Why the study?
Women with adverse pregnancy outcomes have an increased risk of future ASCVD, yet the mechanistic pathways are not well-defined. Potential vascular and inflammatory factors contributing to ASCVD were unknown in women with a history of preeclampsia or spontaneous preterm delivery.
Does a history of preeclampsia or spontaneous preterm delivery increase vascular dysfunction and inflammatory biomarkers at 2–3 years postpartum compared with uncomplicated term delivery?
Cohort (n=51)
Does a history of preeclampsia or spontaneous preterm delivery increase vascular dysfunction and inflammatory biomarkers at 2–3 years postpartum compared with uncomplicated term delivery?
Women with prior preeclampsia exhibit elevated central and brachial blood pressures and central pulse pressure, whereas women with prior spontaneous preterm delivery exhibit elevated interleukin-8 levels at 2–3 years postpartum, suggesting distinct vascular and inflammatory pathways toward future ASCVD risk.
Associations may reflect persistent vascular-inflammatory changes after adverse pregnancy outcomes; leaves open their utility for ASCVD risk stratification.
Background: Women with adverse pregnancy outcomes (APOs) have a 2- to 8-fold increased risk of future atherosclerotic cardiovascular disease (ASCVD), yet the mechanistic pathways are not well-defined. Potential vascular and inflammatory factors contributing to ASCVD are not known in women with a history of preeclampsia (PE) or spontaneous preterm delivery (sPTD). Objective: Describe the vascular and inflammatory factors of women with PE or sPTD and compare differences that may contribute to ASCVD risk. Methods: Women 18 years or older, 2–3 years postpartum, with a history of PE ( N = 19) or sPTD ( N = 13), and reference controls ( N = 19; delivery ≥ 37 weeks’ gestation without APO) were enrolled. All cohorts underwent phlebotomy to measure inflammatory biomarkers and SphygmoCor testing for vascular function, including augmentation index (AIx75), central pulse pressure (CPP), and pulse wave velocity (PWV). Results: Participants with sPTD had higher interleukin-8 concentrations of 6.6 pg/mL (interquartile range [IQR] 5.7, 8.7), compared with 4.7 pg/mL (IQR 2.2, 6.3) in controls ( p = 0.0279). Brachial systolic pressure was higher in PE (120 [standard deviation or SD 12.01]) than in sPTD (110.9 [SD 13.8]) or controls (108.6 [SD 9.22], [ p = 0.0071]). Central systolic pressure was higher in PE (109.8 [SD 11.4]) than in sPTD (99.3 [SD 13.88]) or controls (98.4 [SD 8.94], [ p = 0.0069]). CPP was higher in PE (34.2, SD 3.62) than in sPTD (30.8, SD 3.34) and controls (30.3, SD 3.67 [ p = 0.0027]). Conclusions: Vascular and inflammatory markers in PE or sPTD 2–3 years postpartum are higher compared with reference controls. Future studies should investigate vascular and inflammatory function in larger cohorts and prospectively evaluate contribution to CVD risk.
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Spiro et al. (2026) conducted a cohort in Adverse pregnancy outcomes (preeclampsia or spontaneous preterm delivery) (n=51). History of preeclampsia (PE) or spontaneous preterm delivery (sPTD) vs. Reference controls (delivery ≥37 weeks' gestation without adverse pregnancy outcomes) was evaluated on Vascular function (augmentation index [AIx75], central pulse pressure [CPP], pulse wave velocity [PWV], brachial and central systolic pressure) and inflammatory biomarkers (including interleukin-8) (p=0.0027).
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