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. 2025 May 19;40(6):1409–1418. doi: 10.1111/jgh.16999

Comparison of Carvedilol to Propranolol in Reduction of Hepatic Venous Pressure Gradient in Liver Cirrhosis: A Meta‐Analysis

Amey Joshi 1,✉, Hafsa Arshad Azam Raja 2, Poulami Roy 3, Fakhar Latif 4, Rahul George Reji 5, Novonil Deb 3, Ryan K Mui 6, Ahmed Shady 6
PMCID: PMC12136807  PMID: 40387434

ABSTRACT

Background

Nonselective beta‐blockers, such as propranolol and carvedilol, are used to prevent first decompensation in patients with clinically significant portal hypertension.

Methods

We performed a systematic literature search of English language articles from inception in PubMed, Medline, and Cochrane databases to compare the effect of carvedilol and propranolol on systemic and splanchnic hemodynamics. Mean differences were pooled using a random‐effect model, and a p‐value of < 0.05 was considered statistically significant.

Results

Seven RCTs with a total of 351 patients were involved in the final analysis. Reduction in hepatic venous pressure gradient was significantly greater in the carvedilol group (MD = −0.76, 95% CI = −1.45 to −0.08; p = 0.03). Decrease in systemic vascular resistance and mean arterial pressure was significantly greater in the carvedilol group ([MD = −190.55, 95% CI = −307.5 to −73.58; p = 0.001] and [MD = −3.65, 95% CI = −5.94 to −1.36; p = 0.002], respectively). Decrease in cardiac output was greater in the propranolol group (MD = 0.92, 95% CI = 0.45–1.38; p = 0.004). Decrease in hepatic blood flow and right atrial pressure appeared to be greater in the propranolol group; however, this did not reach statistical significance ([MD = 0.13, 95% CI = −0.06 to 0.32; p = 0.17] and [MD = 0.28, 95% CI = −0.27 to 0.83; p = 0.32], respectively). Decrease in mean pulmonary arterial pressure appeared to be greater in the carvedilol group; however, this was not statistically significant (MD = −0.75, 95% CI = −1.60 to 0.10; p = 0.08). There was no difference in incidence of rebleeding, shortness of breath, hepatic encephalopathy, and hypotension between the two groups.

Conclusion

Carvedilol demonstrated a significantly greater reduction in HVPG, SVR, and MAP compared to propranolol, with no significant difference in adverse effects.

Keywords: beta blockers, cirrhosis, hemodynamic, hepatic venous pressure gradient, meta‐analysis, portal hypertension

1. Introduction

Portal hypertension (PH) is the most common complication of cirrhosis [1]. The development of clinically significant portal hypertension (CSPH) often precedes decompensation events in patients with advanced chronic liver disease (ACLD) [2]. The hepatic venous pressure gradient (HVPG) is an indirect measure of portal pressure and is considered the gold standard for diagnosing PH in patients with cirrhosis [3]. Patients with ACLD may have varying degrees of PH and CSPH with HVPG ≥ 12 mmHg, which can be associated with ascites, variceal bleeding, hepatorenal syndrome, hepatic encephalopathy, and increased mortality [2, 4].

Nonselective beta‐blockers (NSBBs) reduce portal pressures and have been used to reduce first decompensation and secondary prophylaxis for variceal bleeding. These drugs reduce portal pressures by two main mechanisms: (1) reducing cardiac output by β1 adrenergic receptor blockade and (2) promoting splanchnic vasodilation by β2 receptor blockade [5, 6]. Propranolol was one of the first NSBBs utilized to manage portal hypertension in cirrhotic patients [7]. Carvedilol, another NSBB with additional alpha‐1 adrenergic blocking (vasodilator) property, was found to decrease intrahepatic resistance, offering some benefit in lowering portal pressures over other NSBBs [1]. Recent studies comparing the efficacy of carvedilol over propranolol in lowering HVPG in patients with compensated cirrhosis have been mixed [8, 9, 10, 11, 12, 13, 14]; the precise effects of either medication on splanchnic and systemic hemodynamic parameters are not entirely understood. This systematic review and meta‐analysis aimed to compare the effect of carvedilol and propranolol on various systemic and splanchnic hemodynamic parameters.

