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Register a new userInfluence of portal vein occlusion on portal flow and liver elasticity in an animal model
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Hepatic fibrosis causes an increase in liver stiffness, a parameter measured by elastography and widely used as a diagnosis method. The concomitant presence of portal vein thrombosis (PVT) implies a change in hepatic portal inflow that could also affect liver elasticity. The main objective of this study is to determine the extent to which the presence of portal occlusion can affect the mechanical properties of the liver and potentially lead to misdiagnosis of fibrosis and hepatic cirrhosis by elastography. Portal vein occlusion was generated by insertion and inflation of a balloon catheter in the portal vein of four swines. The portal flow parameters peak flow (PF) and peak velocity magnitude (PVM) and liver mechanical properties (shear modulus) were then investigated using 4D-flow MRI and MR elastography, respectively, for progressive obstructions of the portal vein. Experimental results indicate that the reduction of the intrahepatic venous blood flow (PF/PVM decreases of 29.3%/8.5%, 51.0%/32.3% and 83.3%/53.6%, respectively) measured with 50%, 80% and 100% obstruction of the portal vein section results in a decrease of liver stiffness by $0.8%pm0.1%$, $7.7%pm0.4%$ and $12.3%pm0.9%$, respectively. While this vascular mechanism does not have sufficient influence on the elasticity of the liver to modify the diagnosis of severe fibrosis or cirrhosis (F4 METAVIR grade), it may be sufficient to attenuate the increase in stiffness due to moderate fibrosis (F2-F3 METAVIR grades) and consequently lead to false-negative diagnoses with elastography in the presence of PVT.
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The invasive measurement of the hepatic venous pressure gradient is still considered as the reference method to assess the severity of portal hypertension. Even though previous studies have shown that the liver stiffness measured by elastography could predict portal hypertension in patients with chronic liver disease, the mechanisms behind remain today poorly understood. The main reason is that the liver stiffness is not specific to portal hypertension and is also influenced by concomitant pathologies, such as cirrhosis. Portal hypertension is also source of a vascular incidence, with a substantial diversion of portal venous blood to the systemic circulation, bypassing the liver. This study focuses on this vascular effect of portal hypertension. We propose to generate and control the portal venous flow (to isolate the modifications in the portal venous flow as single effect of portal hypertension) in an anesthetized pig and then to quantify its implications on liver stiffness by an original combination of MRE and 4D-Flow Magnetic Resonance Imaging (MRI). A catheter balloon is progressively inflated in the portal vein and the peak flow, peak velocity magnitude and liver stiffness are quantified in a 1.5T MRI scanner (AREA, Siemens Healthcare, Erlangen, Germany). A strong correlation is observed between the portal peak velocity magnitude, the portal peak flow or the liver stiffness and the portal vein intraluminal obstruction. Moreover, the comparison of mechanical and flow parameters highlights a correlation with the possibility of identifying linear relationships. These results give preliminary indications about how liver stiffness can be affected by portal venous flow and, by extension, by hypertension.
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