Evidence map›Paper›PMID 40980715›Full record

ArticleEuropean heart journal open2025

Differences in inflammation biomarkers between patients with paroxysmal and persistent atrial fibrillation in the femoral vein and coronary sinus blood samples; a cohort study.

Carlos Valera Soria, Carl-Johan Carlhäll, Lars O Karlsson, Johan Lindbäck, Ziad Hijazi, Emmanouil Charitakis

Abstract read
In one paragraph

Article in European heart journal open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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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

6 authors.

Carlos Valera SoriaDepartment of Cardiology, Linköping University Hospital, Kardiologiska kliniken, Universitetssjukhuset, Linköping 581 85, Sweden.ORCID https://orcid.org/0009-0000-9016-2924
Carl-Johan CarlhällDepartment of Health, Medicine and Caring Sciences, Linköping University, SE-58183 Linköping, Sweden.ORCID https://orcid.org/0000-0003-2198-9690
Lars O KarlssonDepartment of Cardiology, Linköping University Hospital, Kardiologiska kliniken, Universitetssjukhuset, Linköping 581 85, Sweden.ORCID https://orcid.org/0000-0003-4852-3065
Johan LindbäckUppsala Clinical Research Center, Uppsala University, Uppsala Science Park, HubbenDag Hammarskjölds väg 38, SE-751 85 Uppsala, Sweden.ORCID https://orcid.org/0000-0002-6473-8798
Ziad HijaziUppsala Clinical Research Center, Uppsala University, Uppsala Science Park, HubbenDag Hammarskjölds väg 38, SE-751 85 Uppsala, Sweden.ORCID https://orcid.org/0000-0002-7420-743X
Emmanouil CharitakisDepartment of Health, Medicine and Caring Sciences, Linköping University, SE-58183 Linköping, Sweden.ORCID https://orcid.org/0000-0002-2514-5324

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims: The association between inflammation and atrial fibrillation (AF) is evident, but assessing the specific inflammatory pathways involved in the pathogenesis remains complex. This study aimed to identify inflammatory biomarkers associated with paroxysmal (PAF) and persistent (PeAF) AF by evaluating blood samples from the intra- and extracardiac space. Methods and results: This is an observational, cross-sectional, single-centre study. A total of 92 inflammatory biomarkers were analyzed from blood samples taken from the coronary sinus (CS) and the femoral vein (FV) in 88 patients with AF who had been referred for catheter ablation at the Linköping University Hospital, Sweden. The concentrations of the biomarkers were compared between PAF and PeAF patients in the CS and FV. Significant differences in concentration were found in 36 of 92 biomarkers. Among these, 12 proteins stand out for exhibiting a higher concentration in PeAF patients: Interleukin 6 (IL-6), CUB domain-containing protein 1 (CDCP1), Interleukin 18 receptor 1 (IL-18R1) and cystatin D (CST5) in the FV, β nerve growth factor (β-NGF) and tissue growth factor α (TGF-α) at the CS level, as well as interleukin 18 (IL-18), chemokine ligand 3 (CCL-3) and tumour necrosis factor superfamily 14 (TNFSF-14) in both FV and CS. Moreover, chemokine ligand 25 (CCL-25), chemokine ligand 28 (CCL-28), and artemin (ARTN) were found at a higher concentration in the CS in the overall population. Conclusion: This study supports the involvement of TNFSF-14, IL-6, and IL-18 in the pathogenesis and maintenance of PeAF. Furthermore, it identifies β-NGF and TGF-α as potential participants in the pathogenesis and/or maintenance of PeAF locally in the atria. Novel inflammatory biomarkers, mainly chemokines, are also identified as possibly involved in the pathophysiology of AF.

Indexed as

Atrial fibrillationBiomarkersCoronary sinusInflammationPathophysiological features

Identifiers

PMID40980715
PMCPMC12448471

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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.