Triglyceride- and cholesterol-rich lipoproteins have a differential effect on mild/moderate and severe lesion progression as assessed by quantitative coronary angiography in a controlled trial of lovastatin.

Hodis, Howard N.; Mack, Wendy J.; Azen, Stanley P.; Alaupovic, Petar; Pogoda, Janice M.; LaBree, Laurie; Hemphill, Linda; Kramsch, Dieter M.; Blankenhorn, David H.

doi:10.1161/01.cir.90.1.42

Cited by 312 publications

(152 citation statements)

References 23 publications

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“…Phillips and coworkers showed that angiographic lesion progression was related to IDL cholesterol over a two-year period [116]. Two reports from the Monitored Atherosclerosis Regression Study (MARS) have shown that the apo C-III content of VLDL was associated with lesion progression [117] as well as certain apo B-containing lipoproteins carrying apo C-III and apo E [118]. Recently a novel immunoaffinity method has been established for detection of remnant-like lipoprotein cholesterol (RLP-C) [45].…”

Section: Clinical Evidence For a Link Between Disturbed Metabolism Ofmentioning

confidence: 99%

Postprandial lipoprotein metabolism and atherosclerosis

Karpe

1999

Journal of Internal Medicine

359

242

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Section: Clinical Evidence For a Link Between Disturbed Metabolism Ofmentioning

confidence: 99%

Postprandial lipoprotein metabolism and atherosclerosis

Karpe

1999

Journal of Internal Medicine

359

242

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“…ApoCIII associated with HDL (CIII LpnonB) was negatively correlated with lesion progression in CLAS study 30 whereas apoCIII associated with apoB containing lipoprotein (CIII LpB) was positively correlated with lesion progression in MARS study. 31 Studies on animal models, including transgenic 32 -35 or knock-out mice 36 -40 and familial studies 41,42 suggest that apoE can prevent coronary heart disease. In addition, in vitro studies 43 -49 and animal models 50 have suggested an anti-inflammatory effect of apoE.…”

Section: Introductionmentioning

confidence: 99%

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo

et al. 2001

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BACKGROUND: Obesity is frequently associated with an increase in the early inflammation marker C-reactive protein (CRP), insulin resistance and changes in lipoprotein metabolism. Increased CRP is known as an independent cardiovascular risk factor. Since the apolipoproteins (apo) E and CIII components of HDL are associated with reduced cardiovascular risk and since apoE has in vitro anti-inflammatory effect, we have investigated the relationships between apoE, apoCIII (in apoB and non apoB containing lipoproteins) and CRP in obese adults. METHODS:The following parameters from 34 healthy obese fasting women (age 22 -64 y, body mass index (BMI) 28 -68 kg=m 2 ) were measured: (1) ApoE and apoCIII, in total plasma, in apoB-(E LpB, CIII LpB) and non-apoB-containing lipoproteins (E LpnonB, CIII LpnonB); (2) CRP and cytokine secreted by adipose tissue (TNF-a and its soluble receptor TNFR2); (3) triglyceride, HDL-cholesterol, systolic blood pressure, diastolic blood pressure, waist and hip circumferences, insulin, glucose. HOMA, a marker of insulin sensitivity, and the ratio E=CIII in LpB and LpnonB were calculated. RESULTS: CRP was positively correlated with BMI (P < 0.05), waist circumference (WC, P < 0.05), triglyceride (P < 0.05) and negatively correlated with apoE (P < 0.01) and E LpnonB (P < 0.05). Two multiple regression models including parameters related to CRP with a P < 0.25 were run stepwise to assess their independent contribution to CRP concentration. In the first model (including BMI, WC, HOMA, insulin, triglyceride, apoE, E LpnonB), apoE was the best predictor of CRP (P ¼ 0.01) together with triglyceride (P ¼ 0.02) and BMI (P ¼ 0.08). The second model took into account E=CIII LpnonB ratio with the parameters included in the first model. In this second model, E=CIII LpnonB was the best predictor of CRP (P ¼ 0.007), explaining 39% of CRP variance. CONCLUSION: ApoE is strongly correlated with CRP and could have an anti-inflammatory effect in vivo in obese subjects. This correlation could be limited to LpnonB lipoproteins, depending on their apoE and CIII relative content.

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“…In the Monitored Atherosclerosis Regression Study (MARS) (25), apoC-III, particularly in apoB-containing lipoproteins, was a major risk factor for the severity of CVD in patients with mild and moderate atherosclerosis. In the Cholesterol and Recurrent Events (CARE) study, LpB:C-III was strongly and independently associated with the risk of CVD (26).…”

mentioning

confidence: 99%

Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes

Dallinga‐Thie

Berk-Planken²,

Bootsma³

et al. 2004

Diabetes Care

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OBJECTIVE -Apolipoprotein (apo)C-III is a constituent of HDL (HDL apoC-III) and of apoB-containing lipoproteins (LpB:C-III). It slows the clearance of triglyceride-rich lipoproteins (TRLs) by inhibition of the activity of the enzyme lipoprotein lipase (LPL) and by interference with lipoprotein binding to cell-surface receptors. Elevated plasma LpB:C-III is an independent risk factor for cardiovascular disease. We studied the effect of atorvastatin on plasma LpB:C-III and HDL apoC-III. RESEARCH DESIGN AND METHODS-We studied the effect of 30 weeks' treatment with 10 and 80 mg atorvastatin on plasma apoC-III levels in a randomized, double-blind, placebo-controlled trial involving 217 patients with type 2 diabetes and fasting plasma triglycerides between 1.5 and 6.0 mmol/l.RESULTS -Baseline levels of total plasma apoC-III, HDL apoC-III, and LpB:C-III were 41.5 Ϯ 10.0, 17.7 Ϯ 5.5, and 23.8 Ϯ 7.7 mg/l, respectively. Plasma apoC-III was strongly correlated with plasma triglycerides (r ϭ 0.74, P Ͻ 0.001). Atorvastatin 10-and 80-mg treatment significantly decreased plasma apoC-III (atorvastatin 10 mg, 21%, and 80 mg, 27%), HDL apoC-III (atorvastatin 10 mg, 22%, and 80 mg, 28%) and LpB:C-III (atorvastatin 10 mg, 23%, and 80 mg, 28%; all P Ͻ 0.001). The decrease in plasma apoC-III, mainly in LpB:C-III, strongly correlated with a decrease in triglycerides (atorvastatin 10 mg, r ϭ 0.70, and 80 mg, r ϭ 0.78; P Ͻ 0.001). Atorvastatin treatment also leads to a reduction in the HDL apoC-III-to-HDL cholesterol and HDL apoC-III-to-apoA-I ratios, indicating a change in the number of apoC-III per HDL particle (atorvastatin 10 mg, Ϫ21%, and 80 mg, Ϫ31%; P Ͻ 0.001).CONCLUSIONS -Atorvastatin treatment resulted in a significant dose-dependent reduction in plasma apoC-III, HDL apoC-III, and LpB:C-III levels in patients with type 2 diabetes. These data indicate a potentially important antiatherogenic effect of statin treatment and may explain (part of) the triglyceride-lowering effect of atorvastatin.

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Triglyceride- and cholesterol-rich lipoproteins have a differential effect on mild/moderate and severe lesion progression as assessed by quantitative coronary angiography in a controlled trial of lovastatin.

Cited by 312 publications

References 23 publications

Postprandial lipoprotein metabolism and atherosclerosis

Postprandial lipoprotein metabolism and atherosclerosis

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo

Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes

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