Evidence map›Paper›PMID 37932605›Full record

ReviewHerzschrittmachertherapie & Elektrophysiologie2024

[Genetic basis of atrial fibrillation-on the road to precision medicine].

Shinwan Kany, Renate B Schnabel

Open access · hybridAbstract readEnglish AbstractReview
In one paragraph

Review in Herzschrittmachertherapie & Elektrophysiologie, 2024. 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
0.3field-weighted citation impact, top 28% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

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

2 authors at 2 institutions in 2 countries.

Shinwan KanyKlinik für Kardiologie, Universitäres Herz- und Gefäßzentrum Hamburg-Eppendorf, Universitätsklinikum Hamburg-Eppendorf, Martinistraße 52, 20251, Hamburg, Deutschland. s.kany@uke.de.
Renate B SchnabelKlinik für Kardiologie, Universitäres Herz- und Gefäßzentrum Hamburg-Eppendorf, Universitätsklinikum Hamburg-Eppendorf, Martinistraße 52, 20251, Hamburg, Deutschland.
Broad Institute · USGerman Climate Computing Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia and has complex genetic underpinnings. Despite advancements in treatment, mortality of AF patients remains high. This review discusses the genetic basis of AF and its implications for diagnosis and therapy. Although AF pathology has long been known to include a hereditary component, the first genes associated with AF were not identified until the early 2000s. Subsequent research with genome-wide association studies (GWAS) has implicated other genes and numerous genetic variants in AF. These studies have revealed nearly 140 different regions in the DNA with genome-wide significance associated with AF. In addition to common variants, rare variants with large effects have also been identified. The integration of these genetic findings into clinical practice holds promise for improving AF diagnosis and treatment, moving us closer to precision medicine. However, challenges remain, including the need for more diverse genetic data of non-European ancestry and improved genetic analyses of responses to AF therapy.

Indexed as

Atrial FibrillationGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPrecision MedicineCardiac arrhythmiasGeneticsGenome-wide association studiesPolygenic risk scoresRare variants

Identifiers

PMID37932605
PMCPMC10879292
OpenAlexW4388409291

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.