Evidence map›Paper›PMID 31125424›Full record

ArticleEuropean journal of clinical investigation2019

Autoimmune myocarditis is not associated with left ventricular systolic dysfunction.

Moritz Mirna, Vera Paar, Theo Kraus, Karl Sotlar, Bernhard Wernly, Rudin Pistulli, Uta C Hoppe, Michael Lichtenauer

Open access · hybridAbstract read
In one paragraph

Article in European journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 8 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

8 authors at 2 institutions in 2 countries.

Moritz MirnaDepartment of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.ORCID https://orcid.org/0000-0001-5679-4872
Vera PaarDepartment of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.
Theo KrausInstitute of Pathology, Paracelsus Medical University of Salzburg, Salzburg, Austria.
Karl SotlarInstitute of Pathology, Paracelsus Medical University of Salzburg, Salzburg, Austria.
Bernhard WernlyDepartment of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.
Rudin PistulliDepartment of Cardiology I, Coronary and Peripheral Vascular Diseases, Heart Failure, University Hospital Münster, Münster, Germany.
Uta C HoppeDepartment of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.
Michael LichtenauerDepartment of Cardiology, Clinic of Internal Medicine II, Paracelsus Medical University of Salzburg, Salzburg, Austria.ORCID https://orcid.org/0000-0001-8403-3931
University of Salzburg · ATUniversity Hospital Münster · DE

Funding

PMU-FFF Research Fund (Paracelsus Medical University) R-17/04/099-MIR
6 · The paper itself

Abstract

backgroundExperimental autoimmune myocarditis (EAM) is a common animal model for the investigation of the pathophysiology of myocarditis. Because of diverging findings from previous studies, we performed serial echocardiographic examinations throughout the course of the disease and investigated the dimensions of the murine heart and left ventricular (LV) systolic function. MATERIALS AND

methodsExperimental autoimmune myocarditis was induced in male Balb/c mice by subcutaneous injection of a fragment of the α-myosin heavy chain (MyHC-α 614-629: Ac-SLKLMATLFSTYASAD). Transthoracic echocardiography was performed on days 0, 7 and 21 in healthy animals and mice with EAM.

resultsExperimental autoimmune myocarditis was associated with a reduction in LV systolic function and an increase in LV internal diameter in diastole (LVIDd) and systole (LVIDs) 7 days postimmunization. After 21 days, EAM led to a significant increase in LV-thickness (1.3-fold increase in LV anterior wall diameter in diastole [LVAWDd]), but there was no difference in LV systolic function between immunized animals and healthy controls. LV-thickness correlated well with the severity of myocarditis in the histopathological examination (LVAWDd: rs = 0.603, P = 0.003, LV anterior wall diameter in systole (LVAWDs): rs = 0.718, P < 0.0001).

conclusionOur results indicate that EAM leads to an initial dilatation of the LV that is followed by ventricular "hypertrophy." On day 21, there was no significant difference in LV systolic function between immunized animals and controls. Furthermore, the ageing of the animals had a major impact on the echocardiographic parameters; therefore, the use of healthy age-matched controls seems warranted when echocardiography is performed in rodents.

Indexed as

AnimalsAutoimmune DiseasesDiastoleDisease Models, AnimalEchocardiographyMaleMiceMice, Inbred BALB CMyocarditisMyocardiumSystoleVentricular Dysfunction, LeftVentricular Function, LeftBalb/cechocardiographyexperimental autoimmune myocarditis

Identifiers

PMID31125424
PMCPMC6771695
OpenAlexW2944967994

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.