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Takotsubo Syndrome: From Pathophysiology and Diagnosis to Management
Alexander Marschall1, Jorge Salamanca2, Alberto Cecconi2
1Cardiology Department, La Princesa University Hospital, Princesa Institute for Health Research (IIS-IP), Autonomous University of Madrid, CIBERCV, Madrid, Spain; Cardiology Department, Central Defense Hospital Gómez Ulla, University of Alcalá, Madrid, Spain.
None:
Takotsubo syndrome (TTS) is an acute heart failure syndrome characterized by transient left ventricular dysfunction and characteristic regional wall motion abnormalities extending beyond a single coronary territory in the absence of culprit coronary lesions. Predominantly affecting postmenopausal women, TTS often mimics acute myocardial infarction, with chest pain, dyspnea, electrocardiographic changes, and elevated cardiac biomarkers. Emotional or physical stressors trigger most cases, though one-third occur without identifiable precipitants. Pathophysiology is multifactorial, involving transient catecholamine-mediated cardiotoxicity, coronary microvascular dysfunction, sympathetic hyperactivity, brain-heart axis alterations, and estrogen deficiency, with emerging evidence implicating inflammation and genetic susceptibility. Diagnosis relies on multimodality imaging, including echocardiography, coronary angiography, and cardiac magnetic resonance imaging. Management remains empiric and largely supportive, guided by hemodynamic status and complications, with judicious avoidance of catecholamines. Long-term therapy with beta-blockers ACE inhibitors, ARBs and SGLT2 inhibitors has been proposed to improve prognosis but evidence is observational and limited. TTS is not benign; in-hospital and long-term morbidity and mortality rival those of acute coronary syndromes. Ongoing research is essential to refine risk stratification, elucidate pathophysiology, and develop targeted, evidence-based therapies.
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