Letter regarding article by Tsimikas et al, "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".

Circulation (Impact Factor: 15.2). 06/2005; 111(18):e284-5; author reply e284-5. DOI: 10.1161/01.CIR.0000164264.00913.6D
Source: PubMed

ABSTRACT predominantly associated with Lp(a), 2 the increased OxPL/apoB ratio could be explained by the shift in the Lp(a)/LDL ratio. Similarly, in the placebo-treated group the decreased OxPL/apoB ratio results from a decrease in Lp(a) relative to LDL. It is therefore unlikely that the OxPL/apoB ratio is a surrogate marker of net removal of OxPL from the vessel wall. Moreover, the observed 30% decrease in total plasma apoB-OxPL also argues against an increased net efflux of OxPL from the vessel wall. Recently, using the OxLDL assay from Mercodia in which an oxidation epitope associated with apoB is detected with mono- clonal antibody 4E6, we found that atorvastatin (80 mg/d) and simvastatin (40 mg/d) reduced total plasma Ox-apoB (43% and 35%, respectively) in patients with familial hypercholesterol- emia from the ASAP study.3 Interestingly, we observed no change in the Ox-apoB/apoB ratio when we used the noncom- petitive version of the kit, in which the immobilized antibody captures Ox-apoB from the sample. We did, however, observe a small increase in the Ox-apoB/apoB ratio (18% for atorvastatin, 13% for simvastatin) when we used the competitive version, which unlike the noncompetitive version is sensitive to the number of oxidation epitopes associated with apoB. In addition, the increase in Ox-apoB/apoB ratio can be explained by an increase in Lp(a) relative to LDL. To further address this question, measurements of OxLDL with E06 and 4E6 in well- designed assays (eg, in isolated Lp(a) particles) at different time points after the start of statin treatment are required.

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    ABSTRACT: The aim of the study was to evaluate the association of immunoglobulin G type of autoantibodies to oxidized low-density lipoprotein (oxLDL-lgG) and oxLDL-lgM with the progression of esophageal squamous cell carcinoma (ESSC). Residents from Feicheng, China aged 40 to 69 years were screened for esophageal lesions in a screening program conducted during the period of January 2008 to December 2006. There were 33 controls with normal esophageal squamous epithelium cells, 37 patients with basal cell hyperplasia, 47 with esophageal squamous cell dysplasia, and 43 with ESCC. All the participants were diagnosed by biopsy and histopathological examination. Adiponectin, oxidized low-density lipoprotein (oxLDL), autoantibodies against oxLDL (oxLDL-ab), OxLDL-lgG, and OxLDL-lgM were determined by enzyme linked immunosorbent assay (ELISA). Total cholesterol, High-density lipoprotein (HDL), triglyceride, serum albumin, and blood pressure were co-estimated. Analysis of covariance for lipid levels was used to control the influence of covariates. The level of oxLDL-lgM increased gradually along with esophageal carcinoma progression. The oxLDL-lgM levels in the ESCC group were the highest after possible covariates were controlled. Binary logistic regression showed that oxLDL-lgM had a positive correlation with the development of esophageal carcinoma, while oxLDL and oxLDL-ab had a negative correlation with ESSC. No significant association between the levels of oxLDL-lgG and adiponectin and the different stages of ESSC was observed. The present study shows that the decreased oxLDL and oxLDL-ab and the elevated oxLDL-lgM serum levels may relate to the development and progression of ESSC.
    Lipids in Health and Disease 01/2009; 8:48. · 2.31 Impact Factor
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    ABSTRACT: It has been widely recognized that oxidized low-density lipoprotein (oxLDL) is involved in cardiovascular diseases. However, one of the major questions has been whether oxLDL is a cause or a result of atherosclerotic lesion development. Immunologic detection of human circulating oxLDL has been established, and evidence of a close relationship between oxLDL levels in human circulating plasma and cardiovascular diseases has been accumulating. Recent prospective studies suggest that plasma oxLDL measurement is potentially a predictive marker for cardiovascular diseases. Another question has been how LDL is oxidized in vivo. Recent progress in structural studies has shown evidence that oxLDL in vivo is oxidized differently from copper-induced oxLDL.
    Current Cardiovascular Risk Reports 12/2008; 3(1):18-22.
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    ABSTRACT: Identification of high-risk patients presenting with chest pain remains challenging. The use of a single biomarker or a panel of biomarkers to detect occult plaque destabilization or rupture without frank infarction would allow for appropriate triage of such patients. Current data suggest that plaque vulnerability is determined by the relationship between forces that increase the size of the lipid core and destabilize the overlying thin fibrous cap. A variety of interrelated pathways are imputed to play important roles in this process of plaque evolution, destabilization, and rupture. These mechanisms include increased systemic and local inflammation, increased oxidative stress, matrix metalloproteinase modulation, and hemodynamic variables related to altered shear stress. Select candidate biomarkers that either reflect or influence these underlying processes and may ultimately have clinical application are highlighted in this review, which focuses on emerging biomarkers to define and predict the risks associated with the complex nature of vulnerable plaque biology.
    Current Atherosclerosis Reports 09/2008; 10(4):309-17. · 2.92 Impact Factor

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