2. Methods

This meta‐analysis followed the methods outlined in the Cochrane Handbook for Systematic Reviews of Interventions and adhered to the reporting standards set by the Preferred Reporting Items for Systematic Reviews and Meta‐Analysis (PRISMA). The study was registered with PROSPERO.

2.1. Literature Search and Strategy

Scientific databases of Publisher Medline, Excerpta Medica Database, Web of Science (WoS), and Cochrane Central Registry were searched from inception to June 2024 for studies comparing carvedilol and propranolol in the reduction of hepatic venous pressure in cirrhosis using the comprehensive search strategy. The following terms (“carvedilol”) AND (“liver cirrhosis”) were combined as either keywords or Medical Subject Headings (MeSH). Furthermore, we systematically examined the reference lists of included studies and similar systematic reviews to locate additional pertinent studies.

2.2. Selection Criteria

2.2.1. Inclusion Criteria

Studies with the following characteristics were included in the analysis: (1) double‐armed randomized controlled trials, (2) adults > 18 years of age, and (3) intervention involving carvedilol and propranolol administration in separate arms of the study.

2.2.2. Exclusion Criteria

The following study designs were excluded: (1) study designs other than randomized controlled trials, including non‐randomized clinical trials, cohort studies, and observational studies, (2) animal models, (3) trials with single intervention groups, (4) studies not involving patients with liver cirrhosis, and (5) studies published in languages other than English.

2.3. Study Screening and Data Extraction

The studies obtained via our search strategy were imported on EndNote 20. The duplicates were removed first, and individual studies were searched subsequently. Two authors (N.D. and H.A.A.R.) screened the selected studies that satisfied the inclusion criteria using a Microsoft Excel sheet (Microsoft Corp, Redmond, Washington) to extract the data for characteristics and outcomes. Dichotomous outcomes were reported as events and totals, whereas continuous outcomes were measured with standard deviation and the total number of patients extracted. A third author (R.G.R.) reviewed the extracted data for any discrepancies. The extracted data included Study ID, country, sample size, mean dose, mean age in years, previous history of hypertension, Child–Pugh score, change in hepatic venous pressure gradient in mm Hg (∆HVPG), change in hepatic blood flow in liters per minute (∆HBF), change in mean arterial pressure in mmHg (∆MAP), and adverse events like orthostatic hypotension, encephalopathy, shortness of breath, and worsening of ascites.

2.4. Outcomes Reported

Data were pooled for the primary and secondary outcomes in this meta‐analysis.

2.4.1. Primary Outcome

The primary outcome was a change in HVPG before and after treatment with the beta blocker.

2.4.2. Secondary Outcomes

The secondary outcomes were HBF, mean pulmonary artery pressure (MPAP), MAP (mean arterial pressure), systemic vascular resistance (SVR), and right atrial pressure (RAP).

2.5. Bias Evaluation and Assessment

Version 2 of the Cochrane risk‐of‐bias tool for randomized trials (RoB 2) was used to evaluate the risk of bias assessment. Two authors (R.G.R. and N.D.) independently evaluated the bias in the study assessment. This tool assessed bias under the following five domains: (1) bias stemming from randomization, (2) bias due to deviation from the intended intervention, (3) bias originating from missing outcome data, (4) bias caused by outcome measurement, and (5) selection bias. These were applied to all the studies included, and their bias was rated as high, low, and indistinct, which classified the bias as high, low, and some concerns. Differences in the evaluation were resolved via consultation with a senior author (A.J.).

