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A Tense Race: Correlation of Liver Stiffness with Ultrasound Elastography and Hemodynamics in Fontan Patients
1 Congenital Heart Center, Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA
2 College of Medicine, University of Florida, Gainesville, FL 32610, USA
3 Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL 32610, USA
4 Department of Radiology, Division of Pediatric Radiology and Nuclear Medicine, College of Medicine, University of Florida, Gainesville, FL 32610, USA
* Corresponding Author: Himesh Vyas. Email:
(This article belongs to the Special Issue: Novel Insights into Congenital Heart Disease: Pathophysiology, Biomarkers, and Future Directions)
Congenital Heart Disease 2025, 20(2), 265-272. https://doi.org/10.32604/chd.2025.065661
Received 19 March 2025; Accepted 23 April 2025; Issue published 30 April 2025
Abstract
Background: Patients with Fontan physiology are predisposed to congestive hepatopathy, progressive liver fibrosis, and end-stage liver disease. Ultrasound-based shear wave elastography (SWE) is a non-invasive tool to diagnose and monitor liver fibrosis. We sought to determine whether the degree of hemodynamic derangement prior to and after the Fontan operation is associated with increased liver stiffness measured by SWE. Methods: A single-center retrospective study of patients with Fontan circulation who underwent ultrasound elastography between 2008 and 2024 was conducted. Liver stiffness was measured by SWE and reported as velocity in m/s. Hemodynamic assessment with cardiac catheterization and echocardiograms were collected before and after the Fontan operation. Data was analyzed as a continuous (linear regression model) and a dichotomous variable (t-test). Results: 78 post-Fontan ultrasound elastography studies performed in 56 patients were analyzed. Pre-Fontan hemodynamics included median effective pulmonary flow of 2.45 L/min/m2 [2.21, 3.16] (p = 0.46), ventricular end-diastolic pressure of 10 mmHg [8, 10.5] (p = 0.77), and median Glenn pressure of 12 mmHg [13, 15] (p = 0.83). Post-Fontan median systemic cardiac index was 2.80 L/min/m2 [2.4, 3.34] (p = 0.93), median ventricular end-diastolic pressure of 12 mmHg [13.5, 14] (p = 0.99), median systemic saturation of 93% [87, 96] (p = 0.77), median indexed pulmonary vascular resistance of 1.80 WU·m2 [1.49, 2.37] (p = 0.93), and median Fontan pressure of 18 mmHg [16, 21] (p = 0.86). No correlation was found between SWE and hemodynamics. On echocardiography, no correlation was found between SWE and systemic ventricular systolic function (p = 0.35) or degree of systemic atrioventricular valve regurgitation (p = 0.35). Conclusions: The degree of liver stiffness by SWE in this cohort did not correlate with pre- and post-Fontan hemodynamics on cardiac catheterization, degree of ventricular dysfunction, or severity of atrioventricular valve regurgitation by echocardiography.Keywords
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