# Modelling maternal cardiovascular adaptation to pregnancy: a scoping review

**Authors:** Kathryn Hunt, Ioannis Polydoros, Raoul van Loon, Rosemary C. Townsend, Rebecca M. Reynolds

PMC · DOI: 10.1186/s12884-025-08270-z · BMC Pregnancy and Childbirth · 2025-11-24

## TL;DR

This review explores how computational models can help understand and manage cardiovascular changes during pregnancy and related complications.

## Contribution

The study identifies research gaps and barriers in applying computational models to maternal cardiovascular adaptation in pregnancy.

## Key findings

- 37 studies were identified, including models of maternal circulation and pregnancy-related conditions.
- Nine studies used data from pregnant participants or clinical specimens, with small sample sizes.
- Models covered maternal cardiac remodelling, renal autoregulation, and placental blood flow.

## Abstract

The maternal cardiovascular system undergoes a profound transformation during pregnancy. Disordered cardiovascular adaptation is associated with pre-eclampsia and fetal growth restriction; however, these complications remain challenging to predict and manage. Computational modelling presents an opportunity to study the maternal circulation with unprecedented flexibility.

We conducted a scoping review to assess the potential utility of computational models for studying maternal cardiovascular adaptation to pregnancy and providing insights into disease. We aimed to identify research gaps and barriers to translating this emerging field into clinical practice.

Medline, Embase, and Web of Science Core Collection were searched from 01/01/2013 to 01/09/2025, for articles related to computational haemodynamic models of pregnancy. English-language studies describing models of the maternal circulation in human pregnancy were identified. Information on system modelled, study design, participant or clinical specimen details, and key findings were extracted from original research studies and presented in a narrative synthesis.

Of 662 citations, 37 met inclusion criteria, comprising 28 original research studies, two conference abstracts, and seven reviews. Amongst the original research studies, 27 were basic experimental papers and one was a retrospective cohort study. Nine experimental articles incorporated data from pregnant participants or clinical specimens into personalised models, with sample sizes between one and 21. Four of these included participants or specimens affected by hypertensive disorders of pregnancy or fetal growth restriction. The retrospective cohort study employed haemodynamic modelling to investigate blood loss in 480 patients with abnormally invasive placentas.

Modelling approaches described included those simulating the entire maternal circulation, maternal cardiac remodelling, maternal renal autoregulation, the maternal pelvic circulation in isolation, uterine vascular adaptation, spiral artery remodelling, and blood flows within the placental intervillous space.

Computational modelling could represent a powerful tool to advance understanding of maternal cardiovascular adaptation to pregnancy and guide future approaches to risk stratification, diagnosis, and management of pregnancy complications. Realising this promise will require cardiovascular models to be parameterised with scalable metrics, validated in large pregnancy cohorts, developed alongside robust computational processing pipelines, and integrated into existing clinical workflows.

The review protocol was registered prospectively with the Open Science Framework (osf.io/v3968).

The online version contains supplementary material available at 10.1186/s12884-025-08270-z.

## Linked entities

- **Diseases:** pre-eclampsia (MONDO:0005081), fetal growth restriction (MONDO:0005030)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** FLT1 (fms related receptor tyrosine kinase 1) [NCBI Gene 2321] {aka FLT, FLT-1, VEGFR-1, VEGFR1}
- **Diseases:** diastolic dysfunction (MESH:D018487), complications (MESH:D008107), spiral artery remodelling (MESH:D066253), cardiovascular maladaptation (MESH:D002318), preterm birth (MESH:D047928), ischaemic heart disease (MESH:D006331), endothelial (MESH:D005642), endothelial dysfunction (MESH:D014652), pregnancy (MESH:D011254), prematurity (MESH:C536271), hypertension (MESH:D006973), blood loss (MESH:D016063), Pre-eclampsia (MESH:D011225), cardiac remodelling (MESH:D020257), stillbirth (MESH:D050497), maternal death (MESH:D063130), pernicious placenta praevia (MESH:D010923), pregnancy complications (MESH:D011248), placental disease (MESH:D010922), fetal growth restriction (MESH:D005317), obstetric haemorrhage (MESH:D006470), restriction (MESH:D002313), hypoxic (MESH:D002534)
- **Chemicals:** oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12838005/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC12838005/full.md

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Source: https://tomesphere.com/paper/PMC12838005