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 |
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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 | |
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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Heather Wilson
- School of Medicine, Medical Sciences & Nutrition, Microbiology and Immunity
- School of Medicine, Medical Sciences & Nutrition, Medical Sciences - Chair in Immunology
- School of Medicine, Medical Sciences & Nutrition, Aberdeen Cardiovascular and Diabetes Centre
- School of Medicine, Medical Sciences & Nutrition, Institute of Medical Sciences
Person: Academic