Coincidence of Spontaneous Coronary Artery Dissection With Apical Takotsubo Syndrome

A 48-year-old female was admitted with anterior ST-elevation myocardial infarction (STEMI). The patient’s medical history was unremarkable, except for migraine. Coronary angiography demonstrated a normal right coronary artery (RCA; Figure A) and spontaneous coronary artery dissection (SCAD) type 2 of the distal left anterior descending artery (Figure B) with Thrombolysis in Myocardial Infarction (TIMI)-0 flow. Percutaneous coronary intervention was unsuccessful (Figure C), and dual antiplatelet therapy was initiated. Echocardiography demonstrated midventricular and apical akinesia. Serum creatine kinase peaked at 755 U/L. Cardiac magnetic resonance imaging (MRI) on the following day confirmed midventricular and apical akinesia (Figure D; Supplementary Movie 1) with basal hypercontractility. MRI further showed edema (Figure E) of midventricular and apical left ventricular (LV) segments extending beyond the infarct artery territory. However, non-transmural subendocardial late gadolinium enhancement (LGE) was restricted to the LV apex (Figure F). Four months later, follow-up MRI showed full recovery of midventricular and apical wall motion abnormalities (Figure G; Supplementary Movie 2) and resolution of myocardial edema (Figure H). However, myocardial thinning, akinesia, and transmural LGE of the very apex (Figure G,I) were present, and an apical LV thrombus was found (Figure I). A final diagnosis of apical SCAD-induced myocardial infarction and apical takotsubo syndrome (TS) was made. Antiplatelet therapy was replaced by oral anticoagulation.

Figure.

Angiography of the (A) right coronary artery and (B,C) the left anterior descending artery before (B) and after (C) unsuccessful (arrow) percutaneous coronary intervention. The bottom left image in (B) is a higher-magnification view of the boxed area on the right. (D–I) Images showing cardiac magnetic resonance imaging (2-chamber view) during the acute phase (D–F) and at the elective 4-month follow-up (G–I). During the acute phase, basal hypercontractility was evident (D, arrows). At the 4-month follow-up, an apical left ventricular thrombus was found (I). LGE, late gadolinium enhancement; SCAD, spontaneous coronary artery dissection.

The findings prototypically demonstrate the potential coexistence of SCAD and TS,¹ emphasizing the value of cardiac MRI during the acute phase and follow-up.²

Disclosures

None.

Supplementary Files

Supplementary Movie 1. Cardiac MRI during the acute phase, 2-chamber view, cine sequence.

Supplementary Movie 2. Cardiac MRI at follow-up, 2-chamber view, cine sequence.

Please find supplementary file(s);

http://dx.doi.org/10.1253/circj.CJ-22-0074

References

• 1.   Y-Hassan S. Spontaneous coronary artery dissection and takotsubo syndrome: An often overlooked association; review. Cardiovasc Revasc Med 2018; 19: 717–723.
• 2.   Napp LC, Bauersachs J. Takotsubo syndrome: Between evidence, myths, and misunderstandings. Herz 2020; 45: 252–266.