Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates

Bae, Jang–Ho; Bassenge, E.; Lee, Hee-Ja; Park, Ki-Rack; Park, Chang-Gyo; Park, Keun-Yong; Lee, Moo‐Sik; Schwemmer, Michael

doi:10.1016/s0021-9150(01)00408-7

Cited by 53 publications

(35 citation statements)

References 19 publications

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“…55 (19) 46 (20) 9 (19) 3 (%) 43 (15) 25 (11) 18 (38) We have previously reported that postprandial hypertriglyceridemia can cause endothelial dysfunction to deteriorate further, further increasing the oxidative stress, which in turn is associated with endothelial dysfunction, even in patients with CAD already affected by endothelial dysfunction. 11 Our previous study suggests that increased oxidative stress can further enhance endothelial dysfunction in patients with CAD. In addition, there are relevant reports that antioxidants can improve endothelial function in patients with chronic heart failure, 12 and that the augmented oxidative stress plays an important role initiating endothelial dysfunction in these patients.…”

Section: Discussionmentioning

confidence: 96%

Impact of left ventricular ejection fraction on endothelial function in patients with coronary artery disease

Bae

Bassenge

Kim

et al. 2004

Clinical Cardiology

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SummaryBackground: Endothelial dysfunction is present in patients with coronary artery disease (CAD) or with congestive heart failure.Hypothesis: This study was performed to evaluate the impact of systolic heart function on endothelial function in patients with CAD.Methods: The study population consisted of 283 consecutive patients (mean age 59 years, 176 men) undergoing coronary angiography. Endothelial function was assessed by measuring flow-mediated vasodilation (FMD) of the brachial artery.Results: Patients (n = 236) with an ejection fraction (EF) ≥ 55% on routine echocardiogram were younger (mean age 58 vs. 62 years), showed a lower prevalence of diabetes (15 vs. 38%) and myocardial infarction (13 vs. 66%), and showed a higher FMD (4.8 ± 2.4 vs. 4.0 ± 2.0%, p < 0.05) than patients (n = 47) with an EF < 55%. The correlation coefficient between FMD/endothelial function and EF/systolic heart function was 0.149 (p < 0.02) in the overall study population. Multivariate analysis showed that of age, gender, frequency of

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Section: Discussionmentioning

confidence: 96%

Impact of left ventricular ejection fraction on endothelial function in patients with coronary artery disease

Bae

Bassenge

Kim

et al. 2004

Clinical Cardiology

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“…Postprandial increases in lipids and carbohydrates have been shown to increase oxidative stress, a state implicated in the pathogenesis of cardiovascular disease and diabetic complications (27,28). More specifically, atherosclerosis is correlated with postprandial hyperlipidemia, which is characterized by elevated TGRL levels in the blood, and there is increasing evidence that postprandial TGRLs are more atherogenic than fasting TGRLs (3,(29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation

Wang

Gill

Pedersen

et al. 2009

Journal of Lipid Research

250

181

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Triglyceride-rich lipoprotein (TGRL) lipolysis products provide a pro-inflammatory stimulus that can alter endothelial barrier function. To probe the mechanism of this lipolysis-induced event, we evaluated the pro-inflammatory potential of lipid classes derived from human postprandial TGRL by lipoprotein lipase (LpL). Incubation of TGRL with LpL for 30 min increased the saturated and unsaturated FFA content of the incubation solutions significantly. Furthermore, concentrations of the hydroxylated linoleates 9-hydroxy ocatadecadienoic acid (9-HODE) and 13-HODE were elevated by LpL lipolysis, more than other measured oxylipids. The FFA fractions elicited pro-inflammatory responses inducing TNFa and intracellular adhesion molecule expression and reactive oxygen species (ROS) production in human aortic endothelial cells (HAECs). The FFA-mediated increase in ROS was blocked by both the cytochrome P450 2C9 inhibitor sulfaphenazole and NADPH oxidase inhibitors. Compared with linoleate, 13-HODE was found to be a more potent inducer of ROS production in HAECs, an activity that was insensitive to both NADPH oxidase and cytochrome P450 inhibitors. Therefore, although the oxidative metabolism of FFA in endothelial cells can produce inflammatory responses, TGRL lipolysis can also release preformed mediators of oxidative stress (e.g., HODEs) that may influence endothelial cell function in vivo by stimulating intracellular ROS production.-Wang, L., R. Gill, T. L. Pedersen, L. J. Higgins, J. W. Newman, and J. C. Rutledge. Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation. J. Lipid Res. 2009. 50: 204-213.

