The Role of Inflammation in Takotsubo Syndrome: From Pathogenic Pathways To Imaging Insights and Therapeutic Perspectives

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. 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.