Abstract
L5, the most negatively charged subfraction of low-density lipoprotein (LDL), is implicated in atherogenesis. We examined the relationship between plasma L5 levels and the occurrence of subclinical atherosclerosis in patients with rheumatoid arthritis (RA). Using anion-exchange purification with fast-protein liquid chromatography, we determined the proportion of plasma L5 of LDL (L5%) in 64 RA patients and 12 healthy controls (HC). Plasma L5% and L5 levels were significantly higher in RA patients (median, 1.4% and 1.92 mg/dL) compared with HC (0.9%, p < 0.005; and 1.27 mg/dL, p < 0.05) and further increased in patients with subclinical atherosclerosis (2.0% and 2.88 mg/dL). L5% and L5 levels decreased in patients after 6-months of therapy (p < 0.01). Subclinical atherosclerosis was indicated by plaque and intima-media thickness determined by carotid ultrasonography. Using multivariate analysis, L5% and L5 levels are revealed as the predictors of subclinical atherosclerosis (odds ratio, 4.94 and 1.01; both p < 0.05). Receiver operating characteristic curves showed that cut-off values of L5% ≥ 1.45% and L5 levels ≥ 2.58 mg/dL could predict subclinical atherosclerosis in patients (both p < 0.001). Immunoblotting showed that the expression levels of lectin-like oxidized LDL receptor-1 (LOX-1) was increased in RA patients. Together, our findings suggest that plasma L5% and L5 levels may be predictors of cardiovascular risk in RA patients.
Highlights
Atherosclerosis, a chronic inflammatory vascular disease characterized by atheromatous plaque buildup, is associated with an increased risk of cardiovascular events [1]
We examined the relationship between plasma L5 levels and the occurrence of subclinical atherosclerosis in rheumatoid arthritis (RA) patients and whether L5 may contribute to the increased cardiovascular disease (CVD) risk
Using receiver operating characteristic (ROC) analysis, we found that RA patients with plasma L5% above 1.45% and L5 levels above 2.58 mg/dL may have a high probability of subclinical atherosclerosis, with moderate sensitivity and specificity
Summary
Atherosclerosis, a chronic inflammatory vascular disease characterized by atheromatous plaque buildup, is associated with an increased risk of cardiovascular events [1]. Rheumatoid arthritis (RA) is an inflammatory articular disease [2,3] that is complicated by accelerated atherosclerosis and an increased risk of cardiovascular disease (CVD) [4,5]. Electronegative LDL, which was first separated from its electropositive counterpart by Avogaro and colleagues [10] by using anion-exchange chromatography, has been shown to be atherogenic [11]. The binding of L5 with its specific receptor, lectin-like oxidized LDL receptor-1 (LOX-1), has been shown to induce the release of multiple inflammatory and atherogenic mediators from vascular endothelial cells and monocytes [12,13,14,15]. Whether electronegative L5 contributes to the increased risk of CVD in RA patients has not been explored
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