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