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“…Fasting lipid peroxides did not correlate with VLDL, LDL, or HDL subfractions separated by density-gradient ultracentrifugation; however, postprandial lipid peroxides were strongly correlated with VLDL triglycerides (r ϭ 0.53, P ϭ 0.03). In another study, hypertriglyceridemic and type 2 diabetic subjects administered a high-fat meal (53.4 g fat) recorded increased oxidant stress, as measured by 2-h phorbol myristic acid-activated leukocyte superoxide anion production (4.09 Ϯ 0.93 to 5.49 Ϯ 1.19 nmol ⅐ 10 6 cells Ϫ1 ⅐ min Ϫ1 ) (30). The increased production of superoxide anion correlated with postprandial triglyceride levels (r ϭ 0.798, P Ͻ 0.001).…”

Section: Safety Studiesmentioning

confidence: 97%

Fenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome

et al. 2007

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OBJECTIVE -The aim of this study was to determine the effects of fenofibrate (160 mg/day) on fasting and postprandial lipoproteins, oxidized fatty acids, and inflammatory mediators in subjects with hypertriglyceridemia and the metabolic syndrome.RESEARCH DESIGN AND METHODS -Fifty-nine subjects with fasting hypertriglyceridemia (Ն1.7 and Ͻ6.9 mmol/l) and two or more of the Adult Treatment Panel III criteria for the metabolic syndrome were randomly assigned to fenofibrate (160 mg/day) or placebo in a double-blind, controlled clinical trial.RESULTS -Fenofibrate treatment lowered fasting triglycerides (Ϫ46.1%, P Ͻ 0.0001) and postprandial (area under the curve) triglycerides (Ϫ45.4%, P Ͻ 0.0001) due to significant reductions in postprandial levels of large (Ϫ40.8%, P Ͻ 0.0001) and medium (Ϫ49.5%, P Ͻ 0.0001) VLDL particles. The number of fasting total LDL particles was reduced in fenofibratetreated subjects (Ϫ19.0%, P ϭ 0.0033) primarily due to reductions in small LDL particles (Ϫ40.3%, P Ͻ 0.0001); these treatment differences persisted postprandially. Fasting and postprandial oxidized fatty acids were reduced in fenofibrate-treated subjects compared with placebo-administered subjects (Ϫ15.3%, P ϭ 0.0013, and 31.0%, P Ͻ 0.0001, respectively), and fenofibrate therapy lowered fasting and postprandial soluble vascular cell adhesion molecule-1 (VCAM-1) (Ϫ10.9%, P ϭ 0.0005, and Ϫ12.0%, P ϭ 0.0001, respectively) as well as fasting and postprandial soluble intercellular adhesion molecule-1 (ICAM-1) (Ϫ14.8%, P Ͻ 0.0001, and Ϫ15.3%, P Ͻ 0.0001, respectively). Reductions in VCAM-1 and ICAM-1 were correlated with reductions in fasting and postprandial large VLDL particles (P Ͻ 0.0001) as well as postprandial oxidized fatty acids (P Ͻ 0.0005).CONCLUSIONS -Triglyceride-lowering therapy with fenofibrate reduced fasting and postprandial free fatty acid oxidation and inflammatory responses, and these antiatherosclerotic effects were most highly correlated with reductions in large VLDL particles. Diabetes Care 30:1945-1951, 2007T he metabolic syndrome represents an agglomeration of interrelated risk factors that include abnormally high fasting triglyceride levels (1,2). In a recent analysis, hypertriglyceridemia (Ն1.7 mmol/l) represented the component of the metabolic syndrome most strongly associated with a history of myocardial infarction and stroke (3). Furthermore, elevated fasting triglyceride levels (Ն1.4 mmol/l) and an enlarged waist circumference (Ͼ89 cm) were the two characteristics of the metabolic syndrome that were associated with the greatest increased risk for all-cause mortality and cardiovascular deaths among postmenopausal women (4).Hypertriglyceridemia signifies the presence of increased plasma triglycerideremnant lipoproteins, and the concentrations of remnant-like lipoproteins are further enhanced postprandially among hypertriglyceridemic subjects (5). Remnant-like proteins have been shown to increase intracellular oxidant concentrations and lipid peroxide levels in culture media and to activate nuclear factor-B ...

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Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates

Cited by 53 publications

References 19 publications

Impact of left ventricular ejection fraction on endothelial function in patients with coronary artery disease

Impact of left ventricular ejection fraction on endothelial function in patients with coronary artery disease

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation

Fenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome

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