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Updated: Jun 14, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Long-term microvascular and blood pressure dysregulation after Preeclampsia
Maya Jälmby1, Camilla Edvinsson1, Despoina Lykou1
1Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Abstract:
Preeclampsia (PE) is a pregnancy disorder characterized by systemic endothelial damage that leads to long-term cardiovascular complications. The endothelial glycocalyx (EG) covers the luminal surface of endothelium playing a critical role in vascular homeostasis. In this study we aimed to evaluate EG thickness and blood pressure (BP) trends in women with a history of PE vs. normotensive pregnancy. Fifty-five women participated in the study (18 controls, 34 with PE, and 3 with gestational hypertension). Six years postpartum, we evaluated the sublingual microcirculation by sidestream dark-field microscopy, and assessed BP in the sitting and orthostatic position. At follow-up, women with PE had reduced EG thickness in vessels ≥ 8 µm, expressed by an increased perfused boundary region (PBR), compared to healthy controls (median 3.14 vs. 2.88 µm, p = 0.002). A trend towards increased red blood cell velocity in vessels ≥ 10 µm was also observed in PE vs. controls. The systolic and diastolic BP, as well as within-visit BP variability, were significantly higher in PE vs. controls. Adverse neonatal outcomes, umbilical artery Doppler and BP during both the pregnancy and the follow-up visit, were associated with maternal PBR value in vessels ≥ 8 µm. This study contributes to the existing literature on PE and the increased risk of future cardiovascular disease, highlighting the critical role of EG and BP regulatory mechanisms. Our results showed that the severity of hemodynamic and neonatal impairments during pregnancy may irreversibly affect the EG and thereby be associated with long-term maternal vascular dysfunction.
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