PMC6541970_01
(a) Admission ECG showing minimal anterior ST elevation and concave ST segments in leads II, III, and aVF. (b) ECG 48 hours after presentation demonstrating deep T wave inversion across precordial and limb leads with a prolonged QTc.
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On arrival in the emergency department, a 12-lead ECG showed minimal anterior ST elevation (Figure 1(a)); therefore, a bedside echocardiogram was performed. His ECG evolved to show deep symmetrical T wave inversion across the anterolateral and limb leads, clearly more extensive than the distribution of the infarct artery (Figure 1(b)) associated with the prolongation of the QT interval.
Coronary angiography on admission. (a) Minor disease in the left anterior descending artery. (b) Mild-moderate disease in the right coronary artery. (c) Occluded OM2 branch (arrow) of the left circumflex artery. (d) TIMI III flow post percutaneous coronary intervention (PCI) with drug-eluting stent (DES). Left ventriculogram in the right anterior oblique (RAO) projection during diastole (e) and systole (f) showing mid apical pattern of takotsubo syndrome with sparing of the apical tip.
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Angiography revealed an occluded obtuse marginal 2 (OM2) branch of the circumflex artery (Figure 2(c)) with minor disease in the other major epicardial arteries (Figures 2(a) and 2(b)). The lesion was treated with one 2.5 mm x 15 mm drug-eluting stent resulting in TIMI III flow (Figure 2(d)). Ventriculogram done in the RAO projection revealed mid and apical hypokinesis and ballooning with preserved basal function (Figures 2(e) and 2(f)).
Transthoracic echocardiogram on admission and 6-week follow-up. Apical 4 chamber window at end-diastole (a) and at end-systole (b) showing apical dilatation during acute presentation. (c) Apical 4 chamber window at end-diastole at 6-week follow-up. (d) Apical 4 chamber window at end-systole at 6-week follow-up revealing resolution of apical ballooning.
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Follow-up echocardiography performed 6 weeks after discharge demonstrated restoration of normal LV systolic function and resolution of the previously seen regional wall motion abnormalities (Figure 3).