Evidence map›Paper›PMID 23934857›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2013

Mechanistic insight into prolonged electromechanical delay in dyssynchronous heart failure: a computational study.

Jason Constantino, Yuxuan Hu, Albert C Lardo, Natalia A Trayanova

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Electromechanical wave imaging vs electrocardiographic imaging: a direct comparison of non-invasive ventricular activation mapping modalities.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
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  9. 4D cardiac electromechanical activation imaging.Computers in biology and medicine · 2019
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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

4 authors.

Jason ConstantinoDepartment of Biomedical Engineering and Institute of Computational Medicine, The Johns Hopkins University, Baltimore, Maryland; and.
Yuxuan Hu
Albert C Lardo
Natalia A Trayanova

Funding

Resynchronizing the Failing Heart: Insights from a Multiscale Cardiac ModelR01HL103428 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2011 to 2014
$2.3M
Image-based models of electromechanics in normal and failing heartsF31HL103090 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CONSTANTINO, JASON LANCE · 2010 to 2012
$125k
NHLBI NIH HHS F31-HL-103090NHLBI NIH HHS R01 HL103428NHLBI NIH HHS R01-HL-103428
6 · The paper itself

Abstract

In addition to the left bundle branch block type of electrical activation, there are further remodeling aspects associated with dyssynchronous heart failure (HF) that affect the electromechanical behavior of the heart. Among the most important are altered ventricular structure (both geometry and fiber/sheet orientation), abnormal Ca(2+) handling, slowed conduction, and reduced wall stiffness. In dyssynchronous HF, the electromechanical delay (EMD), the time interval between local myocyte depolarization and myofiber shortening onset, is prolonged. However, the contributions of the four major HF remodeling aspects in extending EMD in the dyssynchronous failing heart remain unknown. The goal of this study was to determine the individual and combined contributions of HF-induced remodeling aspects to EMD prolongation. We used MRI-based models of dyssynchronous nonfailing and HF canine electromechanics and constructed additional models in which varying combinations of the four remodeling aspects were represented. A left bundle branch block electrical activation sequence was simulated in all models. The simulation results revealed that deranged Ca(2+) handling is the primary culprit in extending EMD in dyssynchronous HF, with the other aspects of remodeling contributing insignificantly. Mechanistically, we found that abnormal Ca(2+) handling in dyssynchronous HF slows myofiber shortening velocity at the early-activated septum and depresses both myofiber shortening and stretch rate at the late-activated lateral wall. These changes in myofiber dynamics delay the onset of myofiber shortening, thus giving rise to prolonged EMD in dyssynchronous HF.

Indexed as

AnimalsBundle-Branch BlockCalciumDogsHeartHeart Conduction SystemHeart FailureMagnetic Resonance ImagingMembrane PotentialsModels, CardiovascularMyocardial ContractionMyocytes, CardiacTime FactorsVentricular RemodelingCalciumcardiac electromechanicsdyssynchronous heart failureelectromechanical modeling

Identifiers

PMID23934857
PMCPMC3798786

What OpenQuestion holds

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Registered trials

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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.