Evidence map›Paper›PMID 36722665›Full record

ArticleESC heart failure2023

Omecamtiv mecarbil augments cardiomyocyte contractile activity both at resting and systolic Ca

Arnold Péter Ráduly, Attila Tóth, Fruzsina Sárkány, Balázs Horváth, Norbert Szentandrássy, Péter P Nánási, Zoltán Csanádi, István Édes, Zoltán Papp, Attila Borbély

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 10 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

10 authors at 1 institution in 1 country.

Arnold Péter RádulyDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Attila TóthDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Fruzsina SárkányDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Balázs HorváthDepartment of Physiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Norbert SzentandrássyDepartment of Physiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Péter P NánásiDepartment of Physiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Zoltán CsanádiDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
István ÉdesDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Zoltán PappDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.ORCID 0000-0002-4675-1542
Attila BorbélyDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
University of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHeart failure with reduced ejection fraction (HFrEF) is a disease with high mortality and morbidity. Recent positive inotropic drug developments focused on cardiac myofilaments, that is, direct activators of the myosin molecule and Ca

methodsEnzymatically isolated canine cardiomyocytes with intact cell membranes were loaded with Fura-2AM, a Ca

resultsSL was reduced by about 23% or 9% in the presence of 1 μM OM or 1 μM EMD in the absence of electrical stimulation, whereas 1 μM Levo had no effect on resting SL. Fractional sarcomere shortening was increased by 1 μM EMD or 1 μM Levo to about 152%, but only to about 128% in the presence of 0.03 μM OM. At higher OM concentrations, no significant increase in fractional sarcomere shortening could be recorded. Contraction durations largely increased, whereas the kinetics of contractions and relaxations decreased with increasing OM concentrations. One-micromole EMD or 1 μM Levo had no effects on contraction durations. One-micromole Levo, but not 1 μM EMD, accelerated the kinetics of cardiomyocyte contractions and relaxations. Ca

conclusionsOur data revealed major distinctions between the cellular effects of myofilament targeted agents (OM, EMD, or Levo) depending on their target proteins and binding sites, although they were compatible with the involvement of Ca

Indexed as

Heart FailureMyocytes, CardiacAnimalsDogsMyosinsSimendanStroke VolumeUreaMyosinsomecamtiv mecarbilSimendanUreaHeart failure with reduced ejection fractionMyosin activatorsOmecamtiv mecarbilPositive inotropy, diastolic dysfunction

Identifiers

PMID36722665
PMCPMC10053277
OpenAlexW4318755820

What OpenQuestion holds

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LicenceCC BY-NC
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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.