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

doi:10.1016/j.jacbts.2018.08.006

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

Heather M. Wilson^* (Corresponding Author), Lesley Cheyne, Paul A J Brown, Keith Kerr, Andrew Hannah, Janaki Srinivasan, Natallia Duniak, Graham Horgan, Dana K Dawson

^*Corresponding author for this work

Aberdeen Royal Infirmary

Research output: Contribution to journal › Article › peer-review

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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.

Original language	English
Pages (from-to)	766-778
Number of pages	13
Journal	JACC: Basic to Translational Science
Volume	3
Issue number	6
Early online date	31 Dec 2018
DOIs	https://doi.org/10.1016/j.jacbts.2018.08.006
Publication status	Published - 31 Dec 2018

Bibliographical note

This work was supported by grants from NHS Grampian Endowments and British Heart Foundation Project Grant no. PG/15/108/31928 The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Keywords

histopathology
inflammation
macrophage
pathophysiology
takotsubo cardiomyopathy

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10.1016/j.jacbts.2018.08.006Licence: CC BY

Characterization of the Myocardial Inflammatory Response in Acute StressInduced
Copyright 2018 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY licence http://creativecommons.org/licenses/by/4.0/
Final published version, 1.83 MBLicence: CC BY

Heather Wilson
Person: Academic

Cite this

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title = "Characterization of the Myocardial Inflammatory Response in Acute Stress-Induced (Takotsubo) Cardiomyopathy",

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{\textquoteright}s experimental model. These findings suggest modulators of inflammation could be a potential therapeutic option.",

keywords = "histopathology, inflammation, macrophage, pathophysiology, takotsubo cardiomyopathy",

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note = "This work was supported by grants from NHS Grampian Endowments and British Heart Foundation Project Grant no. PG/15/108/31928 The authors have reported that they have no relationships relevant to the contents of this paper to disclose. ",

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T1 - Characterization of the Myocardial Inflammatory Response in Acute Stress-Induced (Takotsubo) Cardiomyopathy

AU - Wilson, Heather M.

AU - Cheyne, Lesley

AU - Brown, Paul A J

AU - Kerr, Keith

AU - Hannah, Andrew

AU - Srinivasan, Janaki

AU - Duniak, Natallia

AU - Horgan, Graham

AU - Dawson, Dana K

N1 - This work was supported by grants from NHS Grampian Endowments and British Heart Foundation Project Grant no. PG/15/108/31928 The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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Y1 - 2018/12/31

N2 - 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.

AB - 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.

KW - histopathology

KW - inflammation

KW - macrophage

KW - pathophysiology

KW - takotsubo cardiomyopathy

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DO - 10.1016/j.jacbts.2018.08.006

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JO - JACC: Basic to Translational Science

JF - JACC: Basic to Translational Science

IS - 6

ER -

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

Abstract

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Keywords

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