Haopeng Wang, Fu Zhu, Hailing Hu
Hypereosinophilic syndrome (HES) is defined by marked eosinophilia accompanied by eosinophil-mediated organ injury. Cardiac involvement can progress from endomyocardial inflammation to mural thrombosis and fibrosis, with systemic embolization. A 58-year-old man presented with recurrent chest distress and back pain. Laboratory testing showed an absolute eosinophil count of 2.01 × 10⁹/L, cardiac troponin I of 0.25 ng/mL, N-terminal pro-B-type natriuretic peptide of 3,272 pg/mL, and D-dimer of 1.12 mg/L. Coronary angiography excluded fixed obstructive coronary disease and demonstrated dynamic systolic compression of the mid-left anterior descending artery due to myocardial bridging. Brain magnetic resonance imaging, performed because of memory decline and concern for clinically silent embolization, identified multifocal acute cerebral infarctions. Cardiac magnetic resonance imaging demonstrated left ventricular endocardial thickening, subendocardial late gadolinium enhancement, and a non-enhancing mural thrombus, consistent with Löffler endocarditis. Bone marrow eosinophils accounted for 56.4% of nucleated cells. Flow cytometry identified a CLL-phenotype clonal mature B-cell population; however, the peripheral blood CD19-positive B-cell count was only 0.334 × 10⁹/L and no lymphadenopathy or hepatosplenomegaly was found, making overt chronic lymphocytic leukemia unsupported by current criteria. A limited myeloid fusion panel was negative. The patient received dexamethasone 20 mg/day and anticoagulation with enoxaparin and warfarin. The eosinophil count normalized within four days, but six-month cardiac magnetic resonance follow-up showed persistent endocardial disease and a slightly enlarged mural thrombus. This case highlights the need for integrated hematologic, immunologic, and cardiac evaluation in HES, cautious interpretation of coincident lymphoid clones, and long-term imaging and anticoagulation surveillance even after rapid hematologic improvement.