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 apotential therapeutic option.
Highlights
Ejection fraction (EF) = ejection fraction IL = interleukin MHC = major histocompatibility complex MI = myocardial infarction qPCR = quantitative polymerase chain reaction TNFa = tumor necrosis factoralph
Regardless of a spontaneous process of recovery as a recognized feature of takotsubo cardiomyopathy, the mortality risk and long-term mortality are comparable with MI [2,3]
There is no current treatment, and the etiology is unclear, its pathophysiology needs to be resolved before targeted therapies can be trialed
Summary
Our aim was to establish the type and time course of the myocardial inflammatory changes in this stressinduced experimental model and to determine whether similar changes existed in viable, nonfibrotic myocardium from necessarily more complex human post-mortem cases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
