A 66-year old female patient with no previous cardiac history was admitted in a local hospital in December 2021 due to significant weight loss and symptoms of heart failure (exertional dyspnea, fatigue, lower extremity edema). Patient’s initial weight of 79 kg was gradually reduced to 49 kg during past three years, with particular acceleration of weight loss in the past three months before admission. Her past medical history included bronchial asthma, chronic pansinusitis and hypothyroidism.  Due to significant cachexia, patient underwent comprehensive cancer screening - with all negative results including PET/CT scan. At the same time, echocardiographic examination revealed a large right ventricular formation filling up to two thirds of the right ventricle, resembling a tumorous mass. Patient was thus referred to our medical center in order to complete the diagnostic process of presumed malignant cardiac tumor as an underlying cause of cachexia.

At admission to general cardiology department in our medical center in January 2022, asthenic patient with BMI 18 presented with holosystolic apical murmur and right-sided pleural effusion. Lower extremity edemas had already been removed after diuretic treatment. ECG at admission showed signs of subendocardial injury in anterolateral leads (Figure 1).

The initial laboratory findings were as follows (Table 1): the white blood cell count was within normal limits (5.02 x 10*9/l - normal range 4.0-10.0 x 10*9/l), with boundary elevation of peripheral eosinophilia (absolute eosinophil count  0,67 x 10*9/l, normal range 0.0-0.5 x 10*9/l, relative eosinophil count 13.3%, normal range 0.0-5.0%), C-reactive protein level was increased to 51.3mg/l (normal range 1.0-5.0), level of NTproBNP was elevated to 4400ng/l (normal range 0.0-125.0), troponin level was mildly increased (high sensitive troponin T 125ng/l, normal range 0.0-14.0), D-dimer was elevated to 4.03mg/l (normal range 0.0-0.55).

Echocardiography confirmed dilatated right ventricle with a large tumorous mass, dilatated right atrium, normal left chamber size with preserved systolic function, and moderate mitral regurgitation due to retraction of posterior leaflet (Figure 2).

Targeted biopsy of the intracardiac mass was performed. The procedure was carried out in analgosedation with transesophageal echocardiography guidance. Eight samples were obtained from the apical third of the right ventricle. However, the procedure was complicated by right ventricular perforation causing hemopericardium and cardiac tamponade. Immediate pericardiocentesis was conducted in the cath-lab and hemopericardium was successfully removed.

Subsequently, patient was admitted to department of acute cardiology. On follow-up transthoracic echocardiography besides large right ventricle mass an echodense mass was observed in the left ventricular apex (size 12x13mm) (Figure 3). Presence of formations in both ventricular apexes, together with laboratory findings of eosinophilia and pathological EKG, led us to presumption of non-malignant disease etiology, specifically eosinophilic myocarditis.

CMR was added in order to confirm the diagnosis. Results showed late gadolinium enhancement with diffuse subendocardial distribution in apical and midventricular segments of both ventricles and in both papillary muscles (Figure 4). Further, presence of several intracardiac thrombi was detected: besides large thrombus obliterating apex and midventricular part of the right ventricle, smaller thrombi were described in left ventricular apex (9x13mm), right atrium (5x5mm) and right atrial auricle (8x6mm) (Figure 5). CMR thus confirmed distinctive signs of eosinophilic myocarditis.

Histological results from endomyocardial biopsy definitely ruled out initially presumed diagnosis of cardiac tumor, since no signs of malignant proliferation were detected. Histological evaluation of evacuated hemopericardium revealed high concentration of eosinophils (up to 50 eosinophils per one high-power field) without cytogenetic or molecular abnormalities, what represents a characteristic finding in idiopathic hypereosinophilic syndrome.

Consequently, anticoagulant and corticosteroid treatment was initiated, alongside with nutrition support and heart failure treatment. Patient was transferred back to referring hospital for further hematologic examination, including bone marrow biopsy. However, despite the treatment, patient died due to progressive irreversible cachexia with the weight of 42kg in March 2022.