Evidence map›Paper›PMID 31347914›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2019

Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium.

Jae-Hoon Chung, Nima Milani-Nejad, Jonathan P Davis, Noah Weisleder, Bryan A Whitson, Peter J Mohler, Paul M L Janssen

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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 1 institution in 1 country.

Jae-Hoon ChungDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio.
Nima Milani-NejadDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio.
Jonathan P DavisDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio.
Noah WeislederDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio.
Bryan A WhitsonDepartment of Surgery, Division of Cardiac Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio.
Peter J MohlerDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio.
Paul M L JanssenDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio.ORCID 0000-0002-9682-3014
The Ohio State University Wexner Medical Center · US

Funding

Frequency-dependent modulation of cardiac myofilament function in health/diseaseR01HL113084 · NHLBI · OHIO STATE UNIVERSITY · PI JANSSEN, PAULUS ML · 2012 to 2023
$4.6M
Role of Cardiac Troponin in Health and DiseaseR01HL132213 · NHLBI · OHIO STATE UNIVERSITY · PI DAVIS, JONATHAN PAUL · 2017 to 2020
$1.5M
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
NHLBI NIH HHS R01 HL113084NHLBI NIH HHS R01 HL132213NHLBI NIH HHS RC1 HL099538
6 · The paper itself

Abstract

The force-frequency relationship (FFR) is an important regulatory mechanism that increases the force-generating capacity as well as the contraction and relaxation kinetics in human cardiac muscle as the heart rate increases. In human heart failure, the normally positive FFR often becomes flat, or even negative. The rate of cross-bridge cycling, which has been reported to affect cardiac output, could be potentially dysregulated and contribute to blunted or negative FFR in heart failure. We recently developed and herein use a novel method for measuring the rate of tension redevelopment. This method allows us to obtain an index of the rate of cross-bridge cycling in intact contracting cardiac trabeculae at physiological temperature and assess physiological properties of cardiac muscles while preserving posttranslational modifications representative of those that occur in vivo. We observed that trabeculae from failing human hearts indeed exhibit an impaired FFR and a reduced speed of relaxation kinetics. However, stimulation frequencies in the lower spectrum did not majorly affect cross-bridge cycling kinetics in nonfailing and failing trabeculae when assessed at maximal activation. Trabeculae from failing human hearts had slightly slower cross-bridge kinetics at 3 Hz as well as reduced capacity to generate force upon K

Indexed as

Heart RateAdultAgedCardiac OutputFemaleHeart FailureHumansIn Vitro TechniquesKineticsMaleMiddle AgedMyocardial BridgingMyocardial ContractionVentricular Dysfunction, LeftYoung Adultcontractionfrequencyheart failuremyofilamentsrelaxation

Identifiers

PMID31347914
PMCPMC6766727
OpenAlexW2966525610

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.