Inflammation plays a central role in the pathophysiology of Takotsubo syndrome, interacting with sympathetic hyperactivation and microvascular dysfunction to cause myocardial injury.
Abstract Purpose of Review Takotsubo syndrome (TTS), also known as stress-induced cardiomyopathy, is an acute and transient form of myocardial dysfunction that predominantly affects postmenopausal women after emotional or physical stress. Although initially considered benign, growing evidence demonstrates that TTS carries substantial morbidity, recurrence, and mortality risks. This review aims to summarize current knowledge on the pathophysiology of TTS with a focus on inflammation, to explore the interplay between stress and myocardial injury, and to discuss the diagnostic and prognostic value of multimodality imaging together with emerging therapeutic approaches, providing a comprehensive framework for clinical practice and future research. Recent Findings The pathophysiology of TTS is multifactorial, involving sympathetic hyperactivation with catecholamine excess, microvascular dysfunction, epicardial coronary spasm, intracellular calcium overload, and myocardial stunning. Increasing evidence supports a central role of inflammation, including activation of the NLRP3 inflammasome, release of cytokines such as IL-1β, IL-6, and TNF-α, oxidative stress, and macrophage polarization, ultimately leading to myocardial injury, fibrosis, and adverse ventricular remodelling. Multimodality imaging, comprising echocardiography, cardiac magnetic resonance, and nuclear techniques, enables early identification of functional and structural abnormalities, exclusion of differential diagnoses such as acute coronary syndromes or myocarditis, and prognostic assessment. Summary TTS represents a complex stress-related cardiomyopathy with overlapping neurohormonal, inflammatory, and microvascular mechanisms. Current management remains largely supportive, focused on heart failure therapy, anticoagulation when indicated, and hemodynamic stabilization. Novel therapies targeting inflammatory and sympathetic pathways are under investigation and may change the future management of this condition. Understanding the interplay between stress, inflammation, and myocardial injury offers new opportunities for pathophysiology-driven treatment strategies and improved patient outcomes. Graphical Abstract
Madaudo et al. (2026) conducted a review in Takotsubo syndrome. Inflammation and targeted therapies was evaluated. Inflammation plays a central role in the pathophysiology of Takotsubo syndrome, interacting with sympathetic hyperactivation and microvascular dysfunction to cause myocardial injury.
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