JACC. Case reports · 2026
Loeffler's Endomyocarditis With Embolic Stroke Secondary to Chronic Eosinophilic Leukemia With Therapy-Related Molecular Features.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Ramesh Sushmithaa, Yousif Nadia, Affas Ziad, Bajouka John, Haddad Jiries, Thacker Harsh, Zughaib Marcel
Аннотация
BACKGROUND: Loeffler's endomyocarditis is a severe manifestation of hypereosinophilia characterized by eosinophil-mediated myocardial injury, mural thrombus formation, and endomyocardial fibrosis. While often idiopathic, it may arise from clonal eosinophilic disorders carrying higher risk of end-organ damage.
CASE SUMMARY: A 77-year-old man with diffuse large B-cell lymphoma in remission presented 5 years after R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) chemotherapy with subacute confusion and dyspnea. Echocardiography demonstrated a large apical left ventricular thrombus with mildly reduced systolic function. Cardiac magnetic resonance revealed diffuse subendocardial late gadolinium enhancement. Progressive eosinophilia (peak: 3.07 × 109/L) with cytopenias prompted a bone marrow biopsy, which revealed chronic eosinophilic leukemia with monosomy 7 and pathogenic mutations, raising concern for a therapy-related clonal process. Despite emergent systemic anticoagulation followed by high-dose corticosteroids, brain magnetic resonance imaging showed multifocal embolic infarcts.
DISCUSSION: This case highlights clonal, potentially therapy-related eosinophilia as an under-recognized cause of Loeffler's endomyocarditis, requiring early diagnosis to prevent irreversible fibrosis and embolic complications.
CASE SUMMARY: A 77-year-old man with diffuse large B-cell lymphoma in remission presented 5 years after R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) chemotherapy with subacute confusion and dyspnea. Echocardiography demonstrated a large apical left ventricular thrombus with mildly reduced systolic function. Cardiac magnetic resonance revealed diffuse subendocardial late gadolinium enhancement. Progressive eosinophilia (peak: 3.07 × 109/L) with cytopenias prompted a bone marrow biopsy, which revealed chronic eosinophilic leukemia with monosomy 7 and pathogenic mutations, raising concern for a therapy-related clonal process. Despite emergent systemic anticoagulation followed by high-dose corticosteroids, brain magnetic resonance imaging showed multifocal embolic infarcts.
DISCUSSION: This case highlights clonal, potentially therapy-related eosinophilia as an under-recognized cause of Loeffler's endomyocarditis, requiring early diagnosis to prevent irreversible fibrosis and embolic complications.