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Development of portal hypertension is paramount in the natural history of cirrhosis. Longitudinal studies have firmly established that the risk of clinical decompensation (development of ascites, gastroesophageal varices, variceal bleeding, hepatic encephalopathy) and of hepatocellular carcinoma increases fivefold when the portal pressure gradient, evaluated by the hepatic venous pressure gradient (HVPG), increases above a threshold of 10 mm Hg.1 Oesophageal variceal bleeding requires the HVPG to increase to at least 12 mm Hg; going over 16 mm Hg or 20 mm Hg is associated with a shorter survival and to uncontrolled variceal bleeding, respectively. On the contrary, decreasing HVPG by ≥20% of baseline values or to values ≤12 mm Hg by means of medical therapy is associated with a dramatic decrease in the risk of bleeding or rebleeding, of ascites, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome and death.1 ,2 Therefore, it is intuitive that the more powerful an agent is decreasing the HVPG, the greater is its potential for effectively preventing the complications of portal hypertension.
The non-selective β-adrenergic blockers (NSBBs) propranolol and nadolol have been the mainstream in the pharmacological treatment of portal hypertension since its introduction, 30 years ago. Since then, many studies have demonstrated their efficacy in preventing first and recurrent variceal bleeding, and also, reducing the risk of bleeding from portal-hypertensive gastropathy and SBP.1 These beneficial effects are closely associated with the ability of these agents decreasing HVPG (which …
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