Evidence map›Paper›PMID 22920484›Full record

ReviewCurrent cardiology reviews2012

Triggers and anatomical substrates in the genesis and perpetuation of atrial fibrillation.

Damián Sánchez-Quintana, José Ramón López-Mínguez, Gonzalo Pizarro, Margarita Murillo, José Angel Cabrera

Open access · greenAbstract readReview
In one paragraph

Review in Current cardiology reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Superior vena cava and atrial cardiomyopathy: role of adjunctive superior vena cava isolation ablation in atrial fibrillation.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 · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Obesity-Related Atrial Fibrillation: Cardiac Manifestation of a Systemic Disease.Journal of cardiovascular development and disease · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Human Pulmonary Vein Myocardial Sleeve Autonomic Neural Density and Cardiovascular Mortality.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Damián Sánchez-QuintanaDepartamento de Anatomía y Biología Celular, Facultad de Medicina, Universidad de Extremadura, Badajoz, Spain. dasaqui55@yahoo.com
José Ramón López-Mínguez
Gonzalo Pizarro
Margarita Murillo
José Angel Cabrera
Universidad de Extremadura · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The definition of atrial fibrillation (AF) as a functional electrical disorder does not reflect the significant underlying structural abnormalities. Atrial and Pulmonary Vein (PV) muscle sleeve microstructural remodeling is present, and establishes a vulnerable substrate for AF maintenance. In spite of an incomplete understanding of the anatomo-functional basis for AF, current evidence demonstrates that this arrhythmia usually requires a trigger for initiation and a vulnerable electrophysiological and/or anatomical substrate for maintenance. It is still unclear whether the trigger mechanisms include focal enhanced automaticity, triggered activity and/or micro re-entry from myocardial tissue. Initiation of AF can be favored by both parasympathetic and sympathetic stimulation, which also seem to play a role in maintaining AF. Finally, evolving clinical evidence demonstrates that inflammation is associated with new-onset and recurrent AF through a mechanism that possibly involves cellular degeneration, apoptosis, and subsequent atrial fibrosis.

Indexed as

Atrial FibrillationCoronary SinusFibrosisHeart AtriaHumansIon ChannelsMagnetic Resonance AngiographyMyocarditisMyocardiumPulmonary VeinsSinoatrial NodeVena Cava, SuperiorIon Channels

Identifiers

PMID22920484
PMCPMC3492815
OpenAlexW2139875120

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.