Evidence map›Paper›PMID 33982075›Full record

ReviewCardiovascular research2021

Genetics of atrial fibrillation-practical applications for clinical management: if not now, when and how?

Shinwan Kany, Bruno Reissmann, Andreas Metzner, Paulus Kirchhof, Dawood Darbar, Renate B Schnabel

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2021. 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
3.6field-weighted citation impact, top 6% of its field
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, 33 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Common Methylenetetrahydrofolate Reductase PolymorphismDiagnostics (Basel, Switzerland) · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. In Silico TRials guide optimal stratification of ATrIal FIbrillation patients to Catheter Ablation and pharmacological medicaTION: the i-STRATIFICATION study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Discovery ofBiology · 2023
    Article
  17. Polygenic risk scores for prediction of atrial fibrillation.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2023
    Article
  18. Article
  19. Frontiers in physiology · 2022
    Article
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 at 2 institutions in 3 countries.

Shinwan KanyDepartment of Cardiology, University Heart and Vascular Center, University Medical Center Hamburg Eppendorf, Martinistraße 52, 20251 Hamburg, Hamburg, Germany.ORCID 0000-0001-8113-733X
Bruno ReissmannDepartment of Cardiology, University Heart and Vascular Center, University Medical Center Hamburg Eppendorf, Martinistraße 52, 20251 Hamburg, Hamburg, Germany.
Andreas MetznerDepartment of Cardiology, University Heart and Vascular Center, University Medical Center Hamburg Eppendorf, Martinistraße 52, 20251 Hamburg, Hamburg, Germany.
Paulus KirchhofDepartment of Cardiology, University Heart and Vascular Center, University Medical Center Hamburg Eppendorf, Martinistraße 52, 20251 Hamburg, Hamburg, Germany.ORCID 0000-0002-1881-0197
Dawood DarbarDivision of Cardiology, Departments of Medicine, University of Illinois at Chicago and Jesse Brown Veterans Administration, 840 South Wood Street, Suite 928 M/C 715, Chicago, IL 60612, USA.
Renate B SchnabelDepartment of Cardiology, University Heart and Vascular Center, University Medical Center Hamburg Eppendorf, Martinistraße 52, 20251 Hamburg, Hamburg, Germany.ORCID 0000-0001-7170-9509
Universität Hamburg · DEUniversity of Illinois Chicago · US

Funding

Human iPSC-derived atrial cardiomyocytes to model atrial fibrillation in a dishR01HL150586 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DARBAR, DAWOOD, KHETANI, SALMAN R · 2020 to 2023
$2.6M
Deciphering the genetic mechanisms of atrial fibrillationR01HL138737 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DARBAR, DAWOOD · 2017 to 2020
$2.6M
Training Program in Personalized Cardiovascular Medicine (TPIPCVM)T32HL139439 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DARBAR, DAWOOD · 2018 to 2022
$2.1M
British Heart Foundation FS/13/43/30324British Heart Foundation PG/17/30/32961British Heart Foundation PG/20/22/35093NHLBI NIH HHS R01 HL138737NHLBI NIH HHS R01 HL150586NHLBI NIH HHS T32 HL139439
6 · The paper itself

Abstract

The prevalence and economic burden of atrial fibrillation (AF) are predicted to more than double over the next few decades. In addition to anticoagulation and treatment of concomitant cardiovascular conditions, early and standardized rhythm control therapy reduces cardiovascular outcomes as compared with a rate control approach, favouring the restoration, and maintenance of sinus rhythm safely. Current therapies for rhythm control of AF include antiarrhythmic drugs (AADs) and catheter ablation (CA). However, response in an individual patient is highly variable with some remaining free of AF for long periods on antiarrhythmic therapy, while others require repeat AF ablation within weeks. The limited success of rhythm control therapy for AF is in part related to incomplete understanding of the pathophysiological mechanisms and our inability to predict responses in individual patients. Thus, a major knowledge gap is predicting which patients with AF are likely to respond to rhythm control approach. Over the last decade, tremendous progress has been made in defining the genetic architecture of AF with the identification of rare mutations in cardiac ion channels, signalling molecules, and myocardial structural proteins associated with familial (early-onset) AF. Conversely, genome-wide association studies have identified common variants at over 100 genetic loci and the development of polygenic risk scores has identified high-risk individuals. Although retrospective studies suggest that response to AADs and CA is modulated in part by common genetic variation, the development of a comprehensive clinical and genetic risk score may enable the translation of genetic data to the bedside care of AF patients. Given the economic impact of the AF epidemic, even small changes in therapeutic efficacy may lead to substantial improvements for patients and health care systems.

Indexed as

Genetic VariationGenomicsAnimalsAnti-Arrhythmia AgentsAtrial FibrillationCatheter AblationClinical Decision-MakingGenetic Predisposition to DiseaseHumansPhenotypePrecision MedicinePredictive Value of TestsPrognosisRisk AssessmentRisk FactorsAnti-Arrhythmia AgentsAntiarrhythmic drugsArrhythmiasAtrial fibrillationCatheter ablationGenetic variationGenotypeResponse

Identifiers

PMID33982075
PMCPMC8208749
OpenAlexW3162345918

What OpenQuestion holds

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Registered trials

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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.