Evidence map›Paper›PMID 23104912›Full record

ArticleEuropace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology2012

Microscopic variations in interstitial and intracellular structure modulate the distribution of conduction delays and block in cardiac tissue with source-load mismatch.

Marjorie Letitia Hubbard, Craig S Henriquez

Open access · bronzeAbstract read
In one paragraph

Article in 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, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 25 years of basic and translational science in EP Europace: novel insights into arrhythmia mechanisms and therapeutic strategies.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 · 2023
    Review
  5. Article
  6. Article
  7. Reduced NaAmerican journal of physiology. Heart and circulatory physiology · 2020
    Article
  8. Cardiomyocyte-myofibroblast contact dynamism is modulated by connexin-43.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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 at 1 institution in 1 country.

Marjorie Letitia HubbardDepartment of Biomedical Engineering, Duke University, Durham, NC 27708, USA. mlh23@duke.edu
Craig S Henriquez
Duke University · US

Funding

Modeling Cardiac Impulse Propagation at the MicroscaleR01HL093711 · NHLBI · DUKE UNIVERSITY · PI HENRIQUEZ, CRAIG S · 2009 to 2013
$1.8M
NHLBI NIH HHS HL093711-01A2NHLBI NIH HHS R01 HL093711
6 · The paper itself

Abstract

aimsReentrant activity in the heart is often correlated with heterogeneity in both the intracellular structure and the interstitial structure surrounding cells; however, the combined effect of cardiac microstructure and interstitial resistivity in regions of source-load mismatch is largely unknown. The aim of this study was to investigate how microstructural variations in cell arrangement and increased interstitial resistivity influence the spatial distribution of conduction delays and block in poorly coupled regions of tissue. METHODS AND

resultsTwo-dimensional 0.6 cm × 0.6 cm computer models with idealized and realistic cellular structure were used to represent a monolayer of ventricular myocytes. Gap junction connections were distributed around the periphery of each cell at 10 μm intervals. Regions of source-load mismatch were added to the models by increasing the gap junction and interstitial resistivity in one-half of the tissue. Heterogeneity in cell shape and cell arrangement along the boundary between well-coupled and poorly coupled tissue increased variability in longitudinal conduction delays to as much as 10 ms before the onset of conduction block, resulting in wavefront breakthroughs with pronounced curvature at distinct points along the boundary. Increasing the effective interstitial resistivity reduced source-load mismatch at the transition boundary, which caused a decrease in longitudinal conduction delay and an increase in the number of wavefront breakthroughs.

conclusionMicrostructural variations in cardiac tissue facilitate the formation of isolated sites of wavefront breakthrough that may enable abnormal electrical activity in small regions of diseased tissue to develop into more widespread reentrant activity.

Indexed as

Models, CardiovascularAction PotentialsAnimalsComputer SimulationGuinea PigsHeart Conduction SystemMembrane PotentialsMyocytes, CardiacNeural Conduction

Identifiers

PMID23104912
PMCPMC3482616
OpenAlexW2138137694

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.