Takotsubo Syndrome in 2025: Evolving Concepts in Pathophysiology, Diagnosis, and Long-Term Management

Figures

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  Figure 1. Multimodal pathophysiology model of Takotsubo syndrome. Acute emotional, physical, or neurologic stressors trigger sympathetic overactivation and catecholamine excess, leading to myocardial stunning, coronary microvascular dysfunction, and metabolic impairment. Interactions among neurohumoral, microvascular, and myocardial mechanisms result in transient ventricular systolic dysfunction and characteristic clinical manifestations.

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  Figure 2. Schematic illustration of the principal left ventricular contraction patterns observed in Takotsubo syndrome. Arrows indicate segments demonstrating preserved or hyperdynamic systolic contraction.

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  Figure 3. Diagnostic algorithm for Takotsubo syndrome. Flowchart illustrating a structured diagnostic approach incorporating clinical suspicion, ECG and biomarker findings, echocardiography, coronary angiography, cardiac MRI, and exclusion of alternative diagnoses.

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  Figure 4. Apical four-chamber echocardiographic views of a female patient with Takotsubo syndrome following an incident of domestic abuse, admitted with chest pain and elevated cardiac enzymes. (A) Left ventricle during diastole. (B) Left ventricle during systole with akinetic and ballooned LV apex. (C) Coronary angiogram demonstrating patent coronary arteries. RV = right ventricle; RA = right atrium; LV = left ventricle; LA = left atrium; LAD = left anterior descending artery. (Courtesy of Dr. Raed Bargout).