Evidence map›Paper›PMID 29981798›Full record

ArticleJournal of molecular and cellular cardiology2018

Etiology-dependent impairment of relaxation kinetics in right ventricular end-stage failing human myocardium.

Jae-Hoon Chung, Brit L Martin, Benjamin D Canan, Mohammad T Elnakish, Nima Milani-Nejad, Nancy S Saad, Steven J Repas, J Eric J Schultz, Jason D Murray, Jessica L Slabaugh and 16 more

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 26 citations in OpenAlex.

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  20. Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium.American journal of physiology. Heart and circulatory physiology · 2019
    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

26 authors at 2 institutions in 1 country.

Jae-Hoon ChungDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Brit L MartinDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Benjamin D CananDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Mohammad T ElnakishDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Nima Milani-NejadDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Nancy S SaadDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Steven J RepasDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
J Eric J SchultzDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Jason D MurrayDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Jessica L SlabaughDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Rachel L GearingerDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Jennifer ConkleDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Tallib KarazeDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Neha RastogiDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Mei-Pian ChenDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Will CreceliusDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Kyra K PeczkowskiDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States.
Mark T ZioloDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States; Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States.
Vadim V FedorovDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States; Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States.
Ahmet KilicDepartment of Surgery, The Ohio State University, Columbus, OH, United States.
Bryan A WhitsonDepartment of Surgery, The Ohio State University, Columbus, OH, United States.
Robert S D HigginsDepartment of Surgery, The Ohio State University, Columbus, OH, United States.
Sakima A SmithDavis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States; Department of Internal Medicine, The Ohio State University, Columbus, OH, United States.
Peter J MohlerDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States; Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States; Department of Internal Medicine, The Ohio State University, Columbus, OH, United States.
Philip F BinkleyDavis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States; Department of Internal Medicine, The Ohio State University, Columbus, OH, United States.
Paul M L JanssenDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States; Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States; Department of Internal Medicine, The Ohio State University, Columbus, OH, United States. Electronic address: janssen.10@osu.edu.
The Ohio State University · USLung Institute · US

Funding

Defining novel mechanisms for human arrhythmiaR35HL135754 · NHLBI · OHIO STATE UNIVERSITY · PI MOHLER, PETER J. · 2017 to 2023
$6.0M
Targeting the Arrhythmogenic Sources of Human Atrial FibrillationR01HL135109 · NHLBI · OHIO STATE UNIVERSITY · PI Vadim V Fedorov · 2017 to 2026
$6.0M
Frequency-dependent modulation of cardiac myofilament function in health/diseaseR01HL113084 · NHLBI · OHIO STATE UNIVERSITY · PI JANSSEN, PAULUS ML · 2012 to 2023
$4.6M
Integration of structure and signaling in cardiac pacemaker functionR01HL115580 · NHLBI · OHIO STATE UNIVERSITY · PI FEDOROV, VADIM V · 2013 to 2021
$4.2M
Electrical and mechanical behavior of live human myocardium in health and diseaseRC1HL099538 · NHLBI · OHIO STATE UNIVERSITY · PI JANSSEN, PAULUS ML · 2009 to 2010
$1.0M
Defining New Pathways in Heart Failure and ArrhythmiaK08HL135437 · NHLBI · OHIO STATE UNIVERSITY · PI SMITH, SAKIMA AHMAD · 2017 to 2021
$749k
NHLBI NIH HHS K08 HL135437NHLBI NIH HHS R01 HL113084NHLBI NIH HHS R01 HL115580NHLBI NIH HHS R01 HL135109NHLBI NIH HHS R35 HL135754NHLBI NIH HHS RC1 HL099538
6 · The paper itself

Abstract

backgroundIn patients with end-stage heart failure, the primary etiology often originates in the left ventricle, and eventually the contractile function of the right ventricle (RV) also becomes compromised. RV tissue-level deficits in contractile force and/or kinetics need quantification to understand involvement in ischemic and non-ischemic failing human myocardium. METHODS AND

resultsThe human population suffering from heart failure is diverse, requiring many subjects to be studied in order to perform an adequately powered statistical analysis. From 2009-present we assessed live tissue-level contractile force and kinetics in isolated myocardial RV trabeculae from 44 non-failing and 41 failing human hearts. At 1 Hz stimulation rate (in vivo resting state) the developed active force was not different in non-failing compared to failing ischemic nor non-ischemic failing trabeculae. In sharp contrast, the kinetics of relaxation were significantly impacted by disease, with 50% relaxation time being significantly shorter in non-failing vs. non-ischemic failing, while the latter was still significantly shorter than ischemic failing. Gender did not significantly impact kinetics. Length-dependent activation was not impacted. Although baseline force was not impacted, contractile reserve was critically blunted. The force-frequency relation was positive in non-failing myocardium, but negative in both ischemic and non-ischemic myocardium, while the β-adrenergic response to isoproterenol was depressed in both pathologies.

conclusionsForce development at resting heart rate is not impacted by cardiac pathology, but kinetics are impaired and the magnitude of the impairment depends on the underlying etiology. Focusing on restoration of myocardial kinetics will likely have greater therapeutic potential than targeting force of contraction.

Indexed as

AdultAgedAnimalsFemaleHeartHeart FailureHeart TransplantationHeart VentriclesHumansMaleMiddle AgedMyocardial ContractionMyocardiumRelaxation TherapyTissue DonorsExcitation-contraction couplingHeart failureMyocardial biology

Identifiers

PMID29981798
PMCPMC6103886
OpenAlexW2866833960

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.