The role of inflammation in takotsubo syndrome: A new therapeutic target?

Abstract

AbstractTakotsubo syndrome (TTS) is a particular form of acute heart failure that can be challenging to distinguish from acute coronary syndrome at presentation. TTS was previously considered a benign self‐limiting condition, but it is now known to be associated with substantial short‐ and long‐term morbidity and mortality. Because of the poor understanding of its underlying pathophysiology, there are few evidence‐based interventions to treat TTS. The hypotheses formulated so far can be grouped into endogenous adrenergic surge, psychological stress or preexisting psychiatric illness, coronary vasospasm with microvascular dysfunction, metabolic and energetic alterations, and inflammatory mechanisms. Current evidence demonstrates that the infiltration of immune cells such as macrophages and neutrophils play a pivotal role in TTS. At baseline, resident macrophages were the dominant subset in cardiac macrophages, however, it underwent a shift from resident macrophages to monocyte‐derived infiltrating macrophages in TTS. Depletion of macrophages and monocytes in mice strongly protected them from isoprenaline‐induced cardiac dysfunction. It is probable that immune cells, especially macrophages, may be new targets for the treatment of TTS.