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Carvedilol Achieves Higher Hemodynamic Response and Lower Rebleeding Rates Than Propranolol in Secondary Prophylaxis
Mathias Jachs1, Lukas Hartl1, Benedikt Simbrunner2
1Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Insights
Carvedilol significantly reduces hepatic venous pressure gradient (HVPG) more than propranolol for variceal bleeding prophylaxis. This leads to lower rebleeding, liver death, and decompensation rates in patients with cirrhosis.
Area of Science:
- Hepatology
- Gastroenterology
- Clinical Pharmacology
Background:
- Nonselective beta-blockers are standard for variceal bleeding prophylaxis.
- Carvedilol demonstrates superior hepatic venous pressure gradient (HVPG) reduction compared to propranolol.
- Limited data exist on carvedilol's efficacy in secondary variceal bleeding prophylaxis.
Purpose of the Study:
- To compare the efficacy of carvedilol versus propranolol in secondary prophylaxis of variceal bleeding.
- To evaluate the impact of carvedilol and propranolol on HVPG and systemic hemodynamics.
- To assess long-term outcomes including rebleeding, decompensation, and mortality.
Main Methods:
- Retrospective analysis of patients undergoing paired HVPG measurements for prophylaxis.
- Inclusion of patients treated with either carvedilol or propranolol, alongside band ligation.
- Comparison of HVPG changes, hemodynamic parameters, and competing risk regression for long-term outcomes.
Main Results:
- Carvedilol users showed a greater HVPG decrease (20% vs. 11%) and higher chronic HVPG response rates (53.3% vs. 28.6%).
- Carvedilol was associated with significantly lower cumulative incidences of rebleeding (P=.027) and liver-related death (P=.036).
- Ascites development/worsening was less common with carvedilol (P=.012), while acute kidney injury rates did not differ.
Conclusions:
- Carvedilol achieves more significant HVPG reduction than propranolol in secondary variceal bleeding prophylaxis.
- Carvedilol use is linked to reduced rates of rebleeding, liver-related death, and nonbleeding decompensation.
- These findings support carvedilol as a potentially superior option for managing portal hypertension.
Background & Aims:
Carvedilol induces stronger decreases in hepatic venous pressure gradient (HVPG) than conventional nonselective β-blockers (ie, propranolol). Limited data exist on the efficacy of carvedilol in secondary prophylaxis of variceal bleeding.
Methods:
Patients undergoing paired HVPG measurements for guiding secondary prophylaxis with either carvedilol or propranolol were included in this retrospective analysis. All patients also underwent band ligation. Changes in HVPG and systemic hemodynamics were compared between the 2 groups. Long-term follow-up data on rebleeding, acute kidney injury, nonbleeding decompensation, and liver-related death were analyzed applying competing risk regression.
Results:
Eighty-seven patients (carvedilol/propranolol, n = 45/42) were included in our study. The median baseline HVPG was 21 mm Hg (interquartile range, 18-24 mm Hg), and 39.1%/48.3%/12.6% had Child-Turcotte-Pugh A/B/C cirrhosis, respectively. Upon nonselective β-blocker initiation, HVPG decreased more strongly in carvedilol users (median relative decrease, -20% [interquartile range: -29% to -10%] vs -11% [-22% to -5%] for propranolol; P = .027), who also achieved chronic HVPG response more often (53.3% vs 28.6%; P = .034). Cumulative incidences for rebleeding (Gray test, P = .027) and liver-related death (P = .036) were significantly lower in patients taking carvedilol compared with propranolol. Notably, ascites development/worsening also was observed less commonly in carvedilol patients (P = .012). Meanwhile, acute kidney injury rates did not differ between the 2 groups (P = .255). Stratifying patients by HVPG response status yielded similar results. The prognostic value of carvedilol intake was confirmed in competing risk regression models.
Conclusions:
Carvedilol induces more marked reductions in HVPG than propranolol in secondary prophylaxis of variceal bleeding, and thus is associated with lower rates of rebleeding, liver-related death, and further nonbleeding decompensation.
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