2.6. Statistical Analysis

Statistical Analysis was conducted using Review Manager (RevMan) version 5.4.1 (The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen, Denmark). The inverse variance analysis method was utilized for the continuous variables, and mean ± SD was reported along with 95% confidence interval (CI). Studies reporting median and interquartile ranges were converted to mean ± SD using a converter. On the other hand, the dichotomous outcomes were analyzed using the Mantel–Haenszel method and reported in the form of extracted mean difference (MD) with 95% CI. The random effect model was employed for pooled studies. The random effect model was utilized for pooled studies. The study's pooled estimate was represented as a forest plot [15]. The chi‐square test and I‐square statistics were implemented to gauge the heterogeneity of the studies. I‐square values are interpreted in the Cochrane Handbook for Systematic Reviews and Meta‐Analyses Section 10.10.1.

3. Results

The preliminary database search using the pre‐specified keywords yielded 790 articles, of which 156 studies were excluded after removing duplicates. Six hundred ten studies were further excluded from the initial post‐title and abstract screening based on the inclusion and exclusion criteria and comparison arm. The full‐text review was conducted for the remaining 24 articles identified during the search. Twenty‐four full‐text articles were retrieved for screening, and 17 studies were excluded: unmatching target populations, not primary research articles, or lacking a comparison arm. Hence, seven studies met the eligibility criteria and were included in the meta‐analysis (Table 1). The Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) flow diagram is depicted in Figure 1.

TABLE 1.

Baseline characteristics of studies comparing carvedilol to propranolol including in the meta‐analysis.

Study Intervention arms Sample size Dose (range) Time of outcome assessment Age with SD (years) Male (n, %) MELD Child–Pugh (A/B/C) Ascites (N) Bleeding Hx (N) Encephalopathy (N)
[13] Carvedilol 55 6.25 mg/day 6 weeks 51.7 ± 8.1 41 (74.5) 12 23/24/8 33 0
Propranolol 55 40 mg/day 54 ± 8.8 42 (76.4) 9 22/30/3 33 0
[9] Carvedilol 26 31 ± 4 mg/day (12.5–50 mg) 11.1 ± 4.1 weeks 57.9 ± 1.5 19 (73) 13/10/3 10
Propranolol 25 73 ± 10 mg/day (10–160 mg) 58.4 ± 2.2 15 (60) 15/6/4 6
[10] Carvedilol 18 12.5 mg/day 7 days 42.3 ± 11.9 15 (83.3) 5/9/4 12 7 3
Propranolol 18 80 mg/day 47.3 ± 12.9 17 (94.4) 0/13/5 16 7 6
[11] Carvedilol 21 14 ± 7 mg 92.7 ± 13.6 days 58.2 ± 6.8 12 (57.14) 10.7 ± 4.3 8/7/6 5
Propranolol 17 122 ± 64 mg 56.2 ± 6.1 12 (70.6) 10.5 ± 4.0 6/6/4 5

[12]

 Carvedilol 16 14 ± 7 mg/day 3 months 59.2 ± 4.9 9 (56) 4/7/5 6
Propranolol 13 122 ± 64 mg/d 57.9 ± 4.9 8 (62) 1/9/3 5
[8] Carvedilol 14 25 mg 1 h 54.6 ± 8.8 NA 8/4/2 7 9 2
Propranolol 14 0.15 mg/kg IV 51.4 ± 8.5 NA 5/6/3 7 9 2
[14] Carvedilol 30 6.25 mg/day (6.25–12.5 mg) 4–6 weeks 41.7 ± 13.1 29 (96.7) 10/18/2 16 30 0
Propranolol 29 40 mg/day (40–80 mg) 45 ± 9.8 26 (89.7) 4/21/4 21 29 0
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FIGURE 1.

FIGURE 1

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Prisma flow diagram of different search engines and databases.

3.1. Baseline Characteristics of Included Studies

The analysis comprised 7 RCTs with 351 patients (180 in the carvedilol group and 171 in the propranolol group). The propranolol group's mean age was 52.22 years, while the carvedilol group's was 52.88 years. Table 1 displays the demographic details, dose ranges, time to outcome measurement, Child–Pugh score, MELD scores, and signs of decompensation.

