Evidence map›Paper›PMID 28851517›Full record

ArticleProgress in biophysics and molecular biology2017

An integrative appraisal of mechano-electric feedback mechanisms in the heart.

Viviane Timmermann, Lars A Dejgaard, Kristina H Haugaa, Andrew G Edwards, Joakim Sundnes, Andrew D McCulloch, Samuel T Wall

Open access · hybridAbstract read
In one paragraph

Article in Progress in biophysics and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 49 citations in OpenAlex.

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  12. A survey of pathways for mechano-electric coupling in the atria.Progress in biophysics and molecular biology · 2021
    Article
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  17. Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
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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

7 authors at 4 institutions in 2 countries.

Viviane TimmermannSimula Research Laboratory, Martin Linges vei 25, Fornebu, 1364, Norway; Center for Cardiological Innovation, Songsvannsveien 9, Oslo, 0372, Norway; University California San Diego, 9500 Gilman Drive, La Jolla, CA, United States; University of Oslo, Gaustadallen 23 B, Oslo, 0373, Norway. Electronic address: viviane@simula.no.
Lars A DejgaardCenter for Cardiological Innovation, Songsvannsveien 9, Oslo, 0372, Norway; Department of Cardiology, Oslo University Hospital, Norway.
Kristina H HaugaaCenter for Cardiological Innovation, Songsvannsveien 9, Oslo, 0372, Norway; Department of Cardiology, Oslo University Hospital, Norway.
Andrew G EdwardsSimula Research Laboratory, Martin Linges vei 25, Fornebu, 1364, Norway; Center for Cardiological Innovation, Songsvannsveien 9, Oslo, 0372, Norway; University of Oslo, Gaustadallen 23 B, Oslo, 0373, Norway.
Joakim SundnesSimula Research Laboratory, Martin Linges vei 25, Fornebu, 1364, Norway; Center for Cardiological Innovation, Songsvannsveien 9, Oslo, 0372, Norway; University of Oslo, Gaustadallen 23 B, Oslo, 0373, Norway.
Andrew D McCullochUniversity California San Diego, 9500 Gilman Drive, La Jolla, CA, United States.
Samuel T WallSimula Research Laboratory, Martin Linges vei 25, Fornebu, 1364, Norway; Center for Cardiological Innovation, Songsvannsveien 9, Oslo, 0372, Norway. Electronic address: samwall@simula.no.
Simula Research Laboratory · NOOslo University Hospital · NOInnovation Norway (Norway) · NOUniversity of California, San Diego · US

Funding

National Biomedical Computation Resource - Competitive Revision SupplementP41GM103426 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AMARO, ROMMIE E · 2012 to 2019
$14.0M
The Cardiac Atlas ProjectR01HL121754 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D., OMENS, JEFFREY H. · 2014 to 2023
$5.0M
Predictive multiscale in silico cardio-pharmacologyU01HL126273 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CLANCY, COLLEEN E · 2015 to 2019
$3.8M
Multi-scale Systems Model of Murine Heart FailureR01HL105242 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERS, DONALD M, MCCULLOCH, ANDREW D. · 2012 to 2016
$3.5M
Analyzing the Cardiac Power Grid: Adaptive responses to fluctuating local demandU01HL122199 · NHLBI · UNIVERSITY OF WASHINGTON · PI BEARD, DANIEL A, DASH, RANJAN K · 2015 to 2019
$3.3M
Systems Biology of Hypertrophic Heart Disease from Molecular Pathways to Organ SystemR01HL137100 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D. · 2017 to 2020
$2.0M
Multi-Scale Modeling of the Failing Heart for Cardiac Rysynchronization TherapyR01HL096544 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D. · 2009 to 2013
$1.8M
NHLBI NIH HHS R01 HL096544NHLBI NIH HHS R01 HL105242NHLBI NIH HHS R01 HL121754NHLBI NIH HHS R01 HL137100NHLBI NIH HHS U01 HL122199NHLBI NIH HHS U01 HL126273NIGMS NIH HHS P41 GM103426
6 · The paper itself

Abstract

Mechanically-induced alterations in cardiac electrophysiology are referred to as mechano-electric feedback (MEF), and play an important role in electrical regulation of cardiac performance. The influence of mechanical stress and strain on electrophysiology has been investigated at all levels, however the role of MEF in arrhythmia remains poorly understood. During the normal contraction of the heart, mechano-sensitive processes are an implicit component of cardiac activity. Under abnormal mechanical events, stretch-activated mechanisms may contribute to local or global changes in electrophysiology (EP). While such mechanisms have been hypothesised to be involved in mechanically-initiated arrhythmias, the details of these mechanisms and their importance remain elusive. We assess the theoretical role of stretch mechanisms using coupled models of cellular electrophysiology and sarcomere contraction dynamics. Using models of single ventricular myocytes, we first investigated the potential MEF contributions of stretch-activated currents (SAC), and stretch-induced myofilament calcium release, to test how strain and fibrosis may alter cellular electrophysiology. For all models investigated, SACs were alone not sufficient to create a pro-arrhythmic perturbation of the action potential with stretch. However, when combined with stretch-induced myofilament calcium release, the action potential could be shortened depending on the timing of the strain. This effect was highly model dependent, with a canine epicardial EP model being the most sensitive. These model results suggest that known mechanisms of mechano-electric coupling in cardiac myocyte may be sufficient to be pro-arrhythmic, but only in combination and under specific strain patterns.

Indexed as

Electrophysiological PhenomenaFeedback, PhysiologicalMechanical PhenomenaModels, CardiovascularHeartMyocytes, CardiacArrhythmiaComputational modellingHuman electromechanical modelMechano-electric feedback

Identifiers

PMID28851517
PMCPMC5716869
OpenAlexW2746306395

What OpenQuestion holds

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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.