Role of ASpirin in Placental and Maternal Endothelial Cell Regulation IN Pre-eclampsia
Status:
Recruiting
Trial end date:
2023-12-01
Target enrollment:
Participant gender:
Summary
Endothelial dysfunction and defective placental vascularization are hypothesized to be
significant causes of preeclampsia. In preeclampsia, due to vascular endothelial dysfunction,
vasoconstriction and platelet activation can result in severe features which alter pregnancy
outcomes. However, studies have shown that acetylsalicylic acid (Aspirin) can decrease
endothelial dysfunction leading to decreased platelet aggregation which reduces adverse
outcomes. The objective of our study is to determine if Aspirin has a dose-dependent response
for modifying biomarkers reflective of maternal endothelial dysfunction when indicated for
preeclampsia prevention in a cohort of women identified at risk for developing preeclampsia.
Pregnant women who are at risk for preeclampsia will be randomized to receive either 81mg
Aspirin or 162mg Aspirin daily starting from 11-16 weeks of gestation until 36 weeks of
gestation. A third, control group of women at low risk for preeclampsia will not receive
aspirin. All women will be assessed with uterine artery Doppler studies and mean arterial
blood pressures at three time points during pregnancy. Blood, urine, and cord blood samples
will also be collected.