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Over the past decade, Takotsubo syndrome (TTS) has gained increasing recognition as a serious acute cardiovascular condition and now represents an important differential diagnosis in patients with suspected acute coronary syndrome. Current evidence suggests that TTS is likely related to a catecholamine storm leading to coronary microvascular dysfunction in the absence of epicardial coronary artery culprit lesion.1 Recent studies have demonstrated that the rate of acute complications in TTS is comparable to what has been reported in acute coronary syndromes.2 The in-hospital course can be complicated by serious mechanical complications, including dynamic left ventricular outflow tract obstruction (LVOTO), which has been described in a non-negligible proportion of patients and can lead to haemodynamic deterioration.3 4 LVOTO is a dynamic phenomenon precipitated by the hypercontractility of basal left ventricular segments in the context of structural and rheological changes involving the left ventricle, mitral valve apparatus, preload and afterload. Predisposing factors for LVOTO may include a smaller ventricular cavity and hypertrophy of the interventricular septum. As the basal segments contract vigorously and the septum thickens due to myocardial edema, high-velocity flow through the narrowed LVOT creates a Venturi effect, leading to systolic anterior motion of the anterior mitral leaflet and, subsequently, to secondary mitral regurgitation due to leaflet malcoaptation. Furthermore, the increase in afterload caused by LVOTO may exacerbate apical and midventricular myocardial dysfunction by elevating shear stress and disrupting the balance between …
Footnotes
Contributors DDV is the only author of this study and the guarantor.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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