Evidence map›Paper›PMID 21886622›Full record

ArticleFrontiers in physiology2011

Cardiac electromechanical models: from cell to organ.

Natalia A Trayanova, John Jeremy Rice

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. A Contemporary Look at Biomechanical Models of Myocardium.Annual review of biomedical engineering · 2019
    Review
  18. Article
  19. Position Paper Computational Cardiology.IEEE journal of biomedical and health informatics · 2019
    Article
  20. Increased thin filament activation enhances alternans in human chronic atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2018
    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.

Natalia A TrayanovaDepartment of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University Baltimore, MD, USA.
John Jeremy Rice
Johns Hopkins University · US

Funding

Resynchronizing the Failing Heart: Insights from a Multiscale Cardiac ModelR01HL103428 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2011 to 2014
$2.3M
Defibrillation Mechanisms in Infarcted HeartsR01HL082729 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2007 to 2010
$2.1M
NHLBI NIH HHS R01 HL082729NHLBI NIH HHS R01 HL103428
6 · The paper itself

Abstract

The heart is a multiphysics and multiscale system that has driven the development of the most sophisticated mathematical models at the frontiers of computational physiology and medicine. This review focuses on electromechanical (EM) models of the heart from the molecular level of myofilaments to anatomical models of the organ. Because of the coupling in terms of function and emergent behaviors at each level of biological hierarchy, separation of behaviors at a given scale is difficult. Here, a separation is drawn at the cell level so that the first half addresses subcellular/single-cell models and the second half addresses organ models. At the subcellular level, myofilament models represent actin-myosin interaction and Ca-based activation. The discussion of specific models emphasizes the roles of cooperative mechanisms and sarcomere length dependence of contraction force, considered to be the cellular basis of the Frank-Starling law. A model of electrophysiology and Ca handling can be coupled to a myofilament model to produce an EM cell model, and representative examples are summarized to provide an overview of the progression of the field. The second half of the review covers organ-level models that require solution of the electrical component as a reaction-diffusion system and the mechanical component, in which active tension generated by the myocytes produces deformation of the organ as described by the equations of continuum mechanics. As outlined in the review, different organ-level models have chosen to use different ionic and myofilament models depending on the specific application; this choice has been largely dictated by compromises between model complexity and computational tractability. The review also addresses application areas of EM models such as cardiac resynchronization therapy and the role of mechano-electric coupling in arrhythmias and defibrillation.

Indexed as

actinactivationactive tensionelectromechanical modelheartmyofilamentmyosinstretch-induced arrhythmias

Identifiers

PMID21886622
PMCPMC3154390
OpenAlexW1966543040

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.