A 27-year-old man was admitted to the emergency department with fever and thoracic pain. In the previous 6 months, the patient lost a substantial amount of weight (12 kg). His family history was negative for cardiac disease. Electrocardiography revealed sinus rhythm, and diffuse T-wave inversion. T wo-dimensional echocardiography was performed (Fig 1) and revealed normal left systolic function (ejection fraction, 60%). Laboratory tests showed elevated levels of high-sensitivity cardiac troponin (1.07 ng/mL; normal value, ,0.015 ng/mL), high levels of C-reactive protein (16 mg/dL; normal range, 0–5 mg/dL), and leukocytosis with an eosinophilia level of 8710/mL (normal level, ,400/mL). Parasitic and infectious diseases (T oxocara canis, strongyloides, filariasis, cysticercosis, fasciola, trichinella, echinococcosis) were excluded based on blood and fecal test results. Corticosteroid therapy was started, and the patient was dismissed. A few days later, he was readmitted to the emergency department with a headache and suddenly blurred vision. Neurologic and ophthalmologic findings were normal, and MRI of the brain was performed (Fig 2). Cardiac MRI (Fig 3) was performed 2 days later and revealed the following quantitative results: (a) left ventricular end-diastolic volume (LVDV) of 165 mL (LVDV/body surface area [BSA], 89 mL/m2; normal range, 64–100 mL/m2), left ventricular end-systolic volume (LVSV) of 80 mL (LVSV/BSA, 43 mL/m2; normal range, 17–39 mL/m2); stroke volume (SV) of 85 mL (SV/BSA, 46 mL/m2; normal range, 43–67 mL/m2); and ejection fraction of 52% and (b) right ventricular end-diastolic volume (RVDV) of 163 mL (RVDV/BSA, 88 mL/m2; normal range, 63–111 mL/ m2), right ventricular end-systolic volume (RVSV) of 81 mL (RVSV/BSA, 44 mL/m2; normal range, 32–92 mL/m2); stroke volume (SV) of 82 mL (SV/BSA, 44 mL/m2; normal range, 39–71 mL/m2); and ejection fraction of 50%.Two-dimensional transthoracic echocardiography four-chamber end-diastolic (Fig 1A) and end-systolic views showed left ventricle apical thickening (Fig 1B), demonstrating apical myocardial hypertrophy. Diffusion-weighted brain MRI showed small multiple ischemic subacute hyperintense lesions localized in the cortical and subcortical frontal and occipital lobes (Fig 2). Unenhanced three-chamber cine steady-state free precession cardiac MRI (Fig 3A) showed left ventricle apical obliteration by a large thrombus; it was also possible to recognize a very thin hyperintense layer separating the thrombus and myocardium. T riple inversion recovery three-chamber view (Fig 3B) showed massive and diffuse endocardial hyperintensity, showing diffuse endocardial edema. Short-axis cine steady-state free precession images acquired after gadoterate meglumine (0.4 mL/kg of body weight) administration showed thickening and hyperintensity of the endocardium in the end-diastolic (Fig 3C) and end-systolic (Fig 3D) phases, as well as expression of diffuse endocardial hyperemia, which was well visible as hypointensity of the endoventricular thrombotic deposition. Gradient-echo inversion recovery was performed 10 minutes after contrast media injection (late gadolinium enhancement technique), and two-chamber long- (Fig 3E) and short-axis (Fig 3F) images showed left ventricular apical thrombus and apical endocardial delayed enhancement. Note the “V sign” of endomyocardial fibrosis at the apex, characterized by a three-layered appearance of dark overlying thrombus, bright fibrotic endomyocardium, and dark underlying myocardium. In consideration of the cardiac MRI findings (endocardial thickening with diffuse edema or hyperemia and delayed enhancement, apical thrombus) and hypereosinophilia of 8.710 K/mL (normal , 0.4 K/ mL), Loeffler endocarditis was suspected. The patient underwent a bone marrow biopsy that showed numerous cellular aggregates of the bone marrow, with a prevalence of the eosinophilic granulocytic myeloid line, in various stages of maturation and with numerous immature forms, enabling us to confirm myeloidhypereosiniphilic syndrome. After chemotherapy with STI-571 (imatinib) and corticosteroid (25 mg) and heparin administration (eight units per kilogram of body weight per hour, intravenous drip), the patient had a rapid reduction of eosinophilia (1.0 K/mL) and improvement in physical condition, and, subsequently, 1 month later underwent follow-up cardiac MRI. Follow-up unenhanced cardiac short-axis threechamber view cine steady-state free precession MRI (Fig 4A) showed reduction of the left ventricle apical. What is your diagnosis?