Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo 105-8461, Japan.
Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo 105-8461, Japan.
Peptides. 2021 Jan;135:170421. doi: 10.1016/j.peptides.2020.170421. Epub 2020 Oct 12.
Malondialdehyde-modified low-density lipoprotein (MDA-LDL) is recognized as a surrogate marker of lipid oxidation and is associated with arteriosclerosis. However, there are limited reports on the relationship between heart failure and MDA-LDL. Therefore, we aimed to determine whether MDA-LDL is activated in patients with left ventricular (LV) dysfunction and examine our hypothesis that the B-type natriuretic peptide (BNP) masks the enhancement of MDA-LDL in patients with LV dysfunction by its strong antioxidative action. The study population comprised 2,976 patients with various cardiovascular diseases. Patients were divided into four groups depending on the LV ejection fraction (LVEF) or plasma BNP level. A nonparametric analysis with the Kruskal-Wallis test was used to perform an interquartile comparison. In addition, structural equation modeling and Bayesian estimation were used to compare the effects of LVEF and BNP on MDA-LDL. MDA-LDL levels did not significantly change (P > 0.05) with respect to the degree of LVEF among the four groups. In contrast, MDA-LDL levels were significantly decreased (P < 0.001) with respect to the degree of BNP among the four groups. A path model based on structural equation modeling clearly showed a significant effect of LVEF (standardized regression coefficient; β: -0.107, P < 0.001) and BNP (β: -0.114, P < 0.001) on MDA-LDL, with a significant inverse association between LVEF and BNP (correlation coefficient -0.436, P < 0.001). MDA-LDL should be activated in patients with LV dysfunction; however, BNP is thought to exert a strong compensatory suppression on lipid oxidation, masking the relationship between heart failure and lipid oxidation.
丙二醛修饰的低密度脂蛋白(MDA-LDL)被认为是脂质氧化的替代标志物,与动脉粥样硬化有关。然而,关于心力衰竭与 MDA-LDL 之间关系的报道有限。因此,我们旨在确定 MDA-LDL 是否在左心室(LV)功能障碍患者中被激活,并检验我们的假设,即 B 型利钠肽(BNP)通过其强大的抗氧化作用掩盖了 LV 功能障碍患者 MDA-LDL 的增强。研究人群包括 2976 名患有各种心血管疾病的患者。根据 LV 射血分数(LVEF)或血浆 BNP 水平,将患者分为四组。使用 Kruskal-Wallis 检验进行非参数分析,以进行四分位比较。此外,还使用结构方程模型和贝叶斯估计来比较 LVEF 和 BNP 对 MDA-LDL 的影响。MDA-LDL 水平在四组之间与 LVEF 的程度没有显著变化(P > 0.05)。相比之下,MDA-LDL 水平随着四组之间 BNP 程度的降低而显著降低(P < 0.001)。基于结构方程模型的路径模型清楚地显示了 LVEF(标准化回归系数;β:-0.107,P < 0.001)和 BNP(β:-0.114,P < 0.001)对 MDA-LDL 的显著影响,LVEF 和 BNP 之间存在显著的负相关关系(相关系数-0.436,P < 0.001)。MDA-LDL 应该在 LV 功能障碍患者中被激活;然而,BNP 被认为对脂质氧化具有强大的补偿抑制作用,掩盖了心力衰竭与脂质氧化之间的关系。