A 61-year-old man presented with acute cardiogenic shock, elevated troponin level, and left ventricular (LV) ejection fraction of 10%. Coronary angiography was unremarkable. Abdominopelvic CT for abdominal pain revealed incidental diffuse myocardial calcification which was absent at CT 6 weeks earlier (Fig 1), performed for decreasing hemoglobin level. Myocardial biopsy showed marked inflammation and myocyte damage with multinucleated giant cells (Fig 2) consistent with fulminant giant cell myocarditis. The patient subsequently had multisystem organ failure including acute renal failure and died of septic shock on hospital day 83. Autopsy showed patchy subendocardial and midmyocardial fibrosis and calcifications extending from LV apex to base.
Figure 1:
Axial unenhanced CT scan in a 61-year-old man with fulminant giant cell myocarditis. (A) Initial and (B) 6-week posthospitalization axial images demonstrate rapid development and progression of myocardial calcifications involving the right (arrow) and left ventricles (arrowheads)
Figure 2:
(A) Gross pathologic examination demonstrates patchy areas of subendocardial and midmyocardial tan discoloration (arrow) representing fibrosis from apex to base. (B) Hematoxylin-eosin (H-E)–stained photomicrograph at 20× magnification shows collections (black circles) of lymphocytes (black arrows), histiocytes (orange arrows), and eosinophils (red arrows) causing myocyte damage, as indicated by hypereosinophilic myocytes (blue arrows). (C) H-E–stained photomicrograph at 40× magnification reveals histiocyte aggregates (yellow circle) forming a giant cell. Associated lymphocytes (black arrows) and eosinophils (red arrows) are also present. A collection of inflammatory cells surrounds and abuts the damaged, hypereosinophilic myocytes (blue arrows). (D) H-E–stained photomicrograph at 10× magnification shows extensive replacement fibrosis (dotted circles) and calcifications (purple arrows) between surviving myocardiocytes (blue arrows).
Myocardial calcification usually occurs as a consequence of impaired calcium metabolism and hypercalcemia (eg, chronic renal failure) (1) or following severe myocardial damage as seen with chronic myocardial infarction, fibrosis, or inflammation (1–4). Although rarely seen, myocardial calcification following myocarditis is associated with a high risk of mortality (5).
Acknowledgments
Keywords: CT, Cardiac, Thorax, Heart, Calcifications/Calculi
Footnotes
Authors declared no funding for this work.
Disclosures of conflicts of interest: C.W.K. No relevant relationships. J.C.K.C. No relevant relationships. M.C.B. No relevant relationships.
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