Extract

A 75-year-old woman with bronchial asthma presenting with exertional dyspnoea for the past 3 months was referred to our hospital due to elevated C-reactive protein level of 1.64 mg/L, hypereosinophilia (3350/μL), cardiomegaly with pleural effusion, and left ventricular (LV) wall thickening from the mid-ventricular wall to the apex (see Supplementary data online, Video S1, Panels A and B). On admission, she was afebrile with a total white blood cell count of 8900/μL, eosinophil count of 960/μL, C-reactive protein level of 0.36 mg/L, and N-terminal pro-B-type natriuretic peptide level of 5268 pg/mL. The Fip1-like 1-platelet-derived growth factor receptor alpha (FIP1L1/PDGFRA) fusion gene as a pathogenic cause of the hypereosinophilic syndrome was not identified. An electrocardiogram indicated a heart rate of 82 b.p.m. with QS pattern in leads V1–V3 and non-specific ST-T changes in inferior leads (Panel C). Cardiac magnetic resonance imaging showed thrombus formation, and a diffuse high-intensity signal on the T2-weighted image (T2WI) and late gadolinium enhancement (LGE) in the endocardial layer with elevated native T1 value and extracellular volume (Panels D and E). 18F-fluorodeoxyglucose-positron emission tomography combined with computed tomography demonstrated intense uptake in the endocardial layer of the LV, reflecting endocardial inflammatory activity (Panel F). Endomyocardial biopsy of the LV confirmed eosinophilic infiltration with myocardial destruction, leading to a diagnosis of Löffler’s endocarditis (Panel G). Thereafter, corticosteroid with prednisolone (0.5 mg/kg/day) and anticoagulation with warfarin were initiated. One month after the initiation of prednisolone, her eosinophil count decreased to 51/μL. After tapering over the corticosteroid therapy, her eosinophil count and symptom were not increased. Six months after treatments with prednisolone and warfarin, multimodal imaging characteristics except for T2WI and LGE were improved (see Supplementary data online, Video S2, Panels A–F).

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