction distribution among groups of men and women with different fitness levels. Fifty-four men and women (ages 30-53 yr) were recruited based on their previous two-year activity level: sedentary (S), recreational exercisers (R), and endurance trained (T). After a 24-h dietary preparation, blood was collected, and LDL subfractions were separated and analyzed for cholesterol (C) and apoprotein B100. Plasma triglyceride (TG) concentration was assessed before and at 2, 4, 6, and 8 h after fat meal. PP-HTG was significantly higher for the S group compared with the two activity groups. LDL3-C and LDL3-apoprotein B100 were significantly higher for the S group compared with the T group and for men compared with women. These findings suggest that both recreational and competitive aerobic training are associated with a lower TG response after a fatty meal. However, higher volume aerobic training may be necessary to reduce the number of dense LDL molecules and their cholesterol content.

Adult↗
PubMed2004

Rosuvastatin improves the atherogenic and atheroprotective lipid profiles in patients with hypertriglyceridemia.

BACKGROUND: We examined the effects of rosuvastatin treatment on triglyceride levels and lipid measures in a parallel-group multicenter trial (4522IL/0035) in patients with hypertriglyceridemia (Fredrickson Type IIb or IV). METHODS: After a 6-week dietary lead-in period while on a National Cholesterol Education Program step I diet, 156 patients with fasting triglyceride levels >/= 300 and < 800 mg/dl were randomized to 6 weeks of double-blinded treatment: once-daily rosuvastatin of 5, 10, 20, 40 or 80 mg or placebo. The primary end point was mean percentage change from baseline in total serum triglyceride levels at week 6 as determined by analysis of variance. RESULTS: Rosuvastatin at all doses produced significant mean reductions in triglycerides compared with placebo (-18 to -40 compared with +2.9%, P </= 0.001); median reductions in triglycerides with rosuvastatin at 5-80 mg ranged from -21 to -46%. All doses of rosuvastatin significantly reduced levels of atherogenic lipoprotein and apolipoproteins over placebo, including low-density lipoprotein cholesterol, total cholesterol, non-high-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, apolipoprotein B and apolipoprotein C-III. Statistically significant increases in high-density lipoprotein cholesterol were observed with rosuvastatin doses > 5 mg. The occurrence of adverse events was generally low and not dose related, although some adverse events occurred more frequently in the rosuvastatin 80 mg group. CONCLUSIONS: Rosuvastatin reduced triglyceride levels and improved the overall atherogenic and atheroprotective lipid profiles in hypertriglyceridemic patients.

Analysis of Variance↗
PubMed1994

Hypertriglyceridemia and low HDL: therapeutic considerations.

The recently revised guidelines for cholesterol management in Europe and the USA have focused attention on triglycerides and HDL cholesterol as risk factors for coronary heart disease. In the present review, I shall discuss therapeutic considerations in the treatment of patients with hypertriglyceridemia or low HDL cholesterol in the context of these new recommendations. I shall also consider recent studies in which the effect of triglyceride-lowering drugs on the concentrations and metabolism of lipoproteins in patients with dyslipidemia are evaluated.

Cholesterol, HDL↗
PubMed2002

Carbohydrate-induced hypertriglyceridemia: modifying factors and implications for cardiovascular risk.

High-carbohydrate/low-fat, isocaloric diets have repeatedly been shown to increase plasma triglyceride concentrations. The present review addresses recent developments relevant to several important unresolved issues. These include the type of dietary carbohydrate that is most likely to induce hypertriglyceridemia, predictors of individual susceptibility, modifiable physiologic factors that may mitigate the plasma triglyceride response, underlying metabolic mechanisms that are responsible for increased plasma triglycerides, and implications of altered serum lipid profiles for atherogenic risk. Although some progress has been made in this field, the central public health issue - the net effect on cardiovascular risk - remains unresolved.

Arteriosclerosis↗
PubMedDate not supplied

Hypertriglyceridemia and coronaryheart disease risk.

Several angiographic-based trials have established that triglyceride remnant particles are associated with progression of coronary stenosis, and a recent prospective study has shown that triglycerides are associated with coronary heart disease (CHD), even after adjustment for high-density lipoprotein cholesterol. The importance of plasma triglycerides in CHD risk must be interpreted within the context of other plasma lipoproteins, as well as the fasting and postprandial triglyceride levels. Recommendations for triglyceride lowering are empiric because of the lack of randomized clinical trial data that evaluate triglyceride-lowering therapies and CHD prevention. This article presents a clinical approach to the management of hypertriglyceridemia.

Coronary Disease↗