Abstract

A 63-year-old female presented with acute chest pain and ECG showing T wave inversion in the anterior and inferior leads. Troponin T (TnT) was significantly elevated (peak 1378 ng/L; normal <14 ng/L), as was NT-proBNP (3091 ng/L; normal <400 ng/L). Invasive angiography showed unobstructed coronary arteries with mid-ventricular ballooning and hypokinesia on ventriculography (see Supplementary data online, Video S1) and echocardiography (see Supplementary data online, Video S2), suggesting a mid-ventricular tako-tsubo syndrome (TTS). Cardiac magnetic resonance (CMR) was booked but the patient was unable to attend. Focussed history using the InterTAK diagnostic score assessment revealed no emotional or physical triggers. The patient re-presented six months later with similar symptoms and elevated TnT. Inpatient echocardiography showed a reverse TTS pattern (see Supplementary data online, Video S3) and CMR at 1.5T showed basal hypokinesia with matching elevated native T1 (1220 ms; normal 950–1100 ms) and T2 (69 ms; normal <48 ms) (Panels A–B). Quantitative perfusion maps following adenosine stress perfusion to investigate microvascular disease showed basal to mid circumferential hypoperfusion with normal apical myocardial blood flow, not suggestive of specific coronary artery territory ischaemia (Panel D) and no late gadolinium enhancement (LGE) (Panel C), confirming a reverse TTS. The patient further presented two months later with chest pain and TnT elevation. Repeat inpatient CMR on this occasion showed a classic TTS pattern with apical hypokinesia and elevated T1 and T2 (1261 ms and 81 ms, respectively) at the mid to apical segments with no LGE (Panels E–G). The case was further explored but no triggers, including neurological or psychiatric abnormalities were found. Recurrent TTS with different phenotypes has previously been described but is rare, especially without a trigger. Our case illustrates the utility of multimodality imaging in the investigation of TTS; in particular, multiparametric tissue mapping by CMR. Furthermore, the novel quantitative perfusion maps characterising myocardial blood flow added diagnostic utility.

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