Abstract
Löffler's endocarditis (cardiac involvement in hypereosinophilic syndrome) is rare yet life-threatening if left untreated. We describe a case of hypereosinophilic syndrome presenting as a cardiac mass with an abnormal electrocardiogram. Diagnostic studies of the cardiac mass strongly suggested a malignant cardiac tumor invading the papillary muscle. Thus, excision of the cardiac mass and endomyocardial resection with mitral valve replacement were successfully performed. Pathology revealed various stages of thrombosis and irreversible myocardial damage caused by eosinophilic infiltration with no malignancy, leading to the correct diagnosis of late-stage Löffler's endocarditis. The subsequent combination of anticoagulation and corticosteroids was effective with a favorable outcome. This case highlights pitfalls in multimodality imaging of cardiac thrombus and the clinical significance of considering Löffler's endocarditis in the diagnostic work-up of a cardiac mass.
Highlights
Hypereosinophilic syndrome (HES) is an uncommon group of diseases characterized by persistent hypereosinophilia with eosinophil-mediated multiple organ involvement [1]
Diagnosis of HES is based upon the following criteria; an absolute eosinophil count >1,500 cells/μL in the peripheral blood for at least 1 month, organ damage and/or dysfunction caused by eosinophilic infiltration, and exclusion of potential causes of secondary eosinophilia including allergic diseases and parasitic infections
We described a case of histologically proven late-stage Löffler’s endocarditis (LE) presenting as a cardiac mass, which was successfully treated with the combination of surgical intervention and sequential medical treatment
Summary
Hypereosinophilic syndrome (HES) is an uncommon group of diseases characterized by persistent hypereosinophilia with eosinophil-mediated multiple organ involvement [1]. Patients develop cardiac thrombi and present with symptoms and signs based on embolic events such as stroke, or mass effects including secondary mitral regurgitation (MR) and ventricular cavity obliteration, respectively. The patient had a 3-year history of hypereosinophilia, for which etiologies remained unknown despite thorough diagnostic evaluation Eosinophil infiltrations were observed in the endocardium, immunostaining for major basic protein, which is one of eosinophil-specific cardiotoxic granules, showed no remarkable extracellular deposition, indicating no evidence of eosinophilic activation (Figures 4C,D). These findings led to a correct diagnosis of late-stage LE. We present a summarized illustration of the case presentation (Figure 5)
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