Evidence map›Paper›PMID 28964161›Full record

ArticleChaos (Woodbury, N.Y.)2017

Modeling dynamics in diseased cardiac tissue: Impact of model choice.

Tanmay A Gokhale, Eli Medvescek, Craig S Henriquez

Open access · greenAbstract read
In one paragraph

Article in Chaos (Woodbury, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  10. Normal and fibrotic liver parenchyma respond differently to irreversible electroporation.HPB : the official journal of the International Hepato Pancreato Biliary Association · 2019
    Article
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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 at 1 institution in 1 country.

Tanmay A GokhaleDepartment of Biomedical Engineering, Duke University, Durham, North Carolina 27708-0281, USA.ORCID 0000000294362058
Eli MedvescekDepartment of Biomedical Engineering, Duke University, Durham, North Carolina 27708-0281, USA.
Craig S HenriquezDepartment of Biomedical Engineering, Duke University, Durham, North Carolina 27708-0281, USA.
Duke University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007171 · NIGMS · DUKE UNIVERSITY · PI KONTOS, CHRISTOPHER D · 1985 to 2021
$31.2M
In Vitro and In Situ Engineering of Fibroblasts for Cardiac RepairR01HL132389 · NHLBI · DUKE UNIVERSITY · PI BURSAC, NENAD · 2016 to 2019
$2.0M
Engineering of Human Excitable Tissues from Unexcitable CellsR01HL126524 · NHLBI · DUKE UNIVERSITY · PI BURSAC, NENAD · 2016 to 2019
$1.9M
Modeling Cardiac Impulse Propagation at the MicroscaleR01HL093711 · NHLBI · DUKE UNIVERSITY · PI HENRIQUEZ, CRAIG S · 2009 to 2013
$1.8M
NHLBI NIH HHS R01 HL093711NHLBI NIH HHS R01 HL126524NHLBI NIH HHS R01 HL132389NIGMS NIH HHS T32 GM007171
6 · The paper itself

Abstract

Cardiac arrhythmias have been traditionally simulated using continuous models that assume tissue homogeneity and use a relatively large spatial discretization. However, it is believed that the tissue fibrosis and collagen deposition, which occur on a micron-level, are critical factors in arrhythmogenesis in diseased tissues. Consequently, it remains unclear how well continuous models, which use averaged electrical properties, are able to accurately capture complex conduction behaviors such as re-entry in fibrotic tissues. The objective of this study was to compare re-entrant behavior in discrete microstructural models of fibrosis and in two types of equivalent continuous models, a homogenous continuous model and a hybrid continuous model with distinct heterogeneities. In the discrete model, increasing levels of tissue fibrosis lead to a substantial increase in the re-entrant cycle length which is inadequately reflected in the homogenous continuous models. These cycle length increases appear to be primarily due to increases in the tip path length and to altered restitution behavior, and suggest that it is critical to consider the discrete effects of fibrosis on conduction when studying arrhythmogenesis in fibrotic myocardium. Hybrid models are able to accurately capture some aspects of re-entry and, if carefully tuned, may provide a framework for simulating conduction in diseased tissues with both accuracy and efficiency.

Indexed as

Models, CardiovascularCollagenFibrosisHeartCollagen

Identifiers

PMID28964161
PMCPMC5568867
OpenAlexW2747687017

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.