Abstract

Liver cirrhosis remains a leading cause of death worldwide. Non-selective beta blockers (NSBB) have played a key role in the treatment of portal hypertension since Lebrec’s pioneering observations that propranolol significantly reduces portal pressure in patients with cirrhosis (1). At first, the reduction in portal pressure was ascribed to a reduced splanchnic blood flow as a consequence of a demonstrated lowered cardiac output. However, further studies demonstrated that the portal hypertensive state is maintained despite the formation of collaterals because of splanchnic vasodilatation and increased portal venous inflow, the so called hyperdynamic circulation (2). NSBB are known to be more effective in patients presenting with clinical significant portal hypertension (CSPH, i.e., an HVPG >10 mmHg) in which the hyperdynamic circulation is more pronounced (3).

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