Association of maternal endothelial dysfunction with preeclampsia

Context Preeclampsia is believed to result from release of placental factor s that damage maternal vascular endothelium. However, because most studies have been conducted during pregnancy, it has not been possible to separate maternal from placental mechanisms underlying endothelial dysfunction in pr eeclampsia. Objective To determine whether endothelial function is impaired in nonpregn ant women with previous preeclampsia and whether endothelial dysfunction is mediated by oxidative stress. Design and Setting Case-control study conducted at 3 hospital maternity uni ts in London, England, between July 1997 and June 2000. Participants A total of 113 women with previous preeclampsia (n=35 with rec urrent episodes; n=78 with a single episode) and 48 women with previous unc omplicated pregnancies, all of whom were at least 3 months (median, 3 years ) postpartum. Main Outcome Measures Brachial artery flow-mediated (endothelium-dependent) and glyceryl trinitrate-induced (endothelium-independent) dilatation were compared between previously preeclamptic women and controls. To investigate oxidative stress, these measurements were repeated after administration of ascorbic acid, 1 g intravenously, in 15 cases and 15 controls. Results Mean (SD) flow-mediated dilatation was lower in women with previous preeclampsia compared with controls (recurrent group, 0.9% [4.1 %]; single -episode group, 2.7% [3.5%]; and control group, 4.7% [4.3 % ]; P<.001). In contrast, glyceryl trinitrate-induced dilatation was similar in the 3 group s (recurrent, 19.5% [5.9%]; single-episode, 21.0% [8.0%]; and control, 21.0 % [8.3%]; P=.65). Impaired flow-mediated dilatation in previously preeclamp tic women was not accounted for by recognized vascular risk factors. Ascorb ic acid administration increased flow-mediated dilatation in previously pre eclamptic women (baseline, 2.6% [3.3%]; after administration, 5.6% [3.0%]; P=.001) but not in controls (baseline, 6.2% [3.3%]; after administration, 6 .7% [5.0%]; P=.72). Conclusions Our results indicate that endothelial function is impaired in w omen with previous preeclampsia and is not explained by established materna l risk factors but is reversed by antioxidant ascorbic acid administration.