Evidence map›Paper›PMID 41617779›Full record

ArticlePediatric research2026

The hemodynamic impact of congenital heart diseases during fetal-to-neonatal transition: an in-silico investigation.

Bettine G van Willigen, Babette C Krabben, M Beatrijs van der Hout-van der Jagt, Wouter Huberts, Frans N van de Vosse

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Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Bettine G van WilligenCardiovascular Biomechanics, Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands. b.g.v.willigen@tue.nl.
Babette C KrabbenCardiovascular Biomechanics, Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.
M Beatrijs van der Hout-van der JagtCardiovascular Biomechanics, Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.
Wouter HubertsCardiovascular Biomechanics, Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.
Frans N van de VosseCardiovascular Biomechanics, Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCongenital heart disease (CHD) is a significant congenital anomaly, with ventricular septal defect (VSD) and transposition of the great arteries (TGA) being commonly encountered. Despite advancements in prenatal diagnosis and postnatal care, predicting neonatal outcomes remains difficult due to fetal compensatory mechanisms. This study utilizes and adapts existing mathematical models, without patient-specific parameters, to simulate the hemodynamic effects of VSD and TGA during the fetal-to-neonatal transition, validated against literature data.

methodThe model uses a closed-loop 0D-1D cardiovascular system and an oxygen-carbon dioxide exchange model to retrieve clinically relevant information.

resultsResults show realistic replication of flow, pressure profiles, oxygen saturation, and carbon dioxide levels for both normal and CHD-compromised fetuses.

conclusionThe mathematical model offers valuable insights into hemodynamic alterations during the fetal-to-neonatal transition, also under two pathophysiological conditions. It provides a non-invasive means of predicting clinically relevant parameters, which is essential for postnatal treatment planning in the prenatal period, especially given the potential need for immediate postnatal hemodynamic management. Overall, this model presents a promising tool for predicting the impact of CHD postnatally based on prenatal information and for guiding timely and effective treatment strategies. As such, the model may be considered as a potential basis for other applications in perinatal hemodynamics including fetal-to-neonatal transition. IMPACT: This study introduces a mathematical model that simulates the hemodynamic impact of congenital heart disease (CHD) during the fetal-to-neonatal transition, focusing on ventricular septal defect (VSD) and transposition of the great arteries (TGA). By integrating a one-fiber heart model and oxygen and carbon dioxide dynamics, the model gives a prediction of critical clinical parameters like flow, pressure, and oxygen saturation. This mathematical model has a potential to serve as non-invasive tool, providing valuable insights for prenatal planning and postnatal management, helping guide timely interventions for newborns affected by CHD.

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.