OP001. A longitudinal study of maternal vascular reactivity, circulating endothelial progenitor cells and inflammatory response during the second half of pregnancy

Maternal endothelial dysfunction and inflammation are associated with hypertensive pregnancy disorders.

To investigate maternal endothelial function in normal pregnancy using two different methods and explore their association with markers of inflammatory response.

53 women with uncomplicated pregnancies were examined at four-weekly intervals during 22-40weeks gestation. Maternal endothelial function was assessed using flow-mediated vasodilatation (FMD) of brachial artery. FMD was defined as the increase of brachial artery diameter in percent during reactive hyperemia compared to the resting diameter. Circulating EPC were defined as CD45low/CD34+/VEGFR2+ and quantified by flow cytometry. Concentration of the two markers of inflammatory response, i.e. leptin (immunoassay) and highly sensitive CRP (mCRP) (immunoturbidimetric method) were measured in the plasma samples.

FMD decreased from 16.3% to 13.4% and concentration of EPC increased from 6.5 to 12.3 per million mononuclear cells during 22-40 weeks. Leptin increased from 18 to 22ng/L and mCRP did not change significantly (p=0.61). Significant associations were observed between FMD and mCRP (p=0.0016), and between FMD and leptin (p=0.0029). There was no significant association between EPC and FMD or between EPC and mCRP.

FMD decreases, whereas the concentration of circulating EPC increases with advancing gestation during the second half of pregnancy. However, FMD was associated with biomarkers of inflammation but not with EPC. This suggests that the reduced NO-dependent vasodilatation observed in the third trimester of normal pregnancy is related to maternal inflammatory response. Mechanisms other than effective mobilization of EPC to repair endothelial damage are likely to be responsible for gestational age-associated increase in circulating EPC during pregnancy.