JACC. Case reports · 2026
Loeffler Endocarditis: Multimodality Imaging of a Common Cardiac Phenotype in Distinct Hypereosinophilic Syndromes.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Salar Tooba, Feitell Scott, Parikh Vishal, Baibhav Bipul
Аннотация
BACKGROUND: Loeffler endocarditis is a late manifestation of hypereosinophilic syndromes characterized by endomyocardial fibrosis and intracardiac thrombosis. Early recognition is essential yet challenging because presentation is often nonspecific.
CASE SUMMARY: Case 1 involved a 43-year-old man with long-standing atopy and persistent eosinophilia who presented with heart failure symptoms. Echocardiography demonstrated biventricular apical thrombi, and cardiac magnetic resonance confirmed ventricular thrombi and revealed diffuse subendocardial late gadolinium enhancement confirming fibrotic-stage disease. High-dose corticosteroids produced rapid hematologic response, and anticoagulation was initiated. Case 2 involved a 38-year-old man who was admitted for abdominal pain and incidentally found to have eosinophilia and right ventricular apical infiltration. Cardiac magnetic resonance established the diagnosis of Loeffler endocarditis. Molecular testing identified FIP1L1-PDGFRA-positive myeloproliferative hypereosinophilic syndrome. Eosinophil counts normalized promptly with imatinib.
CONCLUSIONS: These cases illustrate a final common cardiac phenotype arising from diverse causes of hypereosinophilia. Imaging was central not only for diagnosis and staging, but also for prompting systemic investigation and directing targeted therapy.
CASE SUMMARY: Case 1 involved a 43-year-old man with long-standing atopy and persistent eosinophilia who presented with heart failure symptoms. Echocardiography demonstrated biventricular apical thrombi, and cardiac magnetic resonance confirmed ventricular thrombi and revealed diffuse subendocardial late gadolinium enhancement confirming fibrotic-stage disease. High-dose corticosteroids produced rapid hematologic response, and anticoagulation was initiated. Case 2 involved a 38-year-old man who was admitted for abdominal pain and incidentally found to have eosinophilia and right ventricular apical infiltration. Cardiac magnetic resonance established the diagnosis of Loeffler endocarditis. Molecular testing identified FIP1L1-PDGFRA-positive myeloproliferative hypereosinophilic syndrome. Eosinophil counts normalized promptly with imatinib.
CONCLUSIONS: These cases illustrate a final common cardiac phenotype arising from diverse causes of hypereosinophilia. Imaging was central not only for diagnosis and staging, but also for prompting systemic investigation and directing targeted therapy.