Modulation of Liver Stiffness by Arterial and Portal Pressure

Abstract

Liver stiffness (LS) can be significantly modulated by inflow pressure through the portal vein and the hepatic artery. The liver perfusion differs from most other organs as it is supplied to a lesser extent of 20% arterially by the hepatic artery but to 80% by the low-pressure portal vein. These two systems merge within the hepatic sinusoids and are further interdependently connected via the hepatic arterial buffer response (HABR). Significant elevation of LS to 8 kPa in non-fibrotic livers almost solely due to arterial pressure changes has been observed under exposure to catecholamines or during physical exercise. An immediate increase of LS by portal pressure has been demonstrated during endoscopic band ligation of esophageal varices while LS decreases after insertion of a transjugular intrahepatic portosystemic shunt (TIPS). Initiation of non-selective betablockers (NSBB) also decrease LS, however, a more complex change of hemodynamic parameters is observed involving both arterial and portal pressures. Notably, the natural onset of esophageal varices can temporarily lower LS values due to lowered portal pressure and falsely suggest an improvement of liver fibrosis. The exact interplay between arterial pressure and LS has not been completely understood in patients with arterial hypertension. In patients with more advanced liver disease, the impact of both arterial and portal pressure seems to be enhanced. Both pressures also seem to contribute to LS elevation during food intake and alcohol consumption, although detailed studies are missing. In summary, both arterial and portal pressure can significantly modulate LS in a complex manner.