Evidence map›Paper›PMID 29921647›Full record

ReviewPharmacological reviews2018

Mechanisms and Drug Development in Atrial Fibrillation.

David Calvo, David Filgueiras-Rama, José Jalife

Abstract readReview
In one paragraph

Review in Pharmacological reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
–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

42 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. mScience China. Life sciences · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Therapeutic advances in atrial fibrillation based on animal models.Journal of Zhejiang University. Science. B · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Advances in basic and translational research in atrial fibrillation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  17. Review
  18. Review
  19. Article
  20. Bioengineered peptibodies as blockers of ion channels.Proceedings of the National Academy of Sciences of the United States of America · 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

3 authors.

David CalvoDepartment of Cardiology, Arrhythmia Unit, Hospital Universitario Central de Asturias and Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain (D.C.); Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain (D.F.-R., J.J.); Department of Cardiology, Arrhythmia Unit, Hospital Clínico Universitario San Carlos, Madrid, Spain (D.F.-R.); Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain (D.F.-R., J.J.); and Center for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan (J.J.).
David Filgueiras-RamaDepartment of Cardiology, Arrhythmia Unit, Hospital Universitario Central de Asturias and Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain (D.C.); Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain (D.F.-R., J.J.); Department of Cardiology, Arrhythmia Unit, Hospital Clínico Universitario San Carlos, Madrid, Spain (D.F.-R.); Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain (D.F.-R., J.J.); and Center for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan (J.J.).
José JalifeDepartment of Cardiology, Arrhythmia Unit, Hospital Universitario Central de Asturias and Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain (D.C.); Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain (D.F.-R., J.J.); Department of Cardiology, Arrhythmia Unit, Hospital Clínico Universitario San Carlos, Madrid, Spain (D.F.-R.); Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain (D.F.-R., J.J.); and Center for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan (J.J.) jjalife@med.umich.edu.

Funding

Intermolecular Interactions of NaV1.5 and Kir2.1 In Ion Channel DiseasesR01HL122352 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERENFELD, OMER · 2015 to 2018
$1.9M
NHLBI NIH HHS R01 HL122352
6 · The paper itself

Abstract

Atrial fibrillation is a highly prevalent cardiac arrhythmia and the most important cause of embolic stroke. Although genetic studies have identified an increasing assembly of AF-related genes, the impact of these genetic discoveries is yet to be realized. In addition, despite more than a century of research and speculation, the molecular and cellular mechanisms underlying AF have not been established, and therapy for AF, particularly persistent AF, remains suboptimal. Current antiarrhythmic drugs are associated with a significant rate of adverse events, particularly proarrhythmia, which may explain why many highly symptomatic AF patients are not receiving any rhythm control therapy. This review focuses on recent advances in AF research, including its epidemiology, genetics, and pathophysiological mechanisms. We then discuss the status of antiarrhythmic drug therapy for AF today, reviewing molecular mechanisms, and the possible clinical use of some of the new atrial-selective antifibrillatory agents, as well as drugs that target atrial remodeling, inflammation and fibrosis, which are being tested as upstream therapies to prevent AF perpetuation. Altogether, the objective is to highlight the magnitude and endemic dimension of AF, which requires a significant effort to develop new and effective antiarrhythmic drugs, but also improve AF prevention and treatment of risk factors that are associated with AF complications.

Indexed as

AnimalsAnti-Arrhythmia AgentsAtrial FibrillationContinuous Positive Airway PressureDrug DevelopmentHumansSleep Apnea SyndromesAnti-Arrhythmia Agents

Identifiers

PMID29921647
PMCPMC6010660

What OpenQuestion holds

Textmetadata
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.