Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (867 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A carbazole and propanol derivative that acts as a non-cardioselective beta blocker and vasodilator. It has blocking activity for alpha 1 adrenergic receptors and, at higher doses, may function as a blocker of calcium channels; it also has antioxidant properties. Carvedilol is used in the treatment of hypertension; angina pectoris; and heart failure. It can also reduce the risk of death following myocardial infarction.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Carvedilol, (+-)-isomer; Carvedilol, 14C-labeled; 14C-labeled Carvedilol; Carvedilol, 14C labeled; Carvedilol, (R)-isomer; Carvedilol, (S)-isomer; Coreg; Dilatrend.
Where it fits in the MeSH classification
- Broader topics
- Propanolamines; Carbazoles
Related concepts
- Alpha
- Adrenergic Receptors
- Calcium Channels
- Hypertension
- Angina Pectoris
- Heart Failure
- Myocardial Infarction
Research landscape
PubMed indexes 3,084 records tagged with the MeSH heading “Carvedilol” (counts retrieved 2026-10-31). 444 of them (14.4%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 1,248 records.
Reviews account for 354 records (11.5%) and meta-analyses for 54. Randomized controlled trials number 519 (16.8%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 452 |
| 2000-2009 | 1,248 |
| 2010-2019 | 940 |
| 2020 onward | 444 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 354 | 11.5% |
| Meta-analyses | 54 | 1.8% |
| Randomized controlled trials | 519 | 16.8% |
Method: PubMed query "Carvedilol"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Long-term use of carvedilol in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundDespite its recommendation by the current guidelines, the role of long-term oral beta-blocker therapy has never been evaluated by randomized trials in uncomplicated ST-segment elevation myocardial infarction (STEMI) patients without heart failure, left ventricular dysfunction or ventricular arrhythmia who underwent primary percutaneous coronary intervention (PCI).
- Closing excerpt
- number, NCT 01155635.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (264 words)
BackgroundDespite its recommendation by the current guidelines, the role of long-term oral beta-blocker therapy has never been evaluated by randomized trials in uncomplicated ST-segment elevation myocardial infarction (STEMI) patients without heart failure, left ventricular dysfunction or ventricular arrhythmia who underwent primary percutaneous coronary intervention (PCI).Methods and resultsIn a multi-center, open-label, randomized controlled trial, STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06).ConclusionLong-term carvedilol therapy added on the contemporary evidence-based medications did not seem beneficial in selected STEMI patients treated with primary PCI.Trial registrationCAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-scale Randomized Controlled Trial) ClinicalTrials.gov.number, NCT 01155635.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30153268 · DOI · PMC6112626
Repositioning of the β-Blocker Carvedilol as a Novel Autophagy Inducer That Inhibits the NLRP3 Inflammasome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The NLRP3 inflammasome is a multiprotein complex that plays a key role in the innate immune system, and aberrant activation of this complex is involved in the pathogenesis of inflammatory diseases.
- Closing excerpt
- Our results indicated that CVL is a novel autophagy inducer that inhibits the NLRP3 inflammasome and can be repositioned for ameliorating NLRP3-associated complications.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (208 words)
The NLRP3 inflammasome is a multiprotein complex that plays a key role in the innate immune system, and aberrant activation of this complex is involved in the pathogenesis of inflammatory diseases. Carvedilol (CVL) is an α-, β-blocker used to treat high blood pressure and congestive heart failure; however, some benefits beyond decreased blood pressure were observed clinically, suggesting the potential anti-inflammatory activity of CVL. In this report, the inhibitory potential of CVL toward the NLRP3 inflammasome and the possible underlying molecular mechanisms were studied. Our results showed that CVL attenuated NLRP3 inflammasome activation and pyroptosis in mouse macrophages, without affecting activation of the AIM2, NLRC4 and non-canonical inflammasomes. Mechanistic analysis revealed that CVL prevented lysosomal and mitochondrial damage and reduced ASC oligomerization. Additionally, CVL caused autophagic induction through a Sirt1-dependent pathway, which inhibited the NLRP3 inflammasome. In the in vivo mouse model of NLRP3-associated peritonitis, oral administration of CVL reduced (1) peritoneal recruitment of neutrophils; (2) the levels of IL-1β, IL-18, active caspase-1, ASC, IL-6, TNF-α, MCP-1, and CXCL1 in the lavage fluids; and (3) the levels of NLRP3 and HO-1 in the peritoneal cells. Our results indicated that CVL is a novel autophagy inducer that inhibits the NLRP3 inflammasome and can be repositioned for ameliorating NLRP3-associated complications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30186288 · DOI · PMC6113403
β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Virus infection may induce excessive interferon (IFN) responses that can lead to host tissue injury or even death.
