Evidence map›Paper›PMID 38848133›Full record

ReviewEuropean heart journal2024

Alcoholic cardiomyopathy: an update.

Fernando Domínguez, Eric Adler, Pablo García-Pavía

Abstract readReview
In one paragraph

Review in European heart journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Observational
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Well-Known and Novel Behavioural Risk Factors for Heart Failure.Journal of cardiovascular development and disease · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Global burden and cross-country inequalities of alcoholic cardiomyopathy: A 1990-2021 analysis.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Article
  17. Quantitative Histological Insights Into Sudden Arrhythmic Death Syndrome: Findings From a Forensic Autopsy Cohort.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Fernando DomínguezDepartment of Cardiology, Heart Failure and Inherited Cardiac Diseases Unit, Hospital Universitario Puerta de Hierro Majadahonda, IDIPHISA, CIBERCV, Manuel de Falla, 2, Majadahonda, Madrid 28222, Spain.ORCID 0000-0001-8408-363X
Eric AdlerSection Head of Heart Failure, University of California, San Diego, CA, USA.ORCID 0000-0002-4765-0188
Pablo García-PavíaDepartment of Cardiology, Heart Failure and Inherited Cardiac Diseases Unit, Hospital Universitario Puerta de Hierro Majadahonda, IDIPHISA, CIBERCV, Manuel de Falla, 2, Majadahonda, Madrid 28222, Spain.ORCID 0000-0002-5470-2257

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcohol-induced cardiomyopathy (AC) is an acquired form of dilated cardiomyopathy (DCM) caused by prolonged and heavy alcohol intake in the absence of other causes. The amount of alcohol required to produce AC is generally considered as >80 g/day over 5 years, but there is still some controversy regarding this definition. This review on AC focuses on pathogenesis, which involves different mechanisms. Firstly, the direct toxic effect of ethanol promotes oxidative stress in the myocardium and activation of the renin-angiotensin system. Moreover, acetaldehyde, the best-studied metabolite of alcohol, can contribute to myocardial damage impairing actin-myosin interaction and producing mitochondrial dysfunction. Genetic factors are also involved in the pathogenesis of AC, with DCM-causing genetic variants in patients with AC, especially titin-truncating variants. These findings support a double-hit hypothesis in AC, combining genetics and environmental factors. The synergistic effect of alcohol with concomitant conditions such as hypertension or liver cirrhosis can be another contributing factor leading to AC. There are no specific cardiac signs and symptoms in AC as compared with other forms of DCM. However, natural history of AC differs from DCM and relies directly on alcohol withdrawal, as left ventricular ejection fraction recovery in abstainers is associated with an excellent prognosis. Thus, abstinence from alcohol is the most crucial step in treating AC, and specific therapies are available for this purpose. Otherwise, AC should be treated according to current guidelines of heart failure with reduced ejection fraction. Targeted therapies based on AC pathogenesis are currently being developed and could potentially improve AC treatment in the future.

Indexed as

Cardiomyopathy, AlcoholicEthanolHumansOxidative StressEthanolAlcoholAlcoholic cardiomyopathyPathogenesisTreatment

Identifiers

PMID38848133
PMCPMC11231944

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.