Acute Hemodynamic Response to β-Blockers and Prediction of Long-term Outcome in Primary Prophylaxis of Variceal Bleeding

Villanueva, Càndid; Aracil, Carles; Colomo, Alan; Hernández‐Gea, Virginia; López-Balaguer, J.M.; Álvarez–Urturi, Cristina; Torras, Xavier; Balanzó, Joaquím; Guarner, Carlos

doi:10.1053/j.gastro.2009.03.048

Cited by 192 publications

(204 citation statements)

References 30 publications

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“…However, the role of carvedilol in primary prophylaxis warrants further confirmation. On the other hand, Villaneuva et al 32 demonstrated that the acute hemodynamic response to beta blockers can be used to predict the long-term risk of first bleeding. Our study did not measure portal pressure.…”

Section: Discussionmentioning

confidence: 99%

Controlled trial of ligation plus nadolol versus nadolol alone for the prevention of first variceal bleeding

Chen

Wang

et al. 2010

Hepatology

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Section: Discussionmentioning

confidence: 99%

Controlled trial of ligation plus nadolol versus nadolol alone for the prevention of first variceal bleeding

Chen

Wang

et al. 2010

Hepatology

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“…The benefit of reduction of HVPG has actually been proven for patients exhibiting a ''good hemodynamic response'' to nonselective beta-adrenergic blockers; i.e., those who exhibit a decrease in HVPG > 20% of baseline or to values below 12 mm Hg during continued therapy, 6,7 or who show a decrease in HVPG >10% of baseline 20 minutes after an intravenous infusion of propranolol. 8,9 Besides the increased intravascular pressure, the risk of bleeding from varices is further influenced by other factors, such as the diameter of the varices and the thickness of the variceal wall. 10 These factors are interrelated by Laplace's law in the concept of wall tension (t), according to which: t ¼ variceal transmural pressure Â variceal radius=wall thickness Abbreviations: EVL, endoscopic variceal ligation; HVPG, hepatic venous pressure gradient; RCT, randomized controlled trial; TIPS, transjugular intrahepatic portosystemic shunt.…”

Section: The Problemmentioning

confidence: 99%

Carvedilol for portal hypertension in patients with cirrhosis

Bosch

2010

Hepatology

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A 48-year-old male with hepatitis C-related cirrhosis is found on endoscopy to have large esophageal varices with red signs. He has never previously had variceal bleeding, and there is no evidence of hepatic encephalopathy. He does have mild ascites. Comorbidity includes diabetes which has been present for many years and is well-controlled on a stable dose of insulin. He has no cardiopulmonary disease. The hemoglobin is 12.4 g/dL, white blood cell count is 6800/mm 3 , and platelets are 112 Â 10 9 /L. Serum bilirubin is 1.8 mg/ dL, creatinine is 1.2 mg/dL, international normalized ratio is 1.3, and the serum albumin is 3.5 g/dL. The electrocardiogram and chest x-ray are normal. The ultrasound examination does not show portal vein thrombosis or hepatocellular carcinoma.What is the role of carvedilol in the prevention of variceal bleeding in this patient? How will the dose of carvedilol be adjusted and how is the patient to be monitored for adverse drug events? When would carvedilol be preferred over nadolol or propranolol? Would the approach be different if the patient was of Child-Pugh class C cirrhosis? The ProblemPortal hypertension is an almost unavoidable complication of cirrhosis, and provides the driving force for most of its complications, such as esophageal and gastric varices, variceal bleeding, portal hypertensive gastropathy, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, thrombopenia, leukopenia and anemia, and portal-systemic encephalopathy.1 Recent studies have shown that for these complications to develop, the portacaval pressure gradient-evaluated clinically by the hepatic venous pressure gradient (HVPG)-should increase above 10 mm Hg and should be above 12 mm Hg for variceal bleeding. 2,3The prevalence of varices is about 40% in asymptomatic compensated patients.2 Development of varices follows an incidence of approximately 6% per year. The incidence is nearly double in patients with a baseline HVPG >10 mm Hg, who therefore represent a high-risk group.2 These patients are also at higher risk of developing decompensation (ascites, bleeding, jaundice, encephalopathy) and hepatocellular carcinoma. 4,5 Because of this, there is a great interest in strategies to revert portal hypertension, since these would prevent portal hypertension-related complications, clinical decompensation, and death. The benefit of reduction of HVPG has actually been proven for patients exhibiting a ''good hemodynamic response'' to nonselective beta-adrenergic blockers; i.e., those who exhibit a decrease in HVPG > 20% of baseline or to values below 12 mm Hg during continued therapy, 6,7 or who show a decrease in HVPG >10% of baseline 20 minutes after an intravenous infusion of propranolol. 8,9 Besides the increased intravascular pressure, the risk of bleeding from varices is further influenced by other factors, such as the diameter of the varices and the thickness of the variceal wall.10 These factors are interrelated by Laplace's law in the concept of wall tension (t), according to which: t ¼ variceal tran...

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“…The hemodynamic response to treatment with b-blockers is considered appropriate when HVPG is decreased below 12 mmHg or by ≥ 20% of baseline values, 1-3 mo after initiation of treatment. The acute hemodynamic response to b-blockers (20 min after administration of propranolol) was shown useful to predict the long-term risk of first bleeding by reducing HVPG ≥ 10% from baseline values [25,26] . In a recent study [27] , patients with esophageal varices with HVPG measurement before and during propranolol treatment were included.…”

Section: Nsbbs Vs No Interventionmentioning

confidence: 99%

Primary prevention of bleeding from esophageal varices in patients with liver cirrhosis

Triantos

Kalafateli

2014

WJH

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Variceal bleeding is a life threatening situation with mortality rates of at least 20%. Prophylactic treatment with non-selective beta blockers (NSBBs) is recommended for patients with small varices that have not bled but with increased risk for bleeding. The recommended treatment strategies on primary prevention of variceal bleeding in patients with medium and largesized varices are NSBBs or endoscopic band ligation. Nitrates, shunt surgery and sclerotherapy are not recommended in this setting. In this review, the most recent data on prevention of esophageal variceal bleeding are presented. Available data derived from randomized-controlled trials suggest both treatment strategies, and according to Baveno V consensus in portal hypertension "the choice of treatment should be based on local resources and expertise, patient preference and characteristics, side-effects and contra-indications". Core tip: The significance of primary prevention of bleeding from esophageal varices in patients with liver cirrhosis is major, considering the high mortality rates that accompany the acute bleeding episode. Current management guidelines suggest the use of either nonselective beta-blockers or endoscopic band ligation with same efficacy between them. In this review, we summarize data from randomized clinical trials or prospective studies together with meta-analytical data, when applicable, to present the most updated recommendations on primary prevention of esophageal variceal bleeding.Triantos C, Kalafateli M. Primary prevention of bleeding from esophageal varices in patients with liver cirrhosis.

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Acute Hemodynamic Response to β-Blockers and Prediction of Long-term Outcome in Primary Prophylaxis of Variceal Bleeding

Cited by 192 publications

References 30 publications

Controlled trial of ligation plus nadolol versus nadolol alone for the prevention of first variceal bleeding

Controlled trial of ligation plus nadolol versus nadolol alone for the prevention of first variceal bleeding

Carvedilol for portal hypertension in patients with cirrhosis

Primary prevention of bleeding from esophageal varices in patients with liver cirrhosis

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