Abstract 20924: Liver Fibrosis Increases Inferior Vena Caval Flow and Power Output of the Heart in Single Ventricle Patients After Fontan
Introduction: The staged Fontan procedure has shown promising short term outcomes in single ventricle patients. However, Fontan-associated liver disease is a marked problem seen in this population as patients age. In this study, we investigate the relationship between hemodynamics and liver fibrosis in Fontan patients.
Hypothesis: The extent of liver fibrosis in Fontan patients is associated with poor total cavopulmonary connection hemodynamics.
Methods: Thirty-three Fontan patients with liver fibrosis were included in this study. Cardiac magnetic resonance (CMR) and phase-contrast CMR data, as well as catheterization measurements and liver biopsies were obtained for each patient. Computational fluid dynamic simulations were performed to quantify TCPC hemodynamics using patient specific anatomies and blood flow waveforms reconstructed from CMR data. Collagen deposition (as a measure of liver fibrosis) was quantified by digital image analysis of Sirius Red stained slides. Statistical analyses were performed to investigate potential relationships between liver fibrosis and Fontan hemodynamics.
Results: Patient clinical data is shown in Figure 1A. Indexed IVC flow showed a significant, positive correlation with liver fibrosis (r=0.563, p=0.001, Figure 1B). Upper and lower Sirius Red tertile comparisons showed a significant difference in indexed IVC flow (p=0.006, Figure 1D). Liver fibrosis was found to be more related to global metrics (IVC flow, ventricle power output) than local TCPC hemodynamics (Figure 1C).
Conclusions: Significant increases in IVC flow consistent with fibrosis induced arterialization and ventricular power output suggests a burden being placed on the single ventricle from liver fibrosis. Local TCPC flow dynamics do not seem to influence the degree of fibrosis. Favorable TCPC hemodynamics may not be enough to overcome the power shortage and elevated venous pressures inherent to a Fontan patient.
Author Disclosures: P.M. Trusty: None. Z. Wei: None. P.A. Russo: None. L.F. Surrey: None. D. Goldberg: None. J. Rychik: None. M.A. Fogel: None. A.P. Yoganathan: None.
- © 2016 by American Heart Association, Inc.