Evidence map›Paper›PMID 34831442›Full record

ReviewCells2021

Electrophysiological Consequences of Cardiac Fibrosis.

Sander Verheule, Ulrich Schotten

Registry-linked trialAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07201363 (The Role of Inflammation and Fibrosis in the Development of Conduction Disorders After Transcatheter Aortic Valve Implantation), which is not on this map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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.

NCT07201363 recruitingnot on this mapstarted 2024, after this paper: background citation

The Role of Inflammation and Fibrosis in the Development of Conduction Disorders After Transcatheter Aortic Valve Implantation

TypeobservationalSponsorClinical Hospital Center RijekaRan2024 to 2026Enrolled102ConditionsTAVI(Transcatheter Aortic Valve Implantation), Conduction Disorder, Aortic Stenosis, Permanent Pacemaker ImplantationArmsBiomarkers of inflammation and fibrosis in pre-procedural serum blood samples, Transthoracic echocardiography with myocardial deformation analysis and staging according to the extent of cardiac damage related to AS
3 · Its place in the literature

Who cites it

58 citing papers in PubMed.

  1. Article
  2. Ventricular tachycardia in mid-ventricular obstructive hypertrophy: electrophysiological and pathological findings, and optimal surgical procedure.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Article
  3. Observational
  4. Article
  5. Article
  6. Histological evaluation of clinically defined atrial cardiomyopathy stages and their association with atrial fibrillation burden under continuous monitoring for a 2.5-year follow-up.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 · 2026
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Low and High Pressor Doses of Ang II Lead to Two Distinct Phenotypes of Hypertensive Heart Disease in Mice.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
  15. Metabolic and Inflammatory Mechanisms Driving Atrial Fibrillation.Annual review of pharmacology and toxicology · 2026
    Review
  16. Review
  17. Article
  18. The spatial ventricular gradient is a non-invasive, vectorcardiographic correlate of cardiac fibrosis.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Article
  19. Full-field surrogate modeling of cardiac electrophysiology encoding geometric variability.Computer methods in applied mechanics and engineering · 2026
    Article
  20. 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

2 authors.

Sander VerheuleDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, 6200 MD Maastricht, The Netherlands.ORCID 0000-0001-5196-5425
Ulrich SchottenDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, 6200 MD Maastricht, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For both the atria and ventricles, fibrosis is generally recognized as one of the key determinants of conduction disturbances. By definition, fibrosis refers to an increased amount of fibrous tissue. However, fibrosis is not a singular entity. Various forms can be distinguished, that differ in distribution: replacement fibrosis, endomysial and perimysial fibrosis, and perivascular, endocardial, and epicardial fibrosis. These different forms typically result from diverging pathophysiological mechanisms and can have different consequences for conduction. The impact of fibrosis on propagation depends on exactly how the patterns of electrical connections between myocytes are altered. We will therefore first consider the normal patterns of electrical connections and their regional diversity as determinants of propagation. Subsequently, we will summarize current knowledge on how different forms of fibrosis lead to a loss of electrical connectivity in order to explain their effects on propagation and mechanisms of arrhythmogenesis, including ectopy, reentry, and alternans. Finally, we will discuss a histological quantification of fibrosis. Because of the different forms of fibrosis and their diverging effects on electrical propagation, the total amount of fibrosis is a poor indicator for the effect on conduction. Ideally, an assessment of cardiac fibrosis should exclude fibrous tissue that does not affect conduction and differentiate between the various types that do; in this article, we highlight practical solutions for histological analysis that meet these requirements.

Indexed as

Electrophysiological PhenomenaAnimalsConfounding Factors, EpidemiologicDisease Models, AnimalFibrosisHeart Conduction SystemHumansMyocardiumarrhythmiasconductionfibrosishearttissue structure

Identifiers

PMID34831442
PMCPMC8625398

What OpenQuestion holds

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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.