A 56-year-old male presented with asthenia for 3 weeks. He had no food or drug allergies, no laboratory evidence of parasite, fungal or virus infection. Vital signs were normal with blood pressure of 130/80 mmHg, heart rate of 80 beats/min and respiratory rate of 12 breaths/min on presentation. Complete blood examination revealed hemoglobin 95 g/dL, total leukocyte count 27.74 × 109/L with an absolute eosinophil count of 12.94 × 109/L, accounting for 59.8% of cells, platelet count 55 × 109/L, elevated N-terminal pro-brain natriuretic peptide (NT-proBNP) level (604.6 ng/L, normal range <450 ng/L) and C-reactive protein (11 mg/L, reference: <8 mg/L). High Sensitivity Cardiac Troponin I (hs-cTnI) level was within the normal range. Other laboratory results were unremarkable, including anti-nuclear antibody screen. The electrocardiogram (ECG) revealed sinus rhythm (). Neither coronary computed tomographic angiography nor encephalic computed tomography showed significant lesions. Echocardiography demonstrated slightly increased chamber size, normal left ventricular systolic function (left ventricular ejection fraction of 57%), and abnormal diastolic function of grade III. There was a large, heterogeneous cardiac mass (39 mm × 22 mm, arrow) in the left ventricle (LV). The most probable diagnosis was Löffler’s endocarditis (LE; cardiac involvement in hypereosinophilia) with intracardiac thrombus (). A cardiac magnetic resonance (CMR) short-axis image showed a curved line of late gadolinium enhancement (LGE) located subendocardial in the apical-middle heart of LV. The arc-shaped unenhanced area in the left ventricular cavity and the medical history were consistent with eosinophilic endocarditis with subendocardial thrombosis () (). Because of the drastically increased eosinophils, we suspected a myeloproliferative disorder. We did a bone marrow examinations including aspiration cytology, biopsy, cytogenetic, and gene rearrangement analysis. While waiting for the results of the examinations, on day 3 of his admission, the patient complained of progressive development of chest pain. The electrocardiographic examination showed a new ST segment depression with T-wave inversion in precordial leads (). Laboratory findings demonstrated an elevated hs-cTnI and NT-proBNP of 2.72 and 1,789 ng/L, respectively, indicating ongoing myocardial damage. After treatment with nitrates to dilate the coronary arteries, the chest pain disappeared. As the symptoms were related to EM, the cause might be coronary artery spasm or a small thromboembolism obstructing the microcirculation, but the patient refused to undergo coronary angiography. Subsequently, bone marrow aspirate revealed dysplastic eosinophilia and eosinophilic promyelocytes. A normal karyotype (46, XY) was present and a FIP1L1-PDGFRA fusion gene (4q12) was detected. The marrow B- and T-cell receptor rearrangement analysis and flow cytometry showed no B- or T-cell clone, confirming EL. The patient was treated with glucocorticoid. The initial medication prescribed was intravenous methylprednisolone (60 mg per day for 3 days and then 40 mg per day for 4 days), then which was switched to oral prednisolone (50 mg per day), with a gradual tapering of the doses and imatinib mesylate (a tyrosine kinase inhibitor) of 100 mg/day was commenced. After only 4 days on imatinib and prednisolone, and the patient’s eosinophil cell levels returned to normal (the lowest level was 0.01 × 109/L). After diagnosis of intracardiac thrombus, he was initially treated with low-molecular-weight heparin (1 mg/kg/dose q12 h) for 7 days. The heparin was gradually switched to warfarin. Warfarin was adjusted to a PT INR of 2–3. Before discharge, the hs-cTnI and NT-proBNP levels had significantly decreased to 0.032 and 617.8 ng/L, respectively. Furthermore, an ECG showed the normalization of ST segment and T wave (). The patient underwent twice 18F-FAPI PET/CT for the visualization of cardiac fibroblast activation during treatment. Before discharge, on whole-body 18F-FAPI PET imaging, heterogeneously increased accumulations of 18F-FAPI were seen in endomyocardial. No other suspected fibrosis with 18F-FAPI accumulation was found (). Given the presence of myocardial fibrosis, he was treated for myocardial fibrosis and heart failure with angiotensin receptor-neprilysin inhibitor (ARNI), β-blockers and spironolactone. Good clinical response was obtained and after 2 months of treatment, follow-up PET/CT revealed that accumulations of 18F-FAPI in endomyocardial were significantly reduced (). The patient was closely followed up in both cardiology and hematology outpatient clinics over a course of 2 months. The eosinophil counts remained within the normal range, when the dose of prednisolone was gradually tapered to 5 mg per day. Peripheral blood examination gave the following results: hemoglobin, 124 g/dL; total leukocyte count 8.66 × 109/L with 6.71% eosinophils; and platelet count, 177 × 109/L. While remaining on warfarin, imatinib mesylate, prednisolone and heart failure therapy, he had no specific symptoms on evaluation in the outpatient clinic. Follow-up echocardiogram revealed normal left ventricular size and rapid regression of the left ventricular mass (6 mm × 13 mm, arrow) (). During a 6-month follow-up, there was no recurrence of hypereosinophilia. The disease remained clinically stable. Echocardiogram showed that left ventricular thrombus had resolved ().