Liver fibrosis emulation: Impact of the vascular fibrotic alterations on hemodynamics.

The liver circulatory system comprises two blood supply vascular trees (the hepatic artery and portal venous networks), microcirculation through the hepatic capillaries (the sinusoids), and a blood drainage vascular tree (the hepatic vein network). Vasculature changes due to fibrosis -located predominantly at the microcirculation level- lead to a marked increase in resistance to flow causing an increase in portal pressure (portal hypertension). Here, we present a liver fibrosis/cirrhosis model. We build on our 1D model of the healthy hepatic circulation, which considers the elasticity of the vessels walls and the pulsatile character of blood flow and pressure, and recreate the deteriorated liver vasculature due to fibrosis. We emulate altered sinusoids by fibrous tissue (stiffened, compressed and splitting) and propose boundary conditions to investigate the impact of fibrosis on hemodynamic variables within the organ. We obtain that the sinusoids stiffness leads to changes in the amplitude and shape of the blood flow and pressure waveforms but not in their mean value. For the compressed and splitting sinusoids, we observe significant increases in the mean value and amplitude of the pressure waveform in the altered sinusoids and in the portal venous network. In other words, we obtain the portal hypertension clinically observed in fibrotic/cirrhotic patients. We also study the extent of the spreading fibrosis by performing the structural fibrotic changes in an increasingly number of sinusoids. Finally, we calculate the portal pressure gradient (PPG) in the model and obtain values in agreement with those reported in the literature for fibrotic/cirrhotic patients.