Background and rationale {6a}
hepatitis B, non-alcoholic steatohepatitis, cirrhosis, Liver cirrhosis, NASH, hepatitis C, [Hepatic venous pressure gradient (HVPG)
HEPATITIS B, VIRUS, NON-ALCOHOLIC STEATOHEPATITIS, CIRRHOSIS, LIVER CIRRHOSIS, ALCOHOL-RELATED LIVER DISEASE, HEPATITIS C, PORTAL HYPERTENSION, CHRONIC LIVER DISEASE, ADVANCED CHRONIC LIVER DISEASE
Liver cirrhosis (i.e. advanced chronic liver disease [ACLD]) develops as a consequence of various chronic liver diseases, with alcohol-related liver disease, hepatitis B virus (HBV), hepatitis C virus (HCV) and non-alcoholic steatohepatitis (NASH) representing the most common causes [Hepatic venous pressure gradient (HVPG) is the current diagnostic gold standard for measuring portal pressure in ACLD [Therefore, the main therapeutic goal in patients with cACLD and CSPH is to prevent decompensation, which may be achieved by eliminating the primary aetiological factor of cirrhosis [In many countries, non-selective beta-blockers (NSBBs) and carvedilol are used off-label as medical treatments for portal hypertension; they act by reducing portal venous inflow via a reduction in cardiac output (βCurrently, there are no approved therapies that directly target or modulate the dynamic component of increased intrahepatic resistance (sinusoidal vasoconstriction), which is an early pathophysiological mechanism of portal hypertension and is largely due to an insufficient bioavailability of nitric oxide (NO) in the intrahepatic circulation [Soluble guanylyl cyclase (sGC) is activated by NO to catalyse the formation of cyclic guanosine monophosphate [