Evidence mapPaperPMID 40095683Full record

ReviewJournal of clinical medicine2025

Serum Lipids, Inflammation, and the Risk of Atrial Fibrillation: Pathophysiological Links and Clinical Evidence.

Alfredo Mauriello, Adriana Correra, Anna Chiara Maratea, Alfredo Caturano, Biagio Liccardo, Marco Alfonso Perrone, Antonio Giordano, Gerardo Nigro, Antonello D'Andrea, Vincenzo Russo

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Thrombaxane-B2 as a predictor marker of atrial fibrillation.International journal of cardiology. Cardiovascular risk and prevention · 2026
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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

10 authors.

Alfredo MaurielloCardiology Unit, Department of Medical and Translational Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, 80131 Naples, Italy.ORCID 0000-0001-7060-6938
Adriana CorreraIntensive Cardiac Care Unit, "San Giuseppe Moscati" Hospital, ASL Caserta 81031 Aversa, Italy.
Anna Chiara MarateaCardiology Unit, Department of Medical and Translational Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, 80131 Naples, Italy.
Alfredo CaturanoInternal Medicine Unit, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Piazza Luigi Miraglia 2, 80138 Naples, Italy.ORCID 0000-0001-7761-7533
Biagio LiccardoCardiology Unit, Department of Medical and Translational Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, 80131 Naples, Italy.
Marco Alfonso PerroneDepartment of Cardiology and CardioLab, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0002-0511-2621
Antonio GiordanoSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.ORCID 0000-0002-5959-016X
Gerardo NigroCardiology Unit, Department of Medical and Translational Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, 80131 Naples, Italy.ORCID 0000-0003-1776-8449
Antonello D'AndreaCardiology and Intensive Care Unit, Department of Cardiology, "Umberto I" Hospital, 84014 Nocera Inferiore, Italy.ORCID 0000-0002-9698-9145
Vincenzo RussoCardiology Unit, Department of Medical and Translational Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, 80131 Naples, Italy.ORCID 0000-0002-9227-0360

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dyslipidemia is a metabolic disorder characterized by quantitative and/or qualitative abnormalities in serum lipid levels. Elevated serum cholesterol levels can modify the turnover and recruitment of ionic channels in myocytes and cellular homeostasis, including those of inflammatory cells. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling, which is the substrate of atrial fibrillation (AF). Data about the association between increased lipid serum levels and AF are few and contrasting. Lipoprotein (a), adiposity, and inflammation seem to be the main drivers of AF; in contrast, low-density lipoproteins, high-density lipoproteins and triglycerides are not directly involved in AF onset. The present review aimed to describe the pathophysiological link between dyslipidemia and AF, the efficacy of lipid-lowering therapies in atherosclerotic cardiovascular disease (ASCVD) patients with and without AF, and the impact of lipid-lowering therapies on AF incidence.

Indexed as

alirocumabatrial fibrillationbempedoic aciddyslipidemiaevolocumabicosapent ethylinclisiranstatins

Identifiers

PMID40095683
PMCPMC11899858

What Socratic holds

Textmetadata
LicenceCC BY
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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.