Cirrhosis is the terminal stage of various chronic liver diseases [1,2]. Patients with compensated cirrhosis are usually asymptomatic, while those in the decompensated stage have clinical manifestations of portal hypertension (PHT) and severe impairment of liver function [2,3]. PHT mainly results from increased resistance to portal outflow, which is accompanied by a rise in splanchnic vascular volume and velocity [3,4]. The pathophysiology of PHT involves local alterations in vascular reactivity (vasodilation and vasoconstriction), angiogenesis, and venous thrombosis [3,4].
