Evidence map›Paper›PMID 39895528›Full record

ArticleJournal of the American Heart Association2025

Telomere Length Is Associated With Adverse Atrial Remodeling in Patients With Atrial Fibrillation.

Kabita Pradhan, Balram Neupane, Paul Niehues, Martin Kirschner, Fabian Beier, Chao-Chung Kuo, Erika Anneliese Hilbold, Christian Bär, Oana-Maria Thoma, Maximilian Waldner and 10 more

Abstract read
In one paragraph

Article in Journal of the American Heart Association, 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
  2. 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

20 authors.

Kabita PradhanDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-8602-6575
Balram NeupaneDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-5818-1981
Paul NiehuesDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.ORCID 0009-0002-3740-380X
Martin KirschnerDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, Medical Faculty University Hospital RWTH Aachen Aachen Germany.
Fabian BeierDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, Medical Faculty University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0002-3718-8217
Chao-Chung KuoGenomics Facility, Interdisciplinary Center for Clinical Research (IZKF) University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-8879-4754
Erika Anneliese HilboldInstitute of Molecular and Translational Therapeutic Strategies (IMTTS) Hannover Medical School Hannover Germany.ORCID 0000-0001-9808-3729
Christian BärInstitute of Molecular and Translational Therapeutic Strategies (IMTTS) Hannover Medical School Hannover Germany.ORCID 0000-0001-9276-9383
Oana-Maria ThomaDepartment of Medicine 1 Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.ORCID 0000-0002-1665-9753
Maximilian WaldnerDepartment of Medicine 1 Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Margherita VieriDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, Medical Faculty University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-5484-4522
Tim H BrümmendorfDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, Medical Faculty University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0002-9677-3723
Vithurithra TharmapalanInstitute for Stem Cell Biology, Helmholtz Institute for Biomedical Engineering University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-5648-0881
Wolfgang WagnerCenter for Integrated Oncology Aachen Bonn Cologne Düsseldorf (CIO ABCD) Cologne Germany.ORCID 0000-0002-1971-3217
Michael KleinesDivision of Virology, Center of Laboratory Diagnostics University Hospital RWTH Aachen Aachen Germany.
Mahdi EmraniDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.
Matthias Daniel ZinkDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.
Andreas NappDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-5329-6675
Nikolaus MarxDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-6141-634X
Michael GramlichDepartment of Cardiology University Hospital RWTH Aachen Aachen Germany.ORCID 0000-0001-5233-6778

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtrial fibrillation (AF) is the most common cardiac arrhythmia with a massive burden on global health. The prevalence of AF increases dramatically with age and can be up to 18% in patients older than 80 years. Telomeres, which are short, repeated DNA sequences at the end of chromosomes, are known to act as a biological aging marker. In this study, we investigated the relation of telomere shortening and AF in the context of atrial remodeling. Furthermore, we assessed changes in the gene expression profiles of patients with AF according to telomere length (TL) and left atrial fibrosis.

methodsWe included 72 patients undergoing catheter ablation for AF. Bipolar voltage maps were obtained to determine left atrial low voltage areas as a surrogate for atrial fibrosis. TL was quantified and correlated to low voltage areas. 3' mRNA sequencing was performed for gene expression profiling. Clonal hematopoiesis of indeterminate potential was assessed by next generation sequencing. Telomerase reverse transcriptase knockout (

resultsPatients with advanced left atrial fibrosis had shorter telomeres compared with patients with healthy left atria. Furthermore, there was a strong correlation between the extent of left atrial low voltage areas, TL, and outcome after catheter ablation of AF. 24 months after ablation, only 26.5% of patients with advanced fibrosis and short TL were in sinus rhythm compared with 62.5% of patients with no/low fibrosis and long TL. Gene expression profiles and clonal hematopoiesis of indeterminate potential frequency differed in patients with AF with short and long telomeres. Finally, atrial tissue of mouse models with shortened telomeres showed marked left atrial fibrosis and over-expression of fibrosis-related genes.

conclusionsTelomere shortening is correlated with left atrial remodeling. Shorter telomeres are associated with a series of molecular events which could eventually lead to cardiac fibrosis and perpetuate AF.

Indexed as

Atrial FibrillationAtrial RemodelingHeart AtriaTelomereTelomere ShorteningAgedAnimalsCatheter AblationDisease Models, AnimalFemaleFibrosisHumansMaleMiceMice, KnockoutMiddle AgedRNATelomeraseTERT protein, humanagingatrial fibrillationfibrosistelomere

Identifiers

PMID39895528
PMCPMC12074728

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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.