irrhosis is a serious complication of liver disease and is commonly caused by viral hepatitis and alcohol consumption. 1,2 Cirrhosis causes abnormal cellular alterations, which increase vascular resistance through the liver. Cirrhosis also comes with cellular damage, tissue fibrosis, liver hardening, nodule formation, and sinusoidal remodeling. Damage to the hepatocytes also results in a disruption of the normal equilibrium between vasodilators and vasoconstrictors and increases total blood flow into the portal system. Endogenous vasodilators such as nitric oxide increase the amount of blood flowing into the portal system by inducing splanchnic arteriolar vasodilation. Following the Ohm law, an increase in vascular resistance along with an increase in portal inflow results in an increase in portal pressure. Subsequently, cirrhosis results in clinical manifestations of portal hypertension.Owing to the variability in severity and progression, cirrhosis is commonly classified into 2 stages: compensated and decompensated. Decompensated cirrhosis is more severe and results in major complications such as ascites, jaundice, encephalopathy and variceal hemorrhage. 1,2 Thus, it is imperative to monitor the progression of compensated cirrhosis and pay close attention to predictive markers of worsening portal hypertension, such as the hepatic venous pressure gradient (HVPG). An HVPG of 10 mm Hg or more is highly