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In cirrhotic patients under pharmacologic treatment for portal hypertension, a reduction in hepatic venous pressure gradient (HVPG) of >20% of baseline or to <12 mm Hg markedly reduces the risk of variceal rebleeding. This study was aimed at evaluating whether these hemodynamic targets also prevent other complications of portal hypertension and improve long-term survival. One hundred five cirrhotic patients included in prospective trials for the prevention of variceal rebleeding were studied. Seventy-three of the patients had 2 separate HVPG measurements, at baseline and under pharmacologic therapy with propranolol ؎ isosorbide mononitrate. Patients were followed for up to 8 years. Survival and risk of developing portal hypertension-related complications were compared between responders and nonresponders. Twenty-eight patients showed a reduction of HVPG >20% of baseline or to <12 mm Hg (responders), and 45 patients were nonresponders. Nonresponders had a significantly greater risk of developing variceal rebleeding (P ‫؍‬ .013), ascites (P ‫؍‬ .025), spontaneous bacterial peritonitis (P ‫؍‬ .003), hepatorenal syndrome (P ‫؍‬ .026), and hepatic encephalopathy (P ‫؍‬ .024) than responders. Eight-year cumulative probability of survival was significantly lower in nonresponders than in responders (52% vs. 95%, respectively, P ‫؍‬ .003). At multivariate analysis, being a nonresponder was independently associated with the risk of developing rebleeding, ascites, spontaneous bacterial peritonitis, and lower survival. In conclusion, in cirrhotic patients receiving pharmacologic treatment for prevention of variceal rebleeding, a decrease in HVPG >20% or to <12 mm Hg is associated with a marked reduction in the long-term risk of developing complications of portal hypertension and with improved survival. (HEPATOLOGY 2003;37:902-908.) P ortal hypertension is responsible for the more frequent and severe complications of cirrhosis: gastrointestinal bleeding from gastroesophageal varices, ascites, renal dysfunction, and hepatic encephalopathy. Because of the combined impact of these complications, portal hypertension represents the main cause of death and liver transplantation in patients with cirrhosis. 1 Previous cross-sectional studies have shown that a portal pressure gradient (determined as the hepatic venous pressure gradient; HVPG) above 12 mm Hg is required for variceal bleeding to develop. 2,3 Indeed, longitudinal studies demonstrated that, when HVPG decreases below this threshold, there is total protection from the risk of bleeding. [4][5][6] Subsequent studies showed that, even without reaching this target, a reduction of HVPG of at least 20% from baseline values is associated with a very low residual risk of rebleeding on follow-up. 7-10 However, no study so far has examined whether the hemodynamic response to drug therapy correlates also with the risk of developing other complications of portal hypertension and survival over a long-term follow-up.The present study was aimed at addressing these issues. For that purpos...

In a randomized controlled trial, addition of simvastatin to standard therapy did not reduce rebleeding, but was associated with a survival benefit for patients with Child-Pugh class A or B cirrhosis. Survival was not the primary end point of the study, so these results require validation. The incidence of rhabdomyolysis in patients receiving 40 mg/d simvastatin was higher than expected. European Clinical Trial Database ID: EUDRACT 2009-016500-24; ClinicalTrials.gov ID: NCT01095185.

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The hemodynamic response in cirrhotic patients is associated with a sustained reduction in the risk of first variceal bleeding over a long-term follow-up. Reduction of HVPG also correlate with a reduced risk of SBP or bacteremia.

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