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Corresponding author at: Alfred Heart Centre and Baker IDI Heart and Diabetes Institute, Commercial Road, Melbourne, Victoria 3004, Australia. Tel.: +61 390762000; fax: +61 390762461.
A 33 year-old female presented with fatigue, dyspnoea, progressive muscle weakness,
signs of clinical heart failure and an elevated CK (4113 U/L). Cardiac magnetic resonance (CMR) demonstrated a mildly dilated left ventricle
(LV) with severe systolic dysfunction (ejection fraction 28%) and a pericardial effusion
(A, Online Video 1). T2-weighted imaging demonstrated normal ratio of myocardial signal
intensity relative to skeletal muscle (<2.0) and visually elevated skeletal muscle signal (arrow) (B). Similarly, early myocardial contrast enhanced T1-weighted imaging demonstrated
normal (<4.0) myocardial to skeletal muscle ratio (C, D), however absolute myocardial enhancement was 82% (normal <45%) [
]. Late gadolinium imaging demonstrated extensive non-ischaemic circumferential enhancement
(arrows) in both long (E) and short axis views (F) with evidence of LV, RV and papillary muscle involvement. Endomyocardial biopsy
(G) showed patchy myocyte loss in association with interstitial oedema and fibrosis
along with scattered lymphocytes and plasma cells, consistent with acute lymphocytic
myocarditis. Skeletal muscle biopsy (H) demonstrated extensive fatty tissue replacement with scattered fascicles of skeletal
muscle, within which there was active degeneration and interstitial lymphocytes, both
perivascular and surrounding individual myocytes, in keeping with a severe inflammatory
myositis (Fig. 1).
Fig. 1(A) Horizontal long axis (four chamber) cine steady-state free precession (SSFP) CMR
image; (B) T2-weighted CMR (STIR); (C,D) T1-weighted imaging pre- and early post-contrast;
(E,F) Late gadolinium enhancement images both long and short axis views; (G) Cardiac
biopsy histology; (H) Skeletal muscle biopsy histology.
