Fulminant eosinophilic myocarditis treated by venoarterial extracorporeal membrane oxygenation and adjunctive immunosuppressive therapy: a case report

Eosinophilic myocarditis can result from drug hypersensitivity or various systemic disorders. Although corticosteroids are effective, treatment strategies are not standardized.

A 78-year-old male presented with dyspnoea. On admission, he was febrile and hypotensive and had sinus tachycardia with a newly developed right bundle branch block. Laboratory findings showed marked eosinophilia with elevated troponin. The patient rapidly progressed to cardiogenic shock, and venoarterial extracorporeal membrane oxygenation (VA-ECMO) was applied. Eosinophilic myocarditis was suspected, and endomyocardial biopsy confirmed dense myocardial eosinophil infiltration consistent with the diagnosis. Review of history revealed recent cefaclor use for a hand injury as the probable cause. The patient’s condition quickly improved after initiation of high-dose intravenous methylprednisolone, allowing weaning from VA-ECMO. However, persistent troponin elevation and myocardial inflammation on fluorodeoxyglucose positron emission tomography (FDG-PET) were observed despite 5 weeks of steroid therapy. Subcutaneous mepolizumab, an anti-interleukin-5 monoclonal antibody, was initiated as an adjunctive immunosuppressive therapy. After seven cycles, troponin levels normalized, cardiac function fully recovered, and follow-up FDG-PET demonstrated a marked reduction in myocardial inflammation.

We describe a case of fulminant eosinophilic myocarditis that was possibly associated with cefaclor use and successfully managed with VA-ECMO and adjunctive immunosuppressive therapy. Fluorodeoxyglucose positron emission tomography imaging helped detect residual inflammation and assess treatment response. Immunosuppressive therapy allowed a reduction of steroid dose, mitigating the risk of steroid-related side effects.