Value of non-invasive imaging in acute chest pain

A 76-year-old lady without prior cardiac history, presented to the hospital with sudden onset, retrosternal chest pain. Her symptoms started while rushing to post office near closing time. She was annoyed as she forgot to bring the letter with her. Her symptoms started when she returned to her car and had an argument with her husband. She was a lifelong non-smoker. She had no history of chest pain and angina. She had no significant past medical history of note. On admission, she was afebrile, normotensive (110/70 mmHg) and slightly tachycardic (110 bpm regular). Clinical examination revealed no signs of heart failure and no other abnormality. Initial laboratory investigation included Haemoglobin 13.1 g/dl (normal range (NR) 11.5–16.5 g/dl), leucocyte count 8.1 × 109/l (NR 4.0–10.0 × 109/l), Na+ 142 mmol/l (NR 135–145 mmol/l), K+ 4.3 mmol/l (NR 3.5–5.0 mmol/l), C-reactive protein 2.6 mg/l (NR 1.0–10.0 mg/l), Mg2+ 0.90 mmol/l (NR 0.75–1.15 mmol/l), Ca2+ 2.29 mmol/l (NR 2.10–2.60 mmol/l). Cardiac troponin-T was raised 12 h after onset of chest pain at 1.6 µg/l (normal <0.03 µg/l). She was clinically and biochemically euthyroid. As electrocardiogram (ECG) on presentation showed ST segment elevation in anterior leads (V1–V4), we proceeded to perform emergency coronary angiography. This was carried out via radial approach and revealed normal coronary anatomy. Transthoracic echocardiogram (Figure 1A) showed severely impaired systolic function with apical and mid segment akinesis and hyper-dynamic basal segments of left ventricle, raising the suspicion of apical ballooning syndrome. It also showed right ventricular apical akinesis. Subsequently, cardiac magnetic resonance (CMR) imaging performed at 60 h from presentation showed impaired left ventricular function (Figure 2A and B) with apical akinesis. This was associated with high-signal intensity areas in the T2-weighted images (Figure 2D, E, F) in the mid and apical region of left ventricle suggestive of myocardial oedema or inflammation. There was no evidence of left ventricular thrombus. The diagnosis was confirmed by the absence of subendocardial late gadolinium enhancement (Figure 2c). She was commenced on Bisoprolol 2.5 mg od and angiotensin-converting enzyme (ACE) inhibitor and discharged. Follow-up echocardiogram at 16 weeks showed complete recovery of left ventricular function with no regional wall motion abnormality (Figure 1B).