CMR can accurately identify lipomatous metaplasia in left ventricular scars following myocardial infarction, as confirmed by histology.
Supports CMR detection of post-MI lipomatous metaplasia in select cases; leaves open routine diagnostic adoption pending larger validation.
A 65-year-old man with history of anterior myocardial infarction 6 years before was admitted for congestive heart failure. Echocardiography revealed a markedly dilated left ventricle with severe systolic dysfunction (EF 32%), apical aneurysm, and diffuse hypokinesis of the other segments. Cardiac catheterization showed three-vessel disease. Gadolinium-enhanced cardiac magnetic resonance (CMR) was performed to assess myocardial viability. Functional CMR with steady-state free precession imaging confirmed echocardiographic findings. Abnormal intramural lineal hyperintense area was detected in thinned anteroseptal mid-ventricular and apical segments. T1-weightened turbo spin-echo sequence also showed intramural lineal hyperintense area in the same segments suggesting myocardial fatty replacement (Panel A) that was confirmed with a fat suppression pulse (Panel B). Transmural gadolinium-enhanced CMR demonstrated non-viable myocardium in the anteroseptal and apical segments and patient underwent surgical coronary revascularization with left ventricular aneurysmectomy (Dor procedure). Histological analysis of specimen revealed fatty metaplasia of scar (Panels C and D) that confirmed CMR findings. Panel (A) Anatomic CMR sequence showing intramural lineal hyperintense area in anteroseptal mid-ventricular and apical segments (arrow). (B) T1-weightened turbo-spin echo with fat suppression that nulls intramural hyperintense area. (C) Histologic specimen from aneurysmectomy (haematoxylin-eosin). (D) (200×). e, endocardium; f, fibrosis; m, myocites; F, fatty tissue.
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Jorge Estornell (2006) studied this question.
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