- Closing excerpt
- Our results thus identify a viral immune-evasion pathway via the degradation of β-arrestin 2, and also hint that carvedilol, approved for treating heart failure, can potentially be repurposed as an antiviral drug candidate.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (164 words)
Virus infection may induce excessive interferon (IFN) responses that can lead to host tissue injury or even death. β-arrestin 2 regulates multiple cellular events through the G protein-coupled receptor (GPCR) signaling pathways. Here we demonstrate that β-arrestin 2 also promotes virus-induced production of IFN-β and clearance of viruses in macrophages. β-arrestin 2 interacts with cyclic GMP-AMP synthase (cGAS) and increases the binding of dsDNA to cGAS to enhance cyclic GMP-AMP (cGAMP) production and the downstream stimulator of interferon genes (STING) and innate immune responses. Mechanistically, deacetylation of β-arrestin 2 at Lys171 facilitates the activation of the cGAS-STING signaling and the production of IFN-β. In vitro, viral infection induces the degradation of β-arrestin 2 to facilitate immune evasion, while a β-blocker, carvedilol, rescues β-arrestin 2 expression to maintain the antiviral immune response. Our results thus identify a viral immune-evasion pathway via the degradation of β-arrestin 2, and also hint that carvedilol, approved for treating heart failure, can potentially be repurposed as an antiviral drug candidate.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33243993 · DOI · PMC7691508
Comparative Risk of Recurrent Esophageal Variceal Hemorrhage and Other Decompensation Events with Carvedilol Versus Propranolol in Patients with Cirrhosis: A Retrospective Study [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Background & aimsNon-selective beta-blockers (NSBBs) have become a cornerstone treatment to prevent complications of cirrhosis and portal hypertension.
- Closing excerpt
- 898, P ConclusionsCompared to propranolol, the use of carvedilol in patients with history of cirrhosis and EVH was associated with lower risk of recurrent EVH, further decompensation episodes, undergoing LT, and mortality.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (231 words)
Background & aimsNon-selective beta-blockers (NSBBs) have become a cornerstone treatment to prevent complications of cirrhosis and portal hypertension. Data supporting the use of a specific beta-blocker are scarce. In this retrospective study, we aimed to compare the effectiveness of carvedilol versus propranolol in: 1) preventing recurrent esophageal hemorrhage (EVH) in patients with prior history of EVH 2) reducing the occurrence of further decompensation episodes in these patients including hepatic encephalopathy (HE), ascites, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome (HRS), and hepatocellular carcinoma (HCC), and 3) reducing all-cause mortality.Approach & resultsThis was a retrospective propensity-matched study using the multi-institutional database TriNetX. We included patients with cirrhosis who had an episode of EVH and were prescribed carvedilol or propranolol between December 2004 and December 2024. The primary outcome was the rate of hospitalization with recurrent EVH within the first 5 years of starting the index NSBB. The secondary outcomes were hospitalization with the principal diagnoses of ascites, SBP, HE, HRS, new diagnosis of HCC, undergoing liver transplant (LT), and all-cause mortality within the observation period of 5 years of NSBB prescription. Kaplan-Meier survival analysis was also performed. Compared to propranolol use, carvedilol use was associated with lower risk of EVH (RR, 0.898, P ConclusionsCompared to propranolol, the use of carvedilol in patients with history of cirrhosis and EVH was associated with lower risk of recurrent EVH, further decompensation episodes, undergoing LT, and mortality.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41108335 · DOI · PMC13144202
