Evidence map›Paper›PMID 30623136›Full record

ArticleJACC. Basic to translational science2018

Characterization of the Myocardial Inflammatory Response in Acute Stress-Induced (Takotsubo) Cardiomyopathy.

Heather M Wilson, Lesley Cheyne, Paul A J Brown, Keith Kerr, Andrew Hannah, Janaki Srinivasan, Natallia Duniak, Graham Horgan, Dana K Dawson

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 125 citations in OpenAlex.

  1. Trial
  2. A novel parameter for risk stratification in patients with takotsubo syndrome.American heart journal plus : cardiology research and practice · 2026
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  13. The role of inflammation in takotsubo syndrome: A new therapeutic target?Journal of cellular and molecular medicine · 2024
    Review
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11 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Heather M WilsonSchool of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Foresterhill, Aberdeen, Scotland, United Kingdom.
Lesley CheyneSchool of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Foresterhill, Aberdeen, Scotland, United Kingdom.
Paul A J BrownDepartment of Pathology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland, United Kingdom.
Keith KerrSchool of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Foresterhill, Aberdeen, Scotland, United Kingdom.
Andrew HannahDepartment of Cardiology NHS Grampian, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland, United Kingdom.
Janaki SrinivasanDepartment of Cardiology NHS Grampian, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland, United Kingdom.
Natallia DuniakDepartment of Pathology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland, United Kingdom.
Graham HorganSchool of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Foresterhill, Aberdeen, Scotland, United Kingdom.
Dana K DawsonSchool of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Foresterhill, Aberdeen, Scotland, United Kingdom.
University of Aberdeen · GBAberdeen Royal Infirmary · GBNHS Grampian · GB

Funding

British Heart Foundation FS/16/39/32174British Heart Foundation PG/15/108/31928
6 · The paper itself

Abstract

Takotsubo cardiomyopathy is an acute stress-induced heart failure syndrome for which the exact pathogenic mechanisms are unclear, and consequently, no specific treatment exists. In an experimental model of stress-induced takotsubo-like cardiomyopathy, the authors describe the temporal course of a chronic inflammatory response post-induction, with an initial early influx of neutrophils into myocardial tissue followed by macrophages that are typical of a proinflammatory M1 phenotype, and a nonsignificant increase in systemic inflammatory cytokines. Post-mortem myocardium from the more complex clinical takotsubo patients share features of the study's experimental model. These findings suggest modulators of inflammation could be a potential therapeutic option.

Indexed as

EF, ejection fractionhistopathologyIL, interleukininflammationmacrophageMHC, major histocompatibility complexMI, myocardial infarctionpathophysiologyqPCR, quantitative polymerase chain reactiontakotsubo cardiomyopathyTNFα, tumor necrosis factor-alpha

Identifiers

PMID30623136
PMCPMC6314973
OpenAlexW2906884822

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.