Prenatal aspirin use is associated with preserved vascular endothelial function measured after pregnancy in women with a history of preeclampsia.

Vascular endothelial dysfunction is a pathophysiological feature of preeclampsia that persists after pregnancy and likely contributes to increased cardiovascular disease (CVD) risk later in life among women with a history of preeclampsia (hxPE). Low-dose aspirin (LDA; 75-150 mg/day) is recommended for pregnant women at high risk of preeclampsia and may help stabilize endothelial function. We hypothesized that endothelial function would be preserved in women with hxPE who used LDA during pregnancy. Three groups were studied: women with a history of uncomplicated pregnancy (hxHC; n = 10; 35 ± 6 years), women with hxPE who used prenatal LDA (hxPE+LDA; n = 10, 34 ± 6 years), and women with hxPE who did not use prenatal LDA (hxPE-LDA; n = 10; 34 ± 5 years). Macrovascular endothelial function was evaluated using brachial artery flow-mediated dilation (FMD). Cutaneous vascular conductance (CVC) responses to acetylcholine alone or with nitric oxide (NO) synthase inhibition were measured to assess microvascular endothelium-dependent and NO-dependent vasodilation. CVC responses to endothelin-1 (ET-1) were used to assess microvascular vasoconstriction. hxPE+LDA did not differ from hxHC across any macrovascular and microvascular function measures (all P > 0.09). In contrast, hxPE-LDA exhibited lower absolute FMD and peak shear rate-normalized FMD compared with hxHC (all P < 0.04). Reduced microvascular endothelium-dependent dilation and increased ET-1-mediated vasoconstriction were observed in hxPE-LDA compared with hxHC (all P ≤ 0.031). These data suggest that prenatal LDA use is associated with preserved endothelial function and normalized ET-1-mediated vasoconstriction after pregnancy in women with hxPE, representing an early opportunity to mitigate progression toward CVD in these high-risk women.