Wang Bin, Xue Yusheng, Shang Fujun, Ni Sifeng, Liu Xiongtao, Fan Boyuan, Wang Haichang
Department of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shanxi, China.
J Clin Lab Anal. 2019 Feb;33(2):e22672. doi: 10.1002/jcla.22672. Epub 2018 Sep 21.
Adropin, a newly identified regulatory protein encoded by Enho gene, suppressed tumor necrosis factor α-induced THP1 monocyte adhesion to human umbilical vein endothelial cells. In addition, inflammation is demonstrated to be involved in the mechanism of atrial fibrillation (AF). Atrial remodeling is correlated with the persistence and progression of AF. Adropin is hypothesized to correlated with AF and atrial remodeling. This study aims to determine the correlation of serum adropin and the presence of AF and remodeling.
This study consisted of 344 AF patients and 210 healthy controls. AF patients were then divided into three subgroups of paroxysmal AF, persistent AF, and permanent AF. Serum adropin concentrations were examined using enzyme-linked immunosorbent assay method. Left atrial diameter (LAD) was measured to evaluate atrial remodeling.
Decreased serum adropin concentrations were found in AF patients compared with healthy controls. Logistic regression analysis confirmed that serum adropin was inversely associated with the presence of AF (OR 0.218, 95% CI 0.15-0.316; P < 0.001). Permanent AF patients had significantly reduced serum adropin concentrations compared with persistent and paroxysmal AF patients. There were decreased serum adropin concentrations in persistent AF group than those in paroxysmal AF group. Simple linear regression analyses showed that serum adropin in AF patients were negatively correlated with BMI, SBP, and LAD. Multiple stepwise regression analysis showed that LAD remained to be inversely associated with serum adropin (β = 0.2, P = 0.010).
Serum adropin concentrations are inversely correlated with the presence of AF and atrial remodeling.
内源性富含半胱氨酸的分泌蛋白（adropin）是一种新发现的由Enho基因编码的调节蛋白，可抑制肿瘤坏死因子α诱导的THP1单核细胞与人脐静脉内皮细胞的黏附。此外，炎症被证明参与心房颤动（房颤）的发病机制。心房重构与房颤的持续和进展相关。推测adropin与房颤及心房重构有关。本研究旨在确定血清adropin与房颤及重构之间的相关性。
本研究纳入344例房颤患者和210例健康对照者。房颤患者随后被分为阵发性房颤、持续性房颤和永久性房颤三个亚组。采用酶联免疫吸附测定法检测血清adropin浓度。测量左心房直径（LAD）以评估心房重构。
与健康对照者相比，房颤患者血清adropin浓度降低。Logistic回归分析证实，血清adropin与房颤的存在呈负相关（OR 0.218，95%CI 0.15 - 0.316；P < 0.001）。与持续性和阵发性房颤患者相比，永久性房颤患者血清adropin浓度显著降低。持续性房颤组血清adropin浓度低于阵发性房颤组。简单线性回归分析显示，房颤患者血清adropin与体重指数、收缩压和LAD呈负相关。多元逐步回归分析显示，LAD仍与血清adropin呈负相关（β = 0.2，P = 0.010）。
血清adropin浓度与房颤及心房重构呈负相关。
