Evidence map›Paper›PMID 25429272›Full record

ReviewFrontiers in physiology2014

Exploring susceptibility to atrial and ventricular arrhythmias resulting from remodeling of the passive electrical properties in the heart: a simulation approach.

Natalia A Trayanova, Patrick M Boyle, Hermenegild J Arevalo, Sohail Zahid

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Towards personalized computational modelling of the fibrotic substrate for atrial arrhythmia.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 · 2016
    Review
  11. Article
  12. Article
  13. Review
  14. Predicting the risk of sudden cardiac death.The Journal of physiology · 2016
    Review
  15. Article
  16. Review
  17. Review
  18. 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

4 authors.

Natalia A TrayanovaDepartment of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University Baltimore, MD, USA.
Patrick M BoyleDepartment of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University Baltimore, MD, USA.
Hermenegild J ArevaloDepartment of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University Baltimore, MD, USA.
Sohail ZahidDepartment of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University Baltimore, MD, USA.

Funding

BIOMEDICAL ENGINEERING TRAINING PROGRAMT32GM007057 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI KANOLD, PATRICK O, KARCHIN, RACHEL · 1985 to 2023
$10.4M
Virtual Electrophysiology LaboratoryDP1HL123271 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2013 to 2017
$4.0M
Redox Modification of the Arrhythmic Substrate in Heart FailureR01HL105216 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN, TRAYANOVA, NATALIA A. · 2011 to 2014
$3.0M
Resynchronizing the Failing Heart: Insights from a Multiscale Cardiac ModelR01HL103428 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2011 to 2014
$2.3M
NHLBI NIH HHS DP1 HL123271NHLBI NIH HHS R01 HL103428NHLBI NIH HHS R01 HL105216NIGMS NIH HHS T32 GM007057
6 · The paper itself

Abstract

Under diseased conditions, remodeling of the cardiac tissue properties ("passive properties") takes place; these are aspects of electrophysiological behavior that are not associated with active ion transport across cell membranes. Remodeling of the passive electrophysiological properties most often results from structural remodeling, such as gap junction down-regulation and lateralization, fibrotic growth infiltrating the myocardium, or the development of an infarct scar. Such structural remodeling renders atrial or ventricular tissue as a major substrate for arrhythmias. The current review focuses on these aspects of cardiac arrhythmogenesis. Due to the inherent complexity of cardiac arrhythmias, computer simulations have provided means to elucidate interactions pertinent to this spatial scale. Here we review the current state-of-the-art in modeling atrial and ventricular arrhythmogenesis as arising from the disease-induced changes in the passive tissue properties, as well as the contributions these modeling studies have made to our understanding of the mechanisms of arrhythmias in the heart. Because of the rapid advance of structural imaging methodologies in cardiac electrophysiology, we chose to present studies that have used such imaging methodologies to construct geometrically realistic models of cardiac tissue, or the organ itself, where the regional remodeling properties of the myocardium can be represented in a realistic way. We emphasize how the acquired knowledge can be used to pave the way for clinical applications of cardiac organ modeling under the conditions of structural remodeling.

Indexed as

arrhythmiacomputer modelingfibrosisinfarctstructural remodeling

Identifiers

PMID25429272
PMCPMC4228852

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.