Evidence map›Paper›PMID 24560668›Full record

ArticleJournal of molecular and cellular cardiology2014

Transmural heterogeneity of cellular level power output is reduced in human heart failure.

Premi Haynes, Kristofer E Nava, Benjamin A Lawson, Charles S Chung, Mihail I Mitov, Stuart G Campbell, Arnold J Stromberg, Sakthivel Sadayappan, Mark R Bonnell, Charles W Hoopes and 1 more

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Stress relaxation rates of myocardium from failing and non-failing hearts.Biomechanics and modeling in mechanobiology · 2025
    Article
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  17. A NovelFrontiers in physiology · 2022
    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

11 authors at 2 institutions in 1 country.

Premi HaynesDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Kristofer E NavaDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Benjamin A LawsonDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Charles S ChungDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Mihail I MitovDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Stuart G CampbellDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Arnold J StrombergDepartment of Statistics, University of Kentucky, Lexington, KY, USA.
Sakthivel SadayappanDepartment of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University, Chicago, USA.
Mark R BonnellDivision of Cardiothoracic Surgery, University of Kentucky, Lexington, KY, USA.
Charles W HoopesDivision of Cardiothoracic Surgery, University of Kentucky, Lexington, KY, USA.
Kenneth S CampbellDepartment of Physiology, University of Kentucky, Lexington, KY, USA; Center for Muscle Biology, University of Kentucky, Lexington, KY, USA. Electronic address: k.s.campbell@uky.edu.
University of Kentucky · USLoyola University Chicago · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
KENTUCKY CENTER FOR CLINICAL AND TRANSLATIONAL SCIENCEUL1RR033173 · NCRR · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2011 to 2011
$3.5M
Myocardial Stiffness in Diastolic Heart FailureR01HL090749 · NHLBI · UNIVERSITY OF KENTUCKY · PI CAMPBELL, KENNETH S · 2008 to 2012
$1.6M
NCATS NIH HHS TR000117NCATS NIH HHS UL1 TR000117NCI NIH HHS P30 CA177558NCRR NIH HHS UL1 RR033173NHLBI NIH HHS HL090749NHLBI NIH HHS R01 HL090749
6 · The paper itself

Abstract

Heart failure is associated with pump dysfunction and remodeling but it is not yet known if the condition affects different transmural regions of the heart in the same way. We tested the hypotheses that the left ventricles of non-failing human hearts exhibit transmural heterogeneity of cellular level contractile properties, and that heart failure produces transmural region-specific changes in contractile function. Permeabilized samples were prepared from the sub-epicardial, mid-myocardial, and sub-endocardial regions of the left ventricular free wall of non-failing (n=6) and failing (n=10) human hearts. Power, an in vitro index of systolic function, was higher in non-failing mid-myocardial samples (0.59±0.06μWmg(-1)) than in samples from the sub-epicardium (p=0.021) and the sub-endocardium (p=0.015). Non-failing mid-myocardial samples also produced more isometric force (14.3±1.33kNm(-2)) than samples from the sub-epicardium (p=0.008) and the sub-endocardium (p=0.026). Heart failure reduced power (p=0.009) and force (p=0.042) but affected the mid-myocardium more than the other transmural regions. Fibrosis increased with heart failure (p=0.021) and mid-myocardial tissue from failing hearts contained more collagen than matched sub-epicardial (p<0.001) and sub-endocardial (p=0.043) samples. Power output was correlated with the relative content of actin and troponin I, and was also statistically linked to the relative content and phosphorylation of desmin and myosin light chain-1. Non-failing human hearts exhibit transmural heterogeneity of contractile properties. In failing organs, region-specific fibrosis produces the greatest contractile deficits in the mid-myocardium. Targeting fibrosis and sarcomeric proteins in the mid-myocardium may be particularly effective therapies for heart failure.

Indexed as

ActinsAdolescentAdultAgedDesminEndocardiumFemaleFibrosisGene ExpressionHeart FailureHeart TransplantationHeart VentriclesHumansIsometric ContractionMaleMiddle AgedActinsDesminMyosin Light ChainsTroponin ICollagenLeft ventricular functionMechanicsMyofilament proteinSarcomere

Identifiers

PMID24560668
PMCPMC4037376
OpenAlexW1996229856

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.