3.2. Quality Assessment

The scientific quality of the included RCTs was evaluated using the Risk of Bias 2 assessment tool. Of the seven studies, Bañares et al. [9] and Hobloth et al. [11] showed high risk, while the rest suggested minimal risk of bias, ensuring the results were robust and accurate (Figures 2 and 3).

FIGURE 2.

FIGURE 2

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Risk of bias.

FIGURE 3.

FIGURE 3

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Risk of bias domains.

3.3. Meta‐Analysis for the Primary and Secondary Endpoints

Reduction in HVPG was significantly greater in the carvedilol group compared to the propranolol group (MD = −0.76, 95% CI = −1.45 to −0.08; p = 0.03) (Figure 4). Decreases in systemic vascular resistance (SVR) and mean arterial pressure (MAP) were also significantly more in the carvedilol group compared to the propranolol group ([MD = −190.55, 95% CI = −307.5 to −73.58; p = 0.001] and [MD = −3.65, 95% CI = −5.94 to −1.36; p = 0.002], respectively). The decrease in cardiac output was greater in the propranolol group than in the carvedilol group (MD = 0.92, 95% CI = 0.45–1.38; p = 0.004). Decreases in hepatic blood flow (HBF) and right atrial pressure (RAP) were greater in the propranolol group; however, this did not reach statistical significance ([MD = 0.13, 95% CI = −0.06 to 0.32; p = 0.17] and [MD = 0.28, 95% CI = −0.27 to 0.83; p = 0.32], respectively). The decrease in mean pulmonary arterial pressure (MPAP) was greater in the carvedilol group; however, this was not statistically significant (MD = −0.75, 95% CI = −1.60 to 0.10; p = 0.08). The incidence of rebleeding, shortness of breath, hepatic encephalopathy, and hypotension after initiation of therapy was not statistically different between the two groups (Figure 5).

FIGURE 4.

FIGURE 4

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Forest plots comparing carvedilol to propranolol in different splanchnic and systemic hemodynamics.

FIGURE 5.

FIGURE 5

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Forest plots comparing adverse effects in carvedilol and propranolol.

4. Discussion

Clinical decompensation of cirrhosis can be characterized by complications like ascites, hepatic encephalopathy, and variceal bleeding, which all carry an increased risk of mortality. Current guidelines recommend starting an NSBB to reduce the risk of the first decompensation event as well as primary and secondary prophylaxis of variceal bleeding in cirrhotic patients with clinically significant portal hypertension [16]. Propranolol, by acting on both β‐1 and β‐2 adrenergic receptors, can reduce cardiac output and portal vein flow by blocking these two receptors, respectively. Carvedilol has emerged as a newer NSBB with the added benefit of blocking α‐1 receptors with β‐1 and β‐2 adrenergic receptors. α‐1 receptor blockade can relax smooth muscles in the splanchnic circulation, decreasing resistance to blood flow and lowering portal pressures.

Furthermore, carvedilol has also demonstrated antioxidant, anti‐inflammatory, and anti‐fibrotic properties in animal and human model studies [17, 18]. Several trials over the last two decades have aimed at comparing carvedilol to propranolol in terms of their efficacy in lowering portal pressures and in specific HVPG. A meta‐analysis by Sinagra et al. assessed HVPG reduction, included five RCTs, and noted a significantly greater reduction in PH with carvedilol than with propranolol [19]. However, the study did not include data on other splanchnic and systemic hemodynamics, including HBF, mPAP, SVR, RAP, and CO. The present study also includes data from two more recent RCTs from 2016 [13, 14].

Our meta‐analysis included seven RCTs and 351 patients and compared the effects of carvedilol and propranolol on various splanchnic and systemic hemodynamics in patients with cirrhosis. Carvedilol demonstrated a significantly greater reduction in HVPG, SVR, and MAP than propranolol, with no significant difference in adverse effects.

