Author/Authors :
Inoue, Tomoko Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Sera, Fusako Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Nishimura, Shunsuke Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Nakamoto, Kei Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Tsukamoto, Yasumasa Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Mizote, Isamu Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Ohtani, Tomohito Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Hikoso, Shungo Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan , Ikeda, Yoshihiko Department of Pathology - National Cardiovascular Center, Osaka, Japan , Hori, Yumiko Department of Pathology - Osaka University Graduate School of Medicine, Osaka, Japan , Ishibashi-Ueda, Hatsue Department of Pathology - National Cardiovascular Center, Osaka, Japan , Morii, Eiichi Department of Pathology - Osaka University Graduate School of Medicine, Osaka, Japan , Minamino, Tetsuo Department of Cardiorenal and Cerebrovascular Medicine - Faculty of Medicine - Kagawa University, Kagawa, Japan , Sakata, Yasushi Department of Cardiovascular Medicine - Osaka University Graduate School of Medicine, Osaka, Japan
Abstract :
A 49-year-old woman was admitted with suspicion of acute myocarditis. On the next day after admission, her serum troponin I
level continued to rise, indicating progression of myocardial damage. Moreover, her symptoms persisted, and left ventricular
ejection fraction did not improve. Because of a predominant infiltration of lymphocytes in the myocardial specimens,
lymphocytic myocarditis was diagnosed. However, a close observation of the specimens revealed eosinophil degranulation.
Based on this finding, intravenous steroid therapy was initiated. High-dose methylprednisolone led to rapid and appreciable
improvements in symptoms and left ventricular function within 12 hours after the first administration, which was followed by
normalization of serum troponin I level. Steroid therapy was switched to oral administration and tapered carefully. There was
no recurrence of left ventricular dysfunction or elevation of serum troponin I level. In eosinophilic myocarditis, eosinophil
degranulation has been recognized as an important finding associated with progression of inflammation and myocardial
damage. However, no attention has been paid to the presence and clinical implications of eosinophil degranulation in
lymphocytic myocarditis. This case indicates that eosinophil degranulation in lymphocytic myocarditis may be an important
finding associated with a high therapeutic response to steroid therapy.
