Evidence mapPaperPMID 40575425Full record

ReviewWorld journal of cardiology2025

Metabolic-dysfunction associated steatotic liver disease and atrial fibrillation: A review of pathogenesis.

Inderjeet Singh Bharaj, Ajit Singh Brar, Jasraj Kahlon, Anmol Singh, Priya Hotwani, Vikash Kumar, Aalam Sohal, Akash Batta

Abstract readReview
In one paragraph

Review in World journal of cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

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

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
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

8 authors.

Inderjeet Singh BharajDepartment of Internal Medicine, Abrazo Health Network, Glendale, AZ 85308, United States.
Ajit Singh BrarDepartment of Internal Medicine, Michigan State University at Hurley Medical Center, Flint, MI 48503, United States.
Jasraj KahlonDepartment of Internal Medicine, Abrazo Health Network, Glendale, AZ 85308, United States.
Anmol SinghDepartment of Medicine, Tristar Centennial Medical Center, Nashville, TN 37203, United States.
Priya HotwaniDepartment of Internal Medicine, Parkview Health Internal Medicine Residency, Fort Wayne, IN 46845, United States.
Vikash KumarDepartment of Gastroenterology and Hepatology, Creighton University School of Medicine, Phoenix, AZ 85012, United States.
Aalam SohalDepartment of Gastroenterology and Hepatology, Creighton University School of Medicine, Phoenix, AZ 85012, United States. aalamsohal@gmail.com.
Akash BattaDepartment of Cardiology, Dayanand Medical College and Hospital, Ludhiana 141001, Punjab, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) significantly contributes to cardiovascular morbidity, with cardiovascular disease being the leading cause of mortality among affected individuals. Atrial fibrillation (AF), the most common cardiac arrhythmia, is frequently observed in patients with MASLD. While shared metabolic risk factors such as obesity, diabetes, dyslipidemia, and hypertension are implicated, underlying pathophysiological mechanisms that include systemic inflammation, oxidative stress, insulin resistance, endothelial dysfunction, and activation of the renin-angiotensin-aldosterone system (RAAS) are proposed to play significant part in the increased risk of AF in MASLD. The aim is to review the pathogenesis linking MASLD and AF. A comprehensive literature review was conducted, focusing on studies that explore the epidemiology, pathogenesis, and clinical implications of MASLD and AF. Databases searched included PubMed, Scopus, and Web of Science, with keywords such as "metabolic associated steatotic liver disease", "non fibrotic metabolic associated steatohepatitis", "Nonalcoholic fatty liver disease", "metabolic syndrome", "atrial fibrillation", "antifibrotic therapies", "pathogenesis", and "cardiovascular risk". Chronic low-grade inflammation and oxidative stress in MASLD contribute to atrial structural and electrical remodeling, fostering an arrhythmogenic substrate. Insulin resistance, a hallmark of MASLD, exacerbates metabolic dysfunction and promotes atrial fibrosis. Dysregulated lipid metabolism and gut microbiota alterations further compound cardiovascular risk. Aldosterone dysregulation and systemic inflammation stemming from RAAS activation contributes to the shared pathophysiology. The severity of MASLD does not seem to directly influence the risk of AF, suggesting that even early stages of liver disease can increase susceptibility to this arrhythmia. Effective management of MASLD requires targeted risk-factor modification strategies, including weight management, glycemic control, and pharmacological interventions. A multidisciplinary approach is essential for comprehensive assessment and management of MASLD patients, with a focus on cardiovascular risk assessment and arrhythmia prevention. Future research should explore the impact of emerging MASLD therapeutic agents on the incidence and recurrence of cardiac arrhythmias. Early detection and comprehensive management of MASLD and AF are crucial to mitigate the dual burden of these conditions.

Indexed as

Atrial fibrillationDyslipidemiaInsulin resistanceMetabolic-dysfunction associated steatotic liver diseaseNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitisObesityOxidative stress

Identifiers

PMID40575425
PMCPMC12186170

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.