4.1. Hepatic Venous Pressure Gradient

HVPG is a key marker for liver decompensation as its elevation indicates the presence of clinically significant portal hypertension. It has been estimated that every one mmHg increase in HVPG above a threshold level of 10 mmHg can mark up to an 11% increase in the risk of clinical decompensation [20]. Studies have found that an HVPG reduction of ≥ 10% reduces the risk of first decompensation in cirrhosis [20]. Carvedilol demonstrated superior efficacy in reducing HVPG compared to propranolol. This effect may be due to the combination of nonselective β blockade and α‐1 receptor blockade to reduce cardiac output, portal vein inflow, and intrahepatic resistance, respectively. Studies have shown that a reduction of HVPG of ≥ 20% from baseline to ≤ 12 mmHg correlates with better outcomes, including risk of variceal bleeding, development of ascites, and mortality [21].

4.2. Systemic Vascular Resistance and Mean Arterial Pressure in Portal Hypertension

Changes in systemic hemodynamics, including a decrease in SVR and MAP, reflect maladaptive responses in multiple organ systems, including the liver, kidney, heart, and peripheral vascular system. SVR is often reduced in patients with portal hypertension due to systemic vasodilation from vasodilating mediators, including nitric oxide. It often reflects a hyperdynamic circulatory state, characteristic of decompensated cirrhosis. When SVR decreases, the body compensates by increasing cardiac output and splanchnic blood inflow. An increase in splanchnic blood flow rate can subsequently contribute to portal hypertension [22]. Carvedilol has been shown to reduce or counteract the increase in HVPG by blocking α‐1 receptors in the splanchnic vascular smooth muscles and causing intrahepatic vasodilation. In concurrence with these observations, we also found that although carvedilol significantly lowered SVR compared to propranolol, the reduction of HVPG was also more significant in the carvedilol group.

Cirrhotic patients often present with lower MAP due to reduced SVR. A significant decrease in MAP can compromise renal perfusion, activate the renin‐angiotensin‐aldosterone system, and even result in complications like hepatorenal syndrome. Studies of blood pressure in patients with cirrhosis and ascites demonstrated that a MAP of 82 mmHg or lower was strongly associated with a reduced probability of survival [23]. We observed that carvedilol significantly lowered MAP compared to propranolol. However, the studies did not involve patients who were hypotensive at baseline (6 studies; 1 study did not measure MAPs). Another study found that the NSBB had a limited role in patients with a low MAP (less than 82 mmHg) and had no role in patients with ascites and a MAP of less than 65 mmHg. If initiated on beta‐blocker therapy, these patients should be monitored closely, and dose adjustments or withdrawal may be warranted if hypotension develops [24]. Furthermore, our study did not find a significant difference in the risk of hypotension between propranolol and carvedilol.

4.3. Mean Pulmonary Artery Pressure and Porto‐Pulmonary Complications

Porto‐pulmonary hypertension is a type of pulmonary artery hypertension that is associated with portal hypertension. Hyperdynamic pulmonary circulation leads to shear stress of the pulmonary vasculature, which can cause obstructive vasculopathy and increased pulmonary resistance. MPAP is an important metric in cirrhosis, particularly in patients with portal‐pulmonary hypertension [25]. Although we observed carvedilol to have a more significant reduction in MPAP than propranolol, this did not reach statistical significance. Of the three studies that compared the impact of these medications on hemodynamics, the study by Bañares et al. [8] showed the superiority of carvedilol in the reduction of MPAP. However, this study had a minimal sample size (27 in total) compared to the subsequent trials, which had 51 and 36, respectively.

