Author:
Martin Anna,Goeser Tobias,Kasper Philipp
Abstract
AbstractIn western industrialized nations, liver cirrhosis is the most common cause of portal hypertension. Portal hypertension is defined by a persistent increase in portal pressure >7mmHg. An HVPG >10mmHg defines the presence of clinically significant portal hypertension. The presence of clinically significant portal hypertension (CSPH) in patients with liver cirrhosis is a key risk factor for the transition from a compensated to a decompensated stage of the disease. CPSH can be determined invasively by measuring HPVG or noninvasively by measuring liver stiffness, platelet count and spleen stiffness. If acute decompensation manifests itself (e.g. ascites, esophageal variceal bleeding), this is associated with a significant increase in patient morbidity and mortality. Non-selective beta blockers (NSBB) are the standard medical therapy for portal hypertension in the presence of CSPH. Due to the additional α1-antiadrenergic effects, carvedilol leads to a greater reduction in portal pressure compared to traditional NSBB (e.g. Propanolol). In patients with compensated liver cirrhosis, carvedilol is better than traditional NSBB at reducing the risk of variceal bleeding and the occurrence of hepatic decompensation. The early identification of CSPH and evaluation of drug therapy to reduce portal hypertension is therefore crucial to improve the prognosis of patients.