Hypereosinophilic syndrome with cardiac involvement in our patient was marked by a myocardial thickening (A, arrows), which resolved after corticosteroid treatment (B, arrows). The artifact in the left ventricular apex was also noted (B, asterisk). LV Z left ventricle; RV Z right ventricle. 

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Context 1

... admission, an episode of acute pulmonary edema occurred. Newly found poor R wave progression in anterior leads on the ECG prompted a subsequent transthoracic echocardiography (TTE) exam, which showed a dilated left atrium (diameter, 4.5 cm in the parasternal long axis view), adequate left ventricular (LV) systolic performance, and thickened mitral valve with restricted motion of PML, leading to severe MR (Fig. 1A) with severe pulmonary hypertension (estimated pulmonary arterial systolic pressure, 73 mmHg). Severe tricuspid regurgitation (TR) was also observed (Fig. 1A). We noted thickening of the LV endocardium, which was a unique pattern caused by eosinophil infiltration (Fig. 2A, arrows). The cardiac magnetic resonance (CMR) imaging showed subendocardial edema (Fig. 3A, arrows) consistent with areas of first-pass perfusion defect (Fig. 3B, arrows), which was clearly delineated via the delayed myocardial enhancement (DME) images ( Fig. 3C and D). In the DME images of LV, we saw an innermost layer of hypointense thrombus and the middle layer of hyperintensity, which was probably encompassed by inflammatory exudate and fibrotic tissue ( Fig. 3C and D). Combining the image findings, the endocardial thickening was a result of eosinophil related myocardium injury and was composed of necrotic tissue, myocardial fibrosis, and thrombi. A myocardial biopsy of the right ventricle showed eosinophil infiltration (Fig. 4, circles). Oral anticoagulant therapy was given to prevent thrombo- embolic events. Intravenous hydrocortisone (200 mg/day) was given initially with a gradual taper in dosage and was shifted to oral prednisolone finally. After treatment with corticosteroid for 2 months, the follow-up TTE showed a resolution of endocardial thickening (Fig. 2B), as well as improvements of MR and TR (Fig. 1B). The peripheral eosin- ophil count was returned to normal (3.2%, reference range, 0e8%) and his diarrhea also ...

Context 2

... admission, an episode of acute pulmonary edema occurred. Newly found poor R wave progression in anterior leads on the ECG prompted a subsequent transthoracic echocardiography (TTE) exam, which showed a dilated left atrium (diameter, 4.5 cm in the parasternal long axis view), adequate left ventricular (LV) systolic performance, and thickened mitral valve with restricted motion of PML, leading to severe MR (Fig. 1A) with severe pulmonary hypertension (estimated pulmonary arterial systolic pressure, 73 mmHg). Severe tricuspid regurgitation (TR) was also observed (Fig. 1A). We noted thickening of the LV endocardium, which was a unique pattern caused by eosinophil infiltration (Fig. 2A, arrows). The cardiac magnetic resonance (CMR) imaging showed subendocardial edema (Fig. 3A, arrows) consistent with areas of first-pass perfusion defect (Fig. 3B, arrows), which was clearly delineated via the delayed myocardial enhancement (DME) images ( Fig. 3C and D). In the DME images of LV, we saw an innermost layer of hypointense thrombus and the middle layer of hyperintensity, which was probably encompassed by inflammatory exudate and fibrotic tissue ( Fig. 3C and D). Combining the image findings, the endocardial thickening was a result of eosinophil related myocardium injury and was composed of necrotic tissue, myocardial fibrosis, and thrombi. A myocardial biopsy of the right ventricle showed eosinophil infiltration (Fig. 4, circles). Oral anticoagulant therapy was given to prevent thrombo- embolic events. Intravenous hydrocortisone (200 mg/day) was given initially with a gradual taper in dosage and was shifted to oral prednisolone finally. After treatment with corticosteroid for 2 months, the follow-up TTE showed a resolution of endocardial thickening (Fig. 2B), as well as improvements of MR and TR (Fig. 1B). The peripheral eosin- ophil count was returned to normal (3.2%, reference range, 0e8%) and his diarrhea also ...