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Takotsubo Cardiomyopathy (TTC), often referred to as stress-induced or "broken heart" syndrome, is characterized by transient left ventricular dysfunction predominantly involving apical hypokinesia and basal hyperkinesia in the absence of obstructive coronary artery disease. Traditionally viewed as an acute and reversible phenomenon, accumulating evidence suggests that TTC may emerge from a preexisting myocardial substrate shaped by chronic stress and hemodynamic loading. Basal Septal Hypertrophy (BSH), a morphological finding commonly observed in elderly, hypertensive, or emotionally stressed individuals, has been increasingly recognized in patients with TTC. This hypertrophic pattern, often accompanied by dynamic contractile gradients and regional perfusion mismatch, reflects a broader adaptive remodeling process conceptualized as Stressed Heart Morphology (SHM). SHM encompasses the structural and functional myocardial responses to cumulative neurohormonal and mechanical stress, with BSH representing a key imaging marker within this spectrum. Advanced echocardiographic techniques, such as tissue Doppler imaging, speckle-tracking strain analysis, and stress echocardiography, consistently reveal overlapping features between SHM and TTC, including basal hyperkinesis, septal thickening, and inducible left ventricular outflow tract obstruction. These findings support a continuum in which SHM serves as a predisposing substrate for TTC, representing a stress-provoked clinical expression within a unified myocardial stress-response framework.
Mahmoud et al. (Tue,) studied this question.