Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis

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...

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Published in:Hepatology (Baltimore, Md.) Md.), 2003-04, Vol.37 (4), p.902-908
Main Authors: Abraldes, Juan G., Tarantino, Ilaria, Turnes, Juan, Garcia-Pagan, Juan Carlos, Rodés, Juan, Bosch, Jaime
Format: Article
Language:English
Subjects:
Antihypertensive Agents - therapeutic use
Ascites - etiology
Bacterial Infections - etiology
Biological and medical sciences
Cohort Studies
Drug Therapy, Combination
Female
Gastroenterology. Liver. Pancreas. Abdomen
Hemodynamics - drug effects
Hemorrhage - etiology
Hemorrhage - physiopathology
Hepatic Encephalopathy - etiology
Hepatorenal Syndrome - etiology
Humans
Hypertension, Portal - drug therapy
Hypertension, Portal - etiology
Hypertension, Portal - physiopathology
Isosorbide Dinitrate - analogs & derivatives
Isosorbide Dinitrate - therapeutic use
Liver Cirrhosis - complications
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Middle Aged
Other diseases. Semiology
Peritonitis - microbiology
Probability
Prognosis
Propranolol - therapeutic use
Recurrence
Risk Factors
Survival Analysis
Time Factors
Varicose Veins - complications
Vasodilator Agents - therapeutic use
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Summary: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. (H epatology 2003;37:902-908.)
ISSN:0270-9139
1527-3350
DOI:10.1053/jhep.2003.50133