Endothelial dysfunction increases preterm delivery risk

Preterm delivery complicates 12-13% of all births in the United States. It is a leading cause of neonatal morbidity and mortality; a positive history may also presage later maternal cardiovascular disease (CVD). We conducted a case (N=240) – control (N=450) study nested within a prospective cohort of low income and minority gravidae (Camden Study) to examine if soluble adhesion molecules which are biomarkers of endothelial dysfunction were associated with preterm delivery. These include soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1) and sE-selectin measured at entry (14.2±0.3 wk) and 3rd trimester (wk 28). After control for potential confounding variables (age, parity, ethnicity, BMI, smoking) we found that high levels (highest tertile) of sICAM-1 at entry (AOR=1.41, 95% CI 1.01-1.98) and 3rd trimester (AOR=1.80, 95% CI 1.25-2.61). sVCAM-1 at entry (AOR= 1.82, 95% CI 1.29-2.57) and 3rd trimester (AOR= 1.94, 95% CI 1.35-2.79) and 3rd trimester sE-selectin (AOR=1.44, 95% CI 1.01-2.15) all were associated with increased risk. When we examined preterm delivery without preeclampsia, risks associated with high sICAM-1 and sVCAM-1 persisted. High sE-selectin was specific to preterm delivery with preeclampsia (AOR= 1.94, 95% CI 1.04-3.64 at entry, AOR= 3.13, 95% CI 1.63-6.02 at 3rd trimester). A history of preeclampsia increases later maternal CVD risk. Consequently, increased endothelial dysfunction during the metabolic stress of pregnancy may well foreshadow later CVD for women whose pregnancies were complicated by preterm delivery.