Pathophysiology of stress cardiomyopathy: A comprehensive literature review

Takotsubo cardiomyopathy is a transient type of acute heart failure with distinct wall motion abnormalities and unclear pathophysiology. This review focuses on the proposed pathophysiological mechanisms that could be involved in the occurrence takotsubo cardiomyopathy.

Acute stress and subsequent excessive activation of the sympathetic nervous system are major factors in the pathophysiology of takotsubo cardiomyopathy. The high levels of catecholamine work in a triggering manner, generate reactive oxygen species, release inflammatory cytokines, and induce endothelial injury. The incidence of Takotsubo cardiomyopathy has increased following COVID-19 infection and vaccination, which suggests that neurohormonal and psychological factors (i.e., fear and anxiety of infection or vaccination) may have an additional role in the pathophysiology. In addition, inflammatory state, cytokine storm, augmented sympathetic activity, and endothelial dysfunction during the acute phase of COVID-19 infection may participate in Takotsubo cardiomyopathy. Chronic stress is also linked to this complex mechanism by accelerating cripple of endocrinal hypothalamic-pituitary-adrenal axis activity, which influences the cortisol effect on releasing catecholamine, which is directly related to the pathogenesis of takotsubo cardiomyopathy.

The excessive activation of the sympathetic nervous system and subsequent high levels of catecholamines could initiate the process. The catecholamines, in turn, generate reactive oxygen species and release inflammatory cytokines (i.e., IL-1, IL-2, IL-6, IL-7, IL-8, CXCL1, TNF-α, and IFN-γ), which causes endothelial injury.