Programa del congreso

1. Introduction

Hypoplastic left heart syndrome (HLHS) is a cyanotic congenital heart disease characterized by the underdevelopment of the left ventricle, aorta, and aortic arch [1]. This structural deficiency results in obstruction to blood flow from the left ventricular outflow tract, altering oxygen delivery throughout the fetal body and potentially impairing organ maturation. We studied this pathology using a computational model of fetal circulation.

2. Materials and Methods

We used our previously published 0D computational model of the fetal cardiovascular system [2], which described the vasculature using Windkessel components, and the ventricles and atria with a single-fiber model [3], with all parameters scaled to represent a 36-week fetus [4].

From its simulated mean blood flows, we estimated oxygen content assuming perfect mixing of blood, computing saturation and partial pressure using Hill’s equation [5]. To simulate placental diffusion, we used Erlich et al.’s [6] model, which estimates oxygen flux through a single villus using geometric features extracted from 3D imaging of the fetoplacental vasculature, assuming 3.5·10⁵ villi in the placenta [7]. Oxygen consumption in fetal organs was derived from the literature, with 57% assigned to the brain [8] and the rest distributed by organ volume [9].

To simulate HLHS, we minimized the left ventricle and mitral and aortic valve dimensions to near-zero, halved the aortic arch diameter, doubled the right ventricle size, enlarged the ductus arteriosus and the main pulmonary artery to 140% of their healthy diameters, and reduced the combined cardiac output to 90% of the healthy value [10]. Additionally, the number of villi was halved since the placenta in HLHS is usually inefficient [11], and organ consumption was reduced proportionally to the cardiac output variation. We compared our blood flows and oxygen saturations with literature MRI data [10].

3. Results

Our simulated blood flows and oxygen saturations are reported in Table 1. In healthy cases, part of the oxygen-rich blood from the left heart perfuses the brain, while the rest mixes with the lower-oxygen blood from the right heart in the descending aorta to supply the lower body. In HLHS, in contrast, the right ventricle supplies the entire body. The combination of complete blood mixing in the right heart and the reduced placental efficiency leads to globally lower oxygen saturation, especially in the brain.

Table 1. Blood flow and oxygen saturation in healthy and HLHS cases simulated (bold, left) compared to [10] (right). CO: cardiac output. PA: pulmonary artery. AA: ascending aorta. DA: descending aorta. UV: umbilical vein. SVC: superior vena cava.

4. Conclusions

Our fetal circulation model simulated blood flow and oxygen distribution in both healthy and HLHS fetuses. It could be used for studying other cyanotic congenital heart defects and birth transition, and as a basis for creating a growth model.

References

[1] J. A. Connor et al., Orphanet J Rare Di., 2:23, 2007

[2] I. Villanueva-Baxarias et al., PLoS Comput Biol, 21:5, 2025

[3] T. Arts et al., Am J Physiol Heart Circ Physiol, 288:4, 2005

[4] G. Pennati et al., Ann Biomed Eng, 28, 2000

[5] E. P. Hill et al., Am J Physiol, 222:3, 1972

[6] A. Erlich et al., Sci Adv, 5:4, 2019

[7] A. R. Clark et al., Interface Focus, 5:2, 2015

[8] L. Sun et al., Circulation, 131:15, 2015

[9] R. H. Luecke et al., Int J Bio-Med Comput, 27:2, 1995

[10] L. Sun et al., Ultrasound Obstet Gynecol, 5:4, 2021

[11] H. N. Jones et al., Placenta, 36:10, 2015