A 59-year-old male patient admitted to our emergency with progredient exertional dyspnea NYHA III, weakening, unspecific headache and rotary vertigo. Angina pectoris was denied. The physical examination showed a normal weighted patient, without congestion or jaundice. Pulmonary examination was normal. No pathologic heart murmur was noticed. Pulse rate was elevated up to 110 bpm, whereas blood pressure was normal. The patient was afebrile and referred no signs of infection.

He had a known history of multiple myeloma after triple autolog transplantation and first allogene transplantation seven months ago with a secondary hypereosinophile syndrom as a manifestated graft-versus-host-reaction, which was already treated with Tacrolimus. The iliac crest biopsy three weeks ago showed an eosiniphilia excess up to 38% (normal range 2-6%). Further diagnosis were chronic kidney disease, diabetes mellitus type II – insulin-dependend and multiple pathologic fractures. Peripheral or central artery disease were not known at time of admission.

Electrocardiogram (ECG) showed ST depression and T-wave inversions in leads V3-V6.  Echocardiography showed a normal right and left ventricular function with an ejection fraction (EF) of 75%. The apical left ventricular myocardium was thickend up to 21 mm with hypocontractility. These findings were not present in a transthoracic echocardiography done 3 months before. A left apical ventricular thrombus was suspected.

Initial Laboratory findings were as follows: mild anemia with hemoglobin 7,0 mmol/l (normal range 8.6-11.0), elevated white blood cell count 10.4 Gpt/l (normal 3.8-9.8) and a peripheral eosinophilia elevation up to 20.7%/2.15 Gpt/l (normal 2-4%/0.01-0.40Gpt/l). Heart enzymes with elevated high-sensitiv Troponin T of 138 ng/l (normal <14 ng/l), NT-proBNP 3625 ng/l (normal <125 ng/l), pathologic ECG and risk factors for coronary artery disease prompted a focused cardiac workup with direct transfer to our cardiac catheter laboratory. However, a coronary artery disease was excluded. 

A Cardiac-MRI confirmed the apcial thickening and a thrombus with 29x22 mm was seen with an „Ace-of-Spades-sign“. In accordance to the laboratory and imaging findings and the history of hypereosinophilia, diagnosis of Loeffler Endocarditis (LE) was made. An anticoagulation was started with low molecular heparin (LMH). In respect to the initial complaints of rotary vertigo and headache, a cranial computertomography with contrast agents was added. No insults or bleedings were seen. Differential diagnosis including infectious, parasites, rheumatological and autoimmune disorders were screened and excluded after laboratory tests. Heart biopsy was discussed for definite diagnosis of hypereosinophilia with cardiac involvement, but in risk of thrombus detachment declined.

In arrangement with our haematologist the existing therapy with Tacrolimus was escalated and supplemented by Prednisolon. During hospitalisation symptoms improved, dyspnea was reduced to NYHA II and vertigo was abscend.

After discharge from hospital our patient was admitted to the haematologic ambulance for further observation. The count of eosinophiles droped down to normal within six months. On LMH twice daily the thrombus was regredient. Left ventricular hypertrophy was still present but no hypokinesia was seen. Our patient was symptom-free.