Related Experiment Video

Updated: Oct 12, 2026

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
09:37

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats

Published on: August 1, 2018

15.6K

Carvedilol for portal hypertension in cirrhosis: systematic review with meta-analysis

Tong Li1, Wenbo Ke1, Ping Sun1

  • 1Hepatobiliary Surgery Centre, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

BMJ Open
|May 6, 2016
PubMed

Insights

Carvedilol shows promise in reducing hepatic venous pressure gradient (HVPG) in cirrhosis patients, potentially outperforming propranolol and nebivolol. However, evidence quality is low, necessitating further research for definitive conclusions on its clinical efficacy.

Area of Science:

  • Hepatology
  • Cardiology
  • Pharmacology

Background:

  • Portal hypertension is a serious complication of cirrhosis.
  • Effective management strategies are crucial for improving patient outcomes.
  • Carvedilol is a beta-blocker with alpha-blocking activity, investigated for its effects in portal hypertension.

Purpose of the Study:

  • To systematically review and meta-analyze the clinical and hemodynamic effects of carvedilol in patients with cirrhosis and portal hypertension.
  • To compare carvedilol's efficacy against other treatments like propranolol, endoscopic variceal band ligation (EVL), and nadolol plus isosorbide-5-mononitrate (ISMN).

Main Methods:

  • Systematic review and meta-analysis of randomized controlled trials (RCTs).
  • Searched major databases (PubMed, Cochrane, EMBASE, Science Citation Index Expanded) up to December 2015.
  • Assessed clinical outcomes (mortality, bleeding) and hemodynamic outcomes (HVPG, MAP).

Main Results:

  • Carvedilol demonstrated a greater reduction in hepatic venous pressure gradient (HVPG) compared to propranolol and nebivolol.
  • No significant differences in mortality or variceal bleeding were observed when comparing carvedilol with EVL or nadolol plus ISMN.
  • Carvedilol did not show a greater reduction in mean arterial pressure (MAP) than propranolol.

Conclusions:

  • Carvedilol may be more effective than propranolol or nebivolol in decreasing HVPG.
  • Carvedilol appears to be as effective as EVL or nadolol plus ISMN in preventing variceal bleeding.
  • The overall quality of evidence is low, and further large-scale RCTs are needed to confirm these findings.
Abstract

Keywords:
CLINICAL PHARMACOLOGYGENERAL MEDICINE (see Internal Medicine)

More Related Videos

Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy07:10

Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy

Published on: June 18, 2020

23.3K
Laparoscopic Splenectomy with Pericardial Devascularization for Hypersplenism and Esophageal Variceal Hemorrhage Due to Portal Hypertension04:00

Laparoscopic Splenectomy with Pericardial Devascularization for Hypersplenism and Esophageal Variceal Hemorrhage Due to Portal Hypertension

Published on: November 15, 2024

954

Related Concept Videos

Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol abuse, or...
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Portal Hypertension01:22

Portal Hypertension

Portal hypertension is an increase in blood pressure within the portal venous system. Normally, this pressure is less than 5 mmHg. It is considered clinically significant when it rises above 10 mmHg. At this threshold, complications from altered blood flow and venous congestion emerge.EtiologyPortal hypertension arises from conditions that impede blood flow through the liver. The most common cause is cirrhosis, in which chronic liver injury leads to fibrotic scarring. This fibrosis narrows or...