Does an imbalance in circulating vascular endothelial growth factors (VEGFs) cause atrial fibrillation in patients with valvular heart disease?
Does an imbalance in circulating vascular endothelial growth factors (VEGFs) cause atrial fibrillation in patients with valvular heart disease?
复制标题
循环血管内皮生长因子 (VEGF) 失衡是否会导致瓣膜性心脏病患者发生心房颤动？
DOI：
10.21037/jtd.2019.11.32
复制
发表时间：
2019
影响因子：
2.5
通讯作者：
Zhongkai Wu
中科院分区：
文献类型：
--
作者：
Keke Wang;Yanyan Liu;Suiqing Huang;Huayang Li;Jian Hou;Jiaxing Huang;Jiantao Chen;Kangni Feng;M. Liang;Guang;Zhongkai Wu
背景
心房颤动（AF）的发病机制尚不清楚。血管内皮生长因子（VEGF）可刺激心房和心室内的纤维化。我们假设，在瓣膜性心脏病（VHD）患者中，血清VEGF/可溶性血管内皮生长因子受体（sVEGFRs）水平与AF之间存在相关性。这为AF的研究提供了一个新的范式。
方法
采用酶联免疫吸附试验（ELISA）检测血浆VEGF-A、VEGF-C、sVEGFR-1、sVEGFR-2水平。本研究共纳入100人，包括AF患者（长期持续性AF; n=49）、窦性心律（SR）患者（n=31）和健康对照组（n=20）。
结果
房颤患者血浆VEGF-A水平显著高于健康对照组（P<0.05）。AF患者血浆sVEGFR-1水平显著高于SR患者（P<0.05）。房颤患者血浆sVEGFR-2水平显著低于SR患者和健康对照组（均P<0.05）。各组sVEGFR-2水平与AF呈显著负相关（r=-0.432，P =0.000）。
结论
VEGF和sVEGF受体的失衡可能通过打破血管生成和淋巴管生成的平衡而导致AF。此外，sVEGFR-2可能是AF的重要生物标志物。
Background
The pathogenesis of atrial fibrillation (AF) remains unclear. Vascular endothelial growth factors (VEGFs) can stimulate fibrosis within the atrium and ventricle. We hypothesized that there is a relationship between the serum VEGFs/soluble vascular endothelial growth factor receptor (sVEGFRs) levels and AF in patients with valvular heart disease (VHD). This provides a new paradigm for studying AF.
Methods
The plasma levels of VEGF-A, VEGF-C, sVEGFR-1 and sVEGFR-2 were detected by enzyme-linked immunosorbent assay (ELISA). A total of 100 people, consisting of AF patients (long-standing, persistent AF; n=49), sinus rhythm (SR) patients (n=31) and healthy controls (n=20), were included in this study.
Results
The plasma levels of VEGF-A were significantly higher in AF patients compared to healthy control (P<0.05). The plasma levels of sVEGFR-1 were significantly higher in AF compared to SR (P<0.05). The plasma levels of sVEGFR-2 were significantly lower in AF patients compared to SR patients and healthy controls (both P<0.05). There was a significant and negative correlation between AF and the sVEGFR-2 levels in the groups (r=-0.432, P=0.000).
Conclusions
An imbalance in VEGFs and sVEGFRs may contribute to AF by breaking the balance of angiogenesis and lymphangiogenesis. Additionally, sVEGFR-2 may be an important biomarker of AF.