Improvement of coronary vasodilatation capacity through single LDL apheresis

Mellwig, Klaus Peter; Baller, D.; Gleichmann, U.; Moll, David; Betker, S; Weise, R.; Notohamiprodjo, G.

doi:10.1016/s0021-9150(98)00055-0

Cited by 117 publications

(76 citation statements)

References 17 publications

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“…9 OxPLs are known to be highly inflammatory and to induce vasoconstriction, 21 and it is possible that removal of such OxPLs contributes to rapid improvement in endothelial function. This is supported by several studies showing improvement in coronary 17 and brachial endothelial function 16 with LDL apheresis or lovastatin treatment. 15 More specifically, Tamai et al 16 have shown that acetylcholine-induced brachial artery vasodilatation improves rapidly within 4 hours after LDL apheresis [Lp(a) is also removed], and the best correlate of improvement was reduced plasma OxLDL levels, measured by use of monoclonal antibody DLH3, which binds to an OxPL epitope nearly identical to that bound by E06.…”

Section: Tsimikas Et Al Oxldl In Acute Coronary Syndromessupporting

confidence: 54%

“…[15][16][17] In mouse and rabbit aortic atherosclerotic lesions, OxLDL becomes depleted after regression diets, out of proportion to LDL depletion or other measures of plaque regression. 8,18 These reductions in OxLDL are associated with increased collagen and smooth muscle cell content, increased endothelial nitric oxide synthase production, and reduced inflammatory markers, 7 which suggests that removal of OxLDL from the vessel wall may serve as an early marker of plaque stabilization.…”

mentioning

confidence: 99%

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High-Dose Atorvastatin Reduces Total Plasma Levels of Oxidized Phospholipids and Immune Complexes Present on Apolipoprotein B-100 in Patients With Acute Coronary Syndromes in the MIRACL Trial

et al. 2004

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Background— Oxidized phospholipids (OxPL) are present within atherosclerotic plaques and bound by lipoprotein (a) [Lp(a)] in plasma. This study evaluated the impact of atorvastatin on oxidized LDL (OxLDL) in patients with acute coronary syndromes (ACS). Methods and Results— OxLDL-E06 (OxPL content on apolipoprotein B-100 [apoB] detected by antibody E06), apoB-100 immune complexes (apoB-IC), OxLDL autoantibodies, and Lp(a) levels were measured in 2341 patients at baseline and after 16 weeks of treatment with atorvastatin 80 mg/d or placebo. The OxLDL-E06 and apoB-IC data are reported per apoB-100 particle (OxPL/apoB, IC/apoB) and as total levels on all apoB-100 particles (total apoB-OxPL and total apoB-IC [eg, OxPL/apoB or IC/apoB×apoB-100 levels]). Compared with baseline values, atorvastatin reduced apoB-100 (−33%), total apoB-OxPL (−29.7%), total apoB-IC IgG (−29.5%), and IgM (−25.7%) ( P <0.0001 for all), whereas no change or an increase was observed with placebo. When normalized per apoB-100, compared with placebo, atorvastatin increased OxPL/apoB (9.5% versus −3.9%, P <0.0001) and Lp(a) (8.8% versus −0.7%, ( P <0.0001). A strong correlation was noted between OxPL/apoB and Lp(a) ( R =0.85, P <0.0001), consistent with previous data that Lp(a) binds OxPL. Conclusions— After atorvastatin treatment, total OxPL on all apoB-100 particles was decreased. However, there was enrichment of OxPL on a smaller pool of apoB-100 particles, in parallel with similar increases in Lp(a), suggesting binding by Lp(a). These data support the hypothesis that atorvastatin promotes mobilization and clearance of proinflammatory OxPL, which may contribute to a reduction in ischemic events after ACS.

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Section: Tsimikas Et Al Oxldl In Acute Coronary Syndromessupporting

confidence: 54%

mentioning

confidence: 99%

High-Dose Atorvastatin Reduces Total Plasma Levels of Oxidized Phospholipids and Immune Complexes Present on Apolipoprotein B-100 in Patients With Acute Coronary Syndromes in the MIRACL Trial

et al. 2004

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“…Interestingly, the Lp-PLA 2 -specifi c activity increased in the intermediate and high Lp(a) groups, suggesting that the remaining LDL particles are defi cient in small dense LDL particles with the lowest specifi c Lp-PLA 2 activity and enriched in large buoyant particles exhibiting higher specifi c activity. These data are also consistent with previous data showing that apheresis enhances endotheliumdependent vasodilation in the brachial ( 32 ) and coronary arteries ( 33 ).…”

Section: Discussionsupporting

confidence: 93%

Acute impact of apheresis on oxidized phospholipids in patients with familial hypercholesterolemia

Arai

Orsoni

Mallat

et al. 2012

Journal of Lipid Research

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“…It is critical to explain how high blood LDL or cholesterol levels can induce a proinflammatory, proatherogenic state and how this state can be reversed or prevented in an intact animal. It has been shown that when human LDL levels are precipitously reduced, rapid correction of vascular change occurs, 21,22 indicating that certain LDL-or cholesterol-induced effects are likely to be reversible. This reversibility effect appears to have been corroborated in our study because there is almost no ICAM-1 or VCAM-1 after 48 hours, when cholesterol levels are again approaching baseline.…”

Section: Verna Et Al Icam-1 and Vcam-1 Correlated With Ap-1mentioning

confidence: 99%

In Vivo Low-Density Lipoprotein Exposure Induces Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 Correlated With Activator Protein-1 Expression

Verna

Ganda

Stemerman

2006

ATVB

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Objective-We tested the hypothesis that direct native low-density lipoprotein (LDL) injection into LDL receptordeficient (LDLR Ϫ/Ϫ ) mice would induce the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in their aortic endothelial cells, and that transcriptional regulation of this pathway involved activator protein-1 (AP-1) but not nuclear factor B (NF-B). Methods and Results-Using tail vein injection of LDL into LDLRϪ/Ϫ mice, we were able to maintain atherogenic LDL blood levels, which induced ICAM-1 and VCAM-1 expression in their aortic endothelial cells after 24 hours. We were able to visualize and quantify this expression using immunohistochemistry and confocal microscopy. Under conditions in which ICAM-1 and VCAM-1 were expressed, the regulatory AP-1 proteins c-Fos and c-Jun were also highly expressed in the endothelial cell cytoplasm and observed within the cell nucleus. The NF-B protein P65, although expressed in the endothelial cell cytoplasm after LDL injection, was not observed within the cell nucleus. Conclusions-Elevated

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Improvement of coronary vasodilatation capacity through single LDL apheresis

Cited by 117 publications

References 17 publications

High-Dose Atorvastatin Reduces Total Plasma Levels of Oxidized Phospholipids and Immune Complexes Present on Apolipoprotein B-100 in Patients With Acute Coronary Syndromes in the MIRACL Trial

High-Dose Atorvastatin Reduces Total Plasma Levels of Oxidized Phospholipids and Immune Complexes Present on Apolipoprotein B-100 in Patients With Acute Coronary Syndromes in the MIRACL Trial

Acute impact of apheresis on oxidized phospholipids in patients with familial hypercholesterolemia

In Vivo Low-Density Lipoprotein Exposure Induces Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 Correlated With Activator Protein-1 Expression

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