ArticleFrontiers in pediatrics2017
Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape.
Article in Frontiers in pediatrics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Long-term neurodevelopmental outcomes in children with hypoplastic left heart syndrome.Annals of medicine and surgery (2012) · 2025Review
- Effects of cardiac growth on electrical dyssynchrony in the single ventricle patient.Computer methods in biomechanics and biomedical engineering · 2024Article
- Hemodynamic Melody of Postnatal Cardiac and Pulmonary Development in Children with Congenital Heart Diseases.Biology · 2024Review
- The dependency of fetal left ventricular biomechanics function on myocardium helix angle configuration.Biomechanics and modeling in mechanobiology · 2023Article
- Ability of the Right Ventricle to Serve as a Systemic Ventricle in Response to the Volume Overload at the Neonatal Stage.Biology · 2022Article
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Evaluation of stimulus-effect relations in left ventricular growth using a simple multiscale model.Biomechanics and modeling in mechanobiology · 2020Article
- miR-486 is modulated by stretch and increases ventricular growth.JCI insight · 2019Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
introductionHypoplastic left heart syndrome (HLHS) is a congenital condition with an underdeveloped left ventricle (LV) that provides inadequate systemic blood flow postnatally. The development of HLHS is postulated to be due to altered biomechanical stimuli during gestation. Predicting LV size at birth using mid-gestation fetal echocardiography is a clinical challenge critical to prognostic counseling. HYPOTHESIS: We hypothesized that decreased ventricular filling
methodsWe developed a novel finite element model of the human fetal heart in which cardiac myocyte growth rates are a function of fiber and cross-fiber strains, which is affected by altered ventricular filling, to simulate alterations in LV growth and remodeling. Model results were tested with echocardiogram measurements from normal and HLHS fetal hearts.
resultsA strain-based fetal growth model with a normal 22-week ventricular filling (1.04 mL) was able to replicate published measurements of changes between mid-gestation to birth of mean LV end-diastolic volume (EDV) (1.1-8.3 mL) and dimensions (long-axis, 18-35 mm; short-axis, 9-18 mm) within 15% root mean squared deviation error. By decreasing volumetric load (-25%) at mid-gestation in the model, which emulates mitral stenosis
conclusionReduced ventricular filling and altered shape may lead to reduced LV growth and a hypoplastic phenotype by reducing myocardial strains that serve as a myocyte growth stimulus. The human fetal growth model presented here may lead to a clinical tool that can help predict LV size and shape at birth based on mid-gestation LV echocardiographic measurements.
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