Does an imbalance in circulating vascular endothelial growth factors (VEGFs) cause atrial fibrillation in patients with valvular heart disease?

J Thorac Dis. 2019 Dec;11(12):5509-5516. doi: 10.21037/jtd.2019.11.32.

Abstract

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.

Keywords: Atrial fibrillation (AF); soluble vascular endothelial growth factor receptor-1 (sVEGFR-1); soluble vascular endothelial growth factor receptor-2 (sVEGFR-2); vascular endothelial growth factor-A (VEGF-A); vascular endothelial growth factor-C (VEGF-C).