Evidence map›Paper›PMID 42161427›Full record

ArticleOpen heart2026

Interaction between clinical and genetic risk of atrial fibrillation in the danish diet, cancer and health cohort.

Tanja Charlotte Frederiksen, Ramesh Nadarajah, Morten Krogh Christiansen, Jianhua Wu, Chris P Gale, Emelia J Benjamin, Anja Olsen, Mette K Andersen, Torben Hansen, Niels Grarup and 2 more

Abstract read
In one paragraph

Article in Open heart, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Tanja Charlotte FrederiksenDepartment of Cardiology, Regional Hospital Horsens, Horsens, Central Denmark Region, Denmark tanja_charlotte@clin.au.dk.ORCID http://orcid.org/0000-0003-3338-9297
Ramesh NadarajahLeeds Institute for Data Analytics, University of Leeds, Leeds, UK.ORCID http://orcid.org/0000-0001-9895-9356
Morten Krogh ChristiansenDepartment of Clinical Medicine, Aarhus University, Aarhus, Central Denmark Region, Denmark.
Jianhua WuQueen Mary University of London Barts and The London School of Medicine and Dentistry, London, UK.ORCID http://orcid.org/0000-0001-6093-599X
Chris P GaleDivision of Epidemiology and Biostatistics, University of Leeds, Leeds, UK.
Emelia J BenjaminEpidemiology Department, Boston University School of Public Health, Framingham, Massachusetts, USA.
Anja OlsenDepartment of Public Health, Aarhus University, Aarhus, Denmark.
Mette K AndersenMedical Sciences, University of Copenhagen, Kobenhavn, Denmark.
Torben HansenMedical Sciences, University of Copenhagen, Kobenhavn, Denmark.
Niels GrarupMedical Sciences, University of Copenhagen, Kobenhavn, Denmark.
Christina C DahmDepartment of Public Health, Aarhus University, Aarhus, Denmark.
Henrik Kjærulf JensenDepartment of Clinical Medicine, Aarhus University, Aarhus, Central Denmark Region, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe interplay between genetic susceptibility and clinical risk for incident atrial fibrillation (AF) is unclear.

methodsWe used a case-cohort study design and included AF cases and a randomly drawn subcohort of 4040 participants from the Danish Diet, Cancer and Health cohort. The simplified version of the Future Innovations in Novel Detection of Atrial Fibrillation (FIND-AF) risk score was used to quantify individual participant clinical risk of incident AF as low (0-3 points), high (4-6 points) and very high risk (7-14 points). We calculated individual participant Genetic Risk Scores (GRS) from 142 variants to categorise participants as low (quintile 1), intermediate (quintile 2-4) or high (quintile 5) genetic risk of AF. We used weighted Cox proportional hazards regression to quantify risk of incident AF according to FIND-AF risk and GRS and assessed the relative excess risk due to interaction (RERI) for interaction on an additive scale.

resultsDuring a median follow-up of 12.9 years, 3094 participants developed AF. Compared with individuals with low FIND-AF risk score and low GRS, the multivariable-adjusted HR for AF was 3.47 (95% CI 2.64 to 4.55) for those with high FIND-AF risk score and high GRS and 12.76 (95% CI 5.07 to 32.11) for those with very high FIND-AF risk score and high GRS. The RERI was 0.56 (95% CI 0.43 to 0.70), indicating a positive additive interaction between GRS and FIND-AF risk score.

conclusionsGenetic susceptibility and clinical risk interacted on an additive scale to elevate AF risk. These results highlight the need for future research on prevention and screening among individuals with both high genetic and clinical risk for AF.

Indexed as

Atrial FibrillationDietGenetic Predisposition to DiseaseNeoplasmsAgedDenmarkFemaleFollow-Up StudiesGenetic Risk ScoreHumansIncidenceMaleMiddle AgedRisk AssessmentRisk FactorsAtrial FibrillationAtrial FlutterEpidemiologyGeneticsRisk Factors

Identifiers

PMID42161427
PMCPMC13201998

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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.