Abstrakt
Background, Aims: As liver disease progresses, scarring results in worsening hemodynamics ultimately culminate in portal hypertension. This process has classically been quantified via the Hepatic Venous Pressure Gradient (HVPG), however HVPG alone does not predict a given patient's clinical presentation with regards to Baveno stage of cirrhosis.
In this study we propose that a patient's 'HVPG-sensitivity' to venous remodelingcould explain disparate disease trajectories. Methods: We created a computational model of liver disease informed by actual physiologic measurements from the field of portal hypertension over the last four decades.
We simulated progression of liver disease, clinical complications, and HVPG in the context of varying 'HVPG-sensitivity' to portal venous remodeling. Results: Our results unify hemodynamics, venous remodeling, and the progression of liver disease.
We demonstrate that in modifying the 'HVPG-sensitivity' to venous remodelingwe can explain multiple trajectories of liver disease. Conclusion: This paper provides a basis for a future, whole-body computational model of decompensated liver disease and highlights the importance of venous remodeling in explaining patients' clinically presentation.