Evidence map›Paper›PMID 27610087›Full record

ArticleFrontiers in physiology2016

Changes in Myocardial Composition and Conduction Properties in Rat Heart Failure Model Induced by Chronic Volume Overload.

David Sedmera, Jan Neckar, Jiri Benes, Jana Pospisilova, Jiri Petrak, Kamil Sedlacek, Vojtech Melenovsky

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2016. 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
1.3field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  14. HIF-1α is required for development of the sympathetic nervous system.Proceedings of the National Academy of Sciences of the United States of America · 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

7 authors at 4 institutions in 1 country.

David SedmeraInstitute of Physiology, Czech Academy of SciencesPrague, Czech Republic; First Faculty of Medicine, Institute of Anatomy, Charles University in PraguePrague, Czech Republic.
Jan NeckarInstitute of Physiology, Czech Academy of SciencesPrague, Czech Republic; Institute of Clinical and Experimental MedicinePrague, Czech Republic.
Jiri BenesInstitute of Physiology, Czech Academy of SciencesPrague, Czech Republic; First Faculty of Medicine, Institute of Anatomy, Charles University in PraguePrague, Czech Republic; Department of Radiology, First Faculty of Medicine, Charles University in PraguePrague, Czech Republic.
Jana PospisilovaFirst Faculty of Medicine, Institute of Pathological Physiology, Charles University in Prague Prague, Czech Republic.
Jiri PetrakFirst Faculty of Medicine, Biotechnology and Biomedicine Center of the Academy of Sciences and Charles University in Vestec Vestec, Czech Republic.
Kamil SedlacekInstitute of Clinical and Experimental Medicine Prague, Czech Republic.
Vojtech MelenovskyInstitute of Clinical and Experimental Medicine Prague, Czech Republic.
Charles University · CZInstitute of Clinical and Experimental Medicine · CZCzech Academy of Sciences · CZCzech Academy of Sciences, Institute of Physiology · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Volume overload leads to development of eccentric cardiac hypertrophy and heart failure. In our previous report, we have shown myocyte hypertrophy with no fibrosis and decrease in gap junctional coupling via connexin43 in a rat model of aorto-caval fistula at 21 weeks. Here we set to analyze the electrophysiological and protein expression changes in the left ventricle and correlate them with phenotypic severity based upon ventricles to body weight ratio. ECG analysis showed increased amplitude and duration of the P wave, prolongation of PR and QRS interval, ST segment elevation and decreased T wave amplitude in the fistula group. Optical mapping showed a prolongation of action potential duration in the hypertrophied hearts. Minimal conduction velocity (CV) showed a bell-shaped curve, with a significant increase in the mild cases and there was a negative correlation of both minimal and maximal CV with heart to body weight ratio. Since the CV is influenced by gap junctional coupling as well as the autonomic nervous system, we measured the amounts of tyrosine hydroxylase (TH) and choline acetyl transferase (ChAT) as a proxy for sympathetic and parasympathetic innervation, respectively. At the protein level, we confirmed a significant decrease in total and phosphorylated connexin43 that was proportional to the level of hypertrophy, and similarly decreased levels of TH and ChAT. Even at a single time-point, severity of morphological phenotype correlates with progression of molecular and electrophysiological changes, with the most hypertrophied hearts showing the most severe changes that might be related to arrhythmogenesis.

Indexed as

aorto-caval fistulaautonomic heart innervationconduction velocityconnexin43hypertrophy

Identifiers

PMID27610087
PMCPMC4997968
OpenAlexW2511190586

What OpenQuestion holds

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LicenceCC BY
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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.