Vascular Adaptations in Pregnancy and Related Complications

Pregnancy induces profound vascular adaptations to meet the growing metabolic demands of the mother and fetus. Central to this process is the remodelling of uteroplacental spiral arteries, whereby specialised extravillous trophoblasts invade and replace the arterial smooth muscle, converting narrow, high-resistance vessels into low-resistance conduits. This transformation increases uterine blood flow five- to tenfold and supports placental perfusion throughout gestation. Systemic changes include expansion of plasma volume, reduced systemic vascular resistance and enhanced cardiac output. In healthy pregnancy these adaptations proceed seamlessly, but in disorders such as preeclampsia and fetal growth restriction, failure of physiological remodelling leads to placental ischaemia, endothelial dysfunction and an anti-angiogenic milieu. Lesions known as acute atherosis—characterised by foam cell accumulation and fibrinoid necrosis in spiral arteries—are frequently observed in such complications and may herald long-term maternal cardiovascular risk. Insights into lipid mediators, inflammatory pathways and advanced imaging have expanded our understanding of the mechanisms linking aberrant placentation to adverse outcomes, offering new avenues for early detection and intervention.

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Vascular Adaptations in Pregnancy and Related Complications publication trend

The graph below shows the total number of articles in vascular adaptations in pregnancy and related complications across all publications each year (not limited to Nature Index journals).

Technical terms

Spiral artery remodelling: The replacement of arterial smooth muscle and elastic lamina by invading trophoblasts and fibrinoid to widen uteroplacental vessels.

Extravillous trophoblast: Fetal-derived cells that invade maternal decidua and spiral arteries to establish low-resistance placental perfusion.

Acute atherosis: A lesion of uteroplacental spiral arteries characterised by foam cells, fibrinoid necrosis and perivascular inflammation, resembling early atherosclerosis.

Angiogenic imbalance: Dysregulation between pro-angiogenic factors (such as placental growth factor) and anti-angiogenic factors (such as soluble fms-like tyrosine kinase-1), leading to endothelial dysfunction.

Lipokine: A bioactive lipid mediator, such as 12,13-diHOME, that influences vascular tone and inflammatory responses in pregnancy.

References

1. Elevated 12,13-diHOME level in maternal and umbilical cord blood complicated with preeclampsia. Frontiers in Endocrinology (2024).
2. Acute Atherosis Lesions at the Fetal-Maternal Border: Current Knowledge and Implications for Maternal Cardiovascular Health. Frontiers in Immunology (2021).
3. Failure of physiological transformation and spiral artery atherosis: their roles in preeclampsia. American Journal of Obstetrics and Gynecology (2020).
4. Quantifying Molecular Changes in the Preeclamptic Rat Placenta with Targeted Contrast-Enhanced Ultrasound Imaging. Molecular Imaging and Biology (2025).
5. Prevalence of placental bed spiral artery pathology in preeclampsia and fetal growth restriction: A prospective cohort study. Placenta (2024).