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Protective role of beta-blockers in chemotherapy-induced cardiotoxicity-a systematic review and meta-analysis of carvedilol [5]
- Research article Meta-Analysis of Carvedilol for the Prevention of Anthracycline-Induced Cardiotoxicity [6]
- Research article Carvedilol versus traditional, non-selective beta-blockers for adults with cirrhosis and gastroesophageal varices [7]
- Research article Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306) [8]
- Research article Preventive use of carvedilol for anthracycline-induced cardiotoxicity: a systematic review and meta-analysis of randomized controlled trials [9]
- Research article The efficacy comparison of carvedilol plus endoscopic variceal ligation and traditional, nonselective β-blockers plus endoscopic variceal ligation in cirrhosis patients for the prevention of variceal rebleeding: a meta-analysis [10]
References
- Watanabe H, Ozasa N, Morimoto T, Shiomi H, Bingyuan B, Suwa S, et al.. Long-term use of carvedilol in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. . 2018. PMID 30153268 · DOI · PMC6112626
- Wong WT, Li LH, Rao YK, Yang SP, Cheng SM, Lin WY, et al.. Repositioning of the β-Blocker Carvedilol as a Novel Autophagy Inducer That Inhibits the NLRP3 Inflammasome. . 2018. PMID 30186288 · DOI · PMC6113403
- Zhang Y, Li M, Li L, Qian G, Wang Y, Chen Z, et al.. β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion. . 2020. PMID 33243993 · DOI · PMC7691508
- Ismail A, Abusuliman M, Kloub M, Abbarh S, Aloum K, Najim MS, et al.. Comparative Risk of Recurrent Esophageal Variceal Hemorrhage and Other Decompensation Events with Carvedilol Versus Propranolol in Patients with Cirrhosis: A Retrospective Study. . 2026. PMID 41108335 · DOI · PMC13144202
- Huang S, Zhao Q, Yang ZG, Diao KY, He Y, Shi K, et al.. Protective role of beta-blockers in chemotherapy-induced cardiotoxicity-a systematic review and meta-analysis of carvedilol. Heart Fail Rev. 2019. PMID 30523513 · DOI · PMC6476829
- Kheiri B, Abdalla A, Osman M, Haykal T, Chahine A, Ahmed S, et al.. Meta-Analysis of Carvedilol for the Prevention of Anthracycline-Induced Cardiotoxicity. Am J Cardiol. 2018. PMID 30292333 · DOI
- Zacharias AP, Jeyaraj R, Hobolth L, Bendtsen F, Gluud LL, Morgan MY. Carvedilol versus traditional, non-selective beta-blockers for adults with cirrhosis and gastroesophageal varices. Cochrane Database Syst Rev. 2018. PMID 30372514 · DOI · PMC6517039
- Liu C, You H, Zeng QL, Wong YJ, Wang B, Grgurevic I, et al.. Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306). Clin Mol Hepatol. 2025. PMID 38988296 · DOI · PMC11791610
- Zhan T, Daniyal M, Li J, Mao Y. Preventive use of carvedilol for anthracycline-induced cardiotoxicity: a systematic review and meta-analysis of randomized controlled trials. Herz. 2020. PMID 30656389 · DOI
- Yang J, Ge K, Chen L, Yang JL. The efficacy comparison of carvedilol plus endoscopic variceal ligation and traditional, nonselective β-blockers plus endoscopic variceal ligation in cirrhosis patients for the prevention of variceal rebleeding: a meta-analysis. Eur J Gastroenterol Hepatol. 2019. PMID 31094853 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.