ArticlePLoS computational biology2025
Understanding the hemodynamic changes in fetuses with coarctation of the aorta using a lumped model of fetal circulation.
Article in PLoS computational biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- First- and Second-Trimester Cardiovascular Anomalies in Trisomy 21 Fetuses: Anatomy, Embryology, Genetics and Imaging.Journal of personalized medicine · 2026Review
- Predictive model integrating two-dimensional ultrasound indicators and hemodynamic features for fetal coarctation of the aorta.BMC pediatrics · 2026Article
- Hemodynamic and developmental biomarkers enhance prenatal coarctation prediction: a validated multiparametric ultrasound model.Archives of gynecology and obstetrics · 2025Article
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12 authors.
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Abstract
Coarctation of the aorta (CoA) is a common congenital heart defect characterized by aortic narrowing. Prenatally, it has mild hemodynamic effects as right ventricular disproportion and ductus arteriosus (DA) dilation occur as adaptive mechanisms, but their impact on CoA hemodynamics remains poorly understood. To investigate this, we built a closed 0D computational model of fetal circulation and simulated different CoA cardiovascular remodeling patterns, including aortic isthmus (AoI) narrowing, ventricular disproportion, and DA dilation. Our results showed mild AoI narrowing (80% of reference diameter) required up to 1.7 right/left ventricular end-diastolic volume ratio and 115% DA dilation to maintain physiological pressures, wall shear stresses, and organ perfusion. In contrast, severe narrowing (20% of reference AoI diameter) required up to 5 right/left ventricular end-diastolic volume ratio and 125% DA dilation, highlighting the necessity of co-occurrence of prenatal ventricular disproportion and DA dilation to compensate for AoI narrowing. These physiological regions were validated with ultrasonographic measurements from 7 controls and 9 CoA patients. We compared blood pressures, velocities, and volumetric flow rates across different fetoplacental anatomical sites. AoI velocity showed a delayed retrograde flow peak and increased antegrade diastolic velocity with greater AoI narrowing, which may aid in diagnosing CoA. Minimal differences were observed in other velocities and pressures. Volumetric flow rates across varying degrees of AoI narrowing decreased in the AoI and mitral and aortic valves, remained stable in the middle cerebral and umbilical arteries, and increased in the DA and tricuspid and pulmonary valves. Therefore, we corroborated that in fetal CoA a redistribution of blood flow occurs to ensure perfusion of the brain and placenta, without a significant alteration in fetal hemodynamics (blood pressure and velocities) except for increased diastolic velocities in the AoI.
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