Takotsubo Cardiomyopathy and Stressed Heart Morphology: Molecular, Hemodynamic, and Imaging Intersections

Abstract

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.

Keywords: Takotsubo Cardiomyopathy; basal septal hypertrophy; stressed heart morphology.

Figure 1

(A) Echocardiography shows a predominant regional LV septal base during end-diastole in a hypertensive patient with basal septal hypertrophy. (B) Protrusion of septal basal tissue into the LV outflow tract during end-systole in the same patient. (B) shows basal septal hypertrophy in a hypertensive patient.

Figure 2

Shows how Superimposed emotional stress amplifies the deleterious cardiovascular effects of chronic hypertension by persistently activating the sympathetic and hypothalamic–pituitary–adrenal (HPA) axes, thereby augmenting systemic arterial pressure and neurohormonal load.

Figure 3

Shows a sharp curvature of more remarkable basal septal hypertrophy from apical four-chamber view during end-diastole in another hypertensive patient.

Figure 4

Shows the stress accumulating effect on HR, BP, and Inflammatory response through HPA, RAAS, Adrenaline, Noradrenaline, and Glucocorticoids release.

Figure 5

TTC apical ballooning underlying the mechanical mechanism involves Adrenergic signaling and the AKT pathway.

Figure 6

Representation of the regional differences in response to high catecholamine levels, explaining stress cardiomyopathy.

Figure 7

Shows a non-stress cMRI of a Caucasian woman with TTC, who then developed apical myocardial edema (pseudohypertrophy) mimicking apical HCM in the recovery phase. Baseline cardiac MRI. Diastolic (A,C) and systolic phases (B,D). Lack of basal to apical wall tapering (C). Elevated mid to apical T1 mapping times (The key feature that proves that this is a TTC rather than HCM) (E). Admission ECG with poor R-wave progression (F). Image permission taken from the author of reference [43].