Fluid-Structure Interaction Simulations for Fontan Hemodynamics

Overview

Congenital heart disease (CHD) affects approximately 1% of all childbirths in the United States, making it the most common type of birth defect. Within this demographic, a critical subset of infants is born with single-ventricle anomalies—a condition where the heart develops with only one functional pumping chamber. To ensure survival, these patients must undergo a complex, three-stage series of palliative surgeries that culminate in the Fontan procedure. The Fontan operation surgically reroutes the cardiovascular system by connecting the superior and inferior vena cavae directly to the pulmonary arteries. This creates a total cavopulmonary connection (TCPC) that entirely bypasses the right side of the heart, leaving the single ventricle to pump oxygenated blood to the body while relying entirely on passive venous pressure to drive deoxygenated blood through the lungs.

While life-saving, the Fontan circulation is highly non-physiologic and inherently creates chronic hemodynamic inefficiencies. The absence of a sub-pulmonary ventricular pump forces the venous system to operate at chronically elevated pressures just to maintain pulmonary perfusion, simultaneously resulting in diminished overall cardiac output. Over decades, this persistent venous hypertension and flow stagnation cascade into severe end-organ complications. The most prominent and life-threatening of these is Fontan-associated liver disease (FALD). FALD encompasses a progressive spectrum of hepatic pathologies—from severe venous congestion to fibrosis, cirrhosis, and eventually liver failure or hepatocellular carcinoma—which significantly impacts the long-term survival and quality of life for aging Fontan patients.

Predicting and mitigating these adverse hemodynamic outcomes requires a granular understanding of patient-specific biomechanics. This project utilizes advanced computational modeling—specifically FSI simulations—to analyze the complex hemodynamics of the Fontan pathway. While traditional rigid-wall CFD provides valuable baseline metrics, FSI uniquely enables the coupled simulation of blood flow and vessel wall deformation. By integrating continuum mechanics stress potentials and evaluating resistance-based RCR Windkessel boundary conditions, these models can accurately capture wave propagation, wall compliance, and energy dissipation across the TCPC. Quantifying these exact pressure landscapes and biomechanical loads is essential for understanding the mechanobiological triggers of hepatic congestion. Ultimately, these high-fidelity FSI models aim to evaluate surgical graft geometries, optimize patient-specific operative planning, and minimize the hemodynamic bottlenecks that drive the progression of FALD.

(Note: Results for this ongoing investigation will be updated as the computational data is finalized and published.)