4.4. Cardiac Output and the Hyperdynamic Circulatory State

CO typically increases in patients with cirrhosis due to complex neurohormonal changes, including increased sympathetic activity and release of vasodilatory substances in response to portal hypertension. This, coupled with decreased SVR, results in a “hyperdynamic circulation” state. High cardiac output worsens portal hypertension by increasing the portal flow rate [26]. In our analysis, propranolol leads to a greater reduction in CO than carvedilol, possibly because propranolol acts primarily by non‐specific β‐adrenergic receptor blockade to decrease cardiac contractility and heart rate. Due to its added effect on α receptors, carvedilol causes vasodilation, which can potentially offset the decrease in CO by decreasing SVR. These findings were also consistent with our observations that propranolol was found to reduce CO to a greater extent than carvedilol. Although a reduction in CO may be beneficial in patients with cirrhosis, hypotension secondary to these medications has to be closely monitored. A CO below 1.5 L/min/m2 was found to predict the development of hepatorenal syndrome and a decreased probability of survival among patients with cirrhosis and ascites [27].

4.5. Hepatic Blood Flow

The combination of increased portal venous inflow and increased intrahepatic resistance due to fibrosis and sinusoidal remodeling can decrease HBF and lead to hypoperfusion of hepatocytes. This imbalance can lead to the progression of liver dysfunction and portal hypertension‐related complications, including encephalopathy and variceal bleeding [28]. In our study, HBF was reduced to a greater extent with propranolol than carvedilol; however, this did not reach statistical significance. This can be attributed to the α‐1 receptor‐blocking properties of carvedilol in intrahepatic vasodilation to improve HBF.

Carvedilol appears to have a more favorable acute and long‐term profile, especially in terms of HVPG reduction and hemodynamic response, while also offering a viable alternative for propranolol non‐responders. While carvedilol's superior efficacy in reducing HVPG is beneficial, particularly in reducing the risk of variceal bleeding, clinicians must balance this with the potential for systemic hypotensive effects. This may require careful patient selection, dose adjustments, or more frequent monitoring, particularly in patients at risk for hemodynamic instability. Therefore, the dose of carvedilol should be carefully titrated, and it should not be increased in patients exhibiting signs of hypotension or with systolic blood pressure (SBP) below 90 mmHg or heart rate (HR) under 50 bpm.

5. Limitations

This meta‐analysis has several limitations. First, the heterogeneity across studies, including differences in patient populations, dosing regimens, and follow‐up periods, introduces variability that may impact the outcomes. While the sample size is relatively large, specific subgroup analyses, especially in advanced cirrhosis patients, are a future scope. The lack of standardized dosing protocols for carvedilol and propranolol complicates direct comparisons.

Short follow‐up durations also limit assessing long‐term outcomes like rebleeding and survival. Potential publication bias and inadequate subgroup analyses further challenge the generalizability of these findings. All the patients included in the meta‐analysis from the RCTs had decompensated cirrhosis; thereby, the extrapolation of this data to CSPH without decompensation remains to be studied. Future research with more standardized protocols and extended follow‐up is needed to strengthen clinical recommendations.

6. Conclusion

Our meta‐analysis comparing carvedilol and propranolol in patients with decompensated cirrhosis demonstrated that carvedilol significantly reduced HVPG compared to propranolol. Additionally, carvedilol significantly lowered SVR and MAP. Despite these changes, the overall incidence of adverse effects, including hypotension, hepatic encephalopathy, and shortness of breath, did not differ significantly between the two groups.

These findings suggest that carvedilol may be more effective than propranolol in reducing portal hypertension in patients with decompensated cirrhosis without the risk of increased adverse outcomes.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Table S1: Search strategy.

JGH-40-1409-s001.docx (14.9KB, docx)

Acknowledgments

Michigan State University funded this project.

Funding: Michigan State University funded this project.

Data Availability Statement

The data supporting the present study's findings are available from the corresponding author upon request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Table S1: Search strategy.

JGH-40-1409-s001.docx (14.9KB, docx)

Data Availability Statement

The data supporting the present study's findings are available from the corresponding author upon request.

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