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Carvedilol for reducing portal pressure in primary prophylaxis of variceal bleeding: a dose-response study
R Schwarzer1,2, D Kivaranovic3, R Paternostro1,2
1Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Insights
Higher doses of carvedilol effectively reduced hepatic venous pressure gradient (HVPG) in patients with portal hypertension. While 12.5 mg/d carvedilol improved HVPG response, careful monitoring for hypotension is advised, particularly in patients with ascites.
Area of Science:
- Hepatology
- Cardiology
- Pharmacology
Background:
- Hepatic venous pressure gradient (HVPG) monitoring assesses hemodynamic response to nonselective betablockers (NSBBs) in portal hypertension.
- HVPG-guided therapy is crucial for managing patients with liver conditions.
Purpose of the Study:
- To evaluate the efficacy of different carvedilol dosages in achieving HVPG response.
- To determine optimal carvedilol dosing for primary prophylaxis of variceal bleeding.
Main Methods:
- Retrospective analysis of 72 cirrhosis patients receiving HVPG-guided carvedilol therapy.
- Carvedilol doses escalated from 6.25 mg/d to 12.5 mg/d based on HVPG response.
- HVPG response defined as ≥20% decrease or ≤12 mm Hg, and Baveno VI criteria (≥10% decrease or ≤12 mm Hg).
Main Results:
- 53% of patients achieved ≥20% HVPG decrease with carvedilol.
- 76% of patients achieved ≥10% HVPG decrease (Baveno VI criteria) with 12.5 mg/d carvedilol.
- Hypotension/bradycardia occurred in 6 patients (4 with ascites) at 12.5 mg/d; no other patients had systolic arterial pressure <90 mm Hg.
Conclusions:
- Carvedilol 12.5 mg/d is more effective than 6.25 mg/d for decreasing HVPG in primary prophylaxis.
- A significant proportion of patients achieve therapeutic HVPG levels with higher carvedilol doses.
- Arterial hypotension is a potential adverse effect, especially in patients with ascites, necessitating vigilant monitoring.
Background:
Sequential measurements of hepatic venous pressure gradient (HVPG) are used to assess the haemodynamic response to nonselective betablockers (NSBBs) in patients with portal hypertension.
Aims:
To assess the rates of HVPG response to different doses of carvedilol.
Methods:
Consecutive patients with cirrhosis undergoing HVPG-guided carvedilol therapy for primary prophylaxis of variceal bleeding between 08/2010 and 05/2015 were retrospectively included. After baseline HVPG measurement, carvedilol 6.25 mg/d was administered and HVPG response (HVPG-decrease ≥20% or to ≤12 mm Hg) was assessed after 3-4 weeks. In case of nonresponse, carvedilol dose was increased to 12.5 mg/d and a third HVPG-measurement was performed after 3-4 weeks. We also assessed HVPG-response rates according to the Baveno VI consensus (HVPG decrease ≥10% or to ≤12 mm Hg) and changes in systolic arterial pressure (SAP).
Results:
Seventy-two patients (Child A, 37%; B, 35%; C, 28%) were included. 28 (39%) patients achieved a HVPG-decrease ≥ 20% with carvedilol 6.25 mg/d and another 10 (14%) with carvedilol 12.5 mg/d. Forty (56%) patients had a HVPG decrease ≥10% with carvedilol 6.25 mg/d and 24 (33%) with carvedilol 12.5 mg/d. Thus, in total, a HVPG-response of ≥20% and ≥10% and was achieved in 38 (53%) and 55 (76%) and of patients respectively. Notably, 6 patients (n = 4 with ascites) did not tolerate an increase to 12.5 mg/d due to hypotension/bradycardia. However, none of the other patients had a SAP < 90 mm Hg at the final HVPG measurement.
Conclusion:
Carvedilol 12.5 mg/d was more effective than 6.25 mg/d in decreasing HVPG in primary prophylaxis. A total of 76% of patients achieved a HVPG-response of ≥ 10% to carvedilol 12.5 mg/d, however, arterial hypotension might occur, especially in patients with ascites.
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