ReviewNature reviews. Cardiology2013
Genetic mechanisms of atrial fibrillation: impact on response to treatment.
Review in Nature reviews. Cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Ethnic Contrasts in Stroke Risk Factors and the Atrial Fibrillation Paradox in the United Kingdom: Population-Based Study and Meta-Analysis.Neurology · 2025Pooled it
- Genetic background is associated with distinct patterns of proarrhythmogenic remodeling leading to atrial fibrillation in pigs with ischemic heart failure.Basic research in cardiology · 2026Article
- Review
- Digital Twin Models in Atrial Fibrillation: Charting the Future of Precision Therapy?Journal of personalized medicine · 2025Review
- EXPRESSION OF CONNEXIN-40 AND INTERLEUKIN 6 GENES IN PATIENTS WITH ATRIAL FIBRILLATION.Acta clinica Croatica · 2025Article
- A novel gain-of-function mutationAmerican journal of cardiovascular disease · 2025Article
- Transient titin-dependent ventricular defects during development lead to adult atrial arrhythmia and impaired contractility.iScience · 2024Article
- Genetics and Pharmacogenetics of Atrial Fibrillation: A Mechanistic Perspective.JACC. Basic to translational science · 2024Review
- The selective RyR2 inhibitor ent-verticilide suppresses atrial fibrillation susceptibility caused by Pitx2 deficiency.Journal of molecular and cellular cardiology · 2023Article
- Association Between rs2200733 Polymorphism of PITX2 Gene and the Risk of Atrial Fibrillation.Anatolian journal of cardiology · 2023Article
- Long-term amelioration of an early-onset familial atrial fibrillation model with AAV-mediated in vivo gene therapy.Fundamental research · 2022Article
- Transcriptional factors in calcium mishandling and atrial fibrillation development.Pflugers Archiv : European journal of physiology · 2021Review
- Bioengineering approaches to mature induced pluripotent stem cell-derived atrial cardiomyocytes to model atrial fibrillation.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Genetics of atrial fibrillation-practical applications for clinical management: if not now, when and how?Cardiovascular research · 2021Review
- Human induced pluripotent stem cell-derived atrial cardiomyocytes carrying an SCN5A mutation identify nitric oxide signaling as a mediator of atrial fibrillation.Stem cell reports · 2021Article
- Expanding the phenotype of CACNA1C mutation disorders.Molecular genetics & genomic medicine · 2021Article
- Predictive Accuracy of a Polygenic Risk Score for Postoperative Atrial Fibrillation After Cardiac Surgery.Circulation. Genomic and precision medicine · 2021Article
- Atrial Fibrillation in Inherited Channelopathies.Cardiac electrophysiology clinics · 2021Review
- Spatial Changes in the Atrial Fibrillation Wave-Dynamics After Using Antiarrhythmic Drugs: A Computational Modeling Study.Frontiers in physiology · 2021Article
- Big Data and Atrial Fibrillation: Current Understanding and New Opportunities.Journal of cardiovascular translational research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Atrial fibrillation (AF) is the most-common sustained arrhythmia observed in clinical practice, but response to therapy is highly variable between patients. Current drug therapies to suppress AF are incompletely and unpredictably effective and carry substantial risk of proarrhythmia and noncardiac toxicities. The limited success of therapy for AF is partially the result of heterogeneity of the underlying substrate, interindividual differences in disease mechanisms, and our inability to predict response to therapies in individual patients. In this Review, we discuss the evidence that variability in response to drug therapy is also conditioned by the underlying genetic substrate for AF. Increased susceptibility to AF is mediated through diverse genetic mechanisms, including modulation of the atrial action-potential duration, conduction slowing, and impaired cell-to-cell communication, as well as novel mechanisms, such as regulation of signalling proteins important in the pathogenesis of AF. However, the translation of genetic data to the care of the patients with AF has been limited because of poor understanding of the underlying mechanisms associated with common AF-susceptibility loci, a dearth of prospective, adequately powered studies, and the challenges associated with determining efficacy of antiarrhythmic drugs. What is apparent, however, is the need for appropriately designed, genotype-directed clinical trials.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.