Evidence map›Paper›PMID 40207039›Full record

ArticleMedizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V2025

Disease mechanism and novel drug therapies for atrial fibrillation.

Constanze Schmidt, Felix Wiedmann

Abstract read
In one paragraph

Article in Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V, 2025. 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
–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

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

2 authors.

Constanze SchmidtMedical University Hospital Heidelberg Department of Cardiology Im Neuenheimer Feld 410 69120 Heidelberg Germany.ORCID https://orcid.org/0000-0001-5897-237X
Felix WiedmannMedical University Hospital Heidelberg Department of Cardiology Im Neuenheimer Feld 410 69120 Heidelberg Germany.ORCID https://orcid.org/0000-0001-8168-0025

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, affects over 3 % of adults globally, increasing risks for stroke, heart failure, and cognitive decline. Early rhythm control shows promise in improving AF prognosis, and catheter ablation remains an effective, safe option, especially for paroxysmal AF. However, high recurrence rates with antiarrhythmic drugs and ablation persist, particularly in cases of persistent AF. Emerging research on molecular mechanisms has led to innovative therapeutic strategies targeting these pathways, offering hope for more effective AF management. This review explores recent insights into the complex pathophysiology of AF, with a particular focus on ion channel dysfunction, calcium mishandling, oxidative stress, and fibrosis. It further considers how these factors will inspire new therapeutic options.

Indexed as

Antiarrhythmic therapyAtrial fibrillationcellular electrophysiologyMolecular pathophysiologyTASK-1 potassium channels

Identifiers

PMID40207039
PMCPMC11976400

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.