Articles techniques et présentations

Hypoplastic left heart syndrome (HLHS) is a severe congenital heart defect characterized by underdevelopment of the left-sided cardiac structures, requiring staged palliation to sustain systemic circulation. The conventional Norwood procedure remains the standard first-stage treatment but is associated with significant surgical complexity, prolonged cardiopulmonary bypass, and considerable perioperative morbidity and mortality. As a less invasive alternative, the hybrid Stage I approach combines ductal stenting with surgical band-mediated pulmonary flow restriction to maintain balanced pulmonary-to-systemic circulation while avoiding cardiopulmonary bypass in the neonatal period, as illustrated in Figure 1a. However, this strategy requires open-chest surgery, and the surgical bands used in the procedure are difficult to adjust for optimal systemic and pulmonary flow balance and can lead to pulmonary artery (PA) distortion. Recently, a new fully endovascular technique has been proposed. This technique involves the replacement of the surgical bands with manually-fenestrated microvascular plug (MVPs) that reduce pulmonary flow, as illustrated in Figure 1b. Though promising, this procedure presents important challenges, including variability in the degree of flow restriction achieved and a limited ability to predict the resulting hemodynamic performance prior to implantation due to the ad hoc nature of the manual fenestration of the MVPs. Consequently, computational tools are needed to evaluate and optimize MVP performance.

This work presents a patient-specific computational fluid dynamics (CFD) framework developed in COMSOL Multiphysics® to investigate the hemodynamic performance of the fenestrated MVPs and establish a reproducible workflow for their evaluation and optimization. A three-dimensional pulmonary artery model, including the main pulmonary artery (MPA), right pulmonary artery (RPA), left pulmonary artery (LPA), and patent ductus arteriosus (PDA), was reconstructed from CT data using SimVascular and imported into COMSOL Multiphysics®, as shown in Figure 2a. A simplified model of the MVP was designed directly within COMSOL and incorporated into the reconstructed anatomy. Blood flow was simulated using the Laminar Flow interface of the CFD Module, assuming incompressible Newtonian flow with rigid vessel walls. A mesh independence study was performed to ensure solution accuracy, and the final computational mesh is shown in Figure 2b. Stready flow simulations were carried out using a prescribed inlet velocity and literature-based resistance outlet boundary conditions to reproduce physiologically relevant pulmonary flow. The developed workflow provides a foundation for future pulsatile flow simulations.

As illustrated in Figure 3, the computational framework successfully captures the hemodynamic effects of pulmonary flow restriction. Flow streamlines reveal flow acceleration through the pulmonary flow restriction devices and changes in flow patterns following intervention. Compared with the pre-intervention model, the post-intervention simulations demonstrate increased blood flow through the patent ductus arteriosus (PDA), redirecting flow toward the systemic circulation while reducing flow to both pulmonary arteries. These preliminary results demonstrate the capability of the proposed computational framework to quantify and visualize the hemodynamic effects of pulmonary flow restriction devices.

The proposed framework establishes a reproducible workflow for evaluating and optimizing pulmonary flow restriction devices for HLHS. More broadly, this study demonstrates how patient-specific CFD simulations in COMSOL Multiphysics® can support preclinical device assessment, treatment planning, and the design of next-generation cardiovascular devices for congenital heart disease.