BSPED2012 Oral Communications Oral Communications 1 (8 abstracts)
1University of Manchester, Manchester, UK; 2Kings College and Health Partners, London, UK.
Cardiovascular risk factors are more prevalent in south Asian (SA) adults compared to White Europeans (WE), although the reasons for this are not fully known. Vascular growth factors (VGFs) are increasingly recognised to have various roles in arterial development, function and remodelling. We hypothesised that ethnic differences in VGFs in early life contribute to the later differences in CV risk. We further hypothesised that arterial stiffness, as a measure of large artery structure and function, could correlate to VGF levels
Methods: Serum samples were obtained from children (WE 95, SA 45, and other 12) at various ages between 3 and 48 months, with repeated sampling in some children. Samples (n=80151) were assayed for platelet derived GF, osteoprotogerin, fibroblast GF, vascular endothelial GF, epidermal GF, hepatocyte GF, and placental GF. Aortic pulse wave velocity (aPWV) was measured in 63 children.
Results: Across ethnic groups, significant differences were seen in VEGF (KruskalWallis, P value=0.04), HGF (P=0.016), and PlGF (P=0.011). Even with these small numbers, SA samples showed significantly higher levels of EGF (median (range); SA 15.7 pg/ml (0.9119) vs WE 8.6 (1.650), P=0.036), HGF (0.79 ng/ml (0.12.8) vs 0.47 (0.013.1), P=0.039), and PIGF (58.5 pg/ml (7.8193) vs 30.8 (3.4160), P=0.014) compared to WE samples. Across all ethnic groups, only EGF was significantly correlated to aPWV (rs=+0.31, P=0.034). When this correlation was analyzed by ethnicity, the slope of the regression line for SA children was markedly steeper than that for WE children (SA: EGF=(7.2×PWV)−31 vs WE: EGF=(1.4×PWV)+4.4)), suggesting possible ethnic differences in the effect of EGF on aPWV.
Conclusions: VGF levels in early life differ between ethnic groups and EGF is related to aPWV, as a marker of arterial status. These relationships need to be reassessed through childhood and adolescence and may be relevant to the genesis of later life CV risk.