Wilson Heather M, Cheyne Lesley, Brown Paul A J, Kerr Keith, Hannah Andrew, Srinivasan Janaki, Duniak Natallia, Horgan Graham, Dawson Dana K
School of Medicine, Medical Sciences & Nutrition, University of Aberdeen, Foresterhill, Aberdeen, Scotland, United Kingdom.
Department of Pathology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, Scotland, United Kingdom.
JACC Basic Transl Sci. 2018 Dec 31;3(6):766-778. doi: 10.1016/j.jacbts.2018.08.006. eCollection 2018 Dec.
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.
应激性心肌病是一种急性应激诱导的心力衰竭综合征,其确切的致病机制尚不清楚,因此不存在特异性治疗方法。在应激诱导的类应激性心肌病实验模型中,作者描述了诱导后慢性炎症反应的时间进程,最初是中性粒细胞早期流入心肌组织,随后是具有促炎M1表型特征的巨噬细胞,全身炎症细胞因子无显著增加。更复杂的临床应激性心肌病患者的死后心肌具有该研究实验模型的特征。这些发现表明,炎症调节剂可能是一种潜在的治疗选择。