A 66-year-old woman was admitted with NYHA class II congestive heart failure, oedema of the lower extremities, and slight jugular vein enlargement. She had no history of drug allergy but was known for an adult form of bronchial asthma, treated with oral corticosteroids, and for a newly diagnosed type-2 diabetes mellitus. She complained of headaches, low-grade fever, painful ears, decreased appetite and 12 kg weight lost during the last six months. The results of a routine haematological study showed a total eosinophil count of 5750/ml. The routine clinical chemistry demonstrated small augmentation of troponin T level, creatine phosphokinase, lactic dehydrogenase and pro-BNP. Transthoracic and then transoesophagial echocardiography [1] revealed a thickening of the anterior left ventricular wall, appearing bright (Figure 1 – arrows) and a mass-like lesion in the left ventricle. An invasive examination showed normal coronary arteries, modest impaired left ventricular function due to apical hypokinesia and a restrictive filling pattern. The endomyocardial biopsy (Figure 2 and Figure 3) from the right ventricle illustrated oedematous changes, thickening of the endocardium (Figure 2– arrowheads), necrosis and degeneration of the myocytes. Fibrosis and infiltration of lymphocytes admixed with marked eosinophils (Figure 3 – arrows) were seen in the interstitial space of the myocardium, and eosinophils had infiltrated the endocardium. These findings finally assessed the diagnosis of Loeffler’s syndrome or so-called idiopathic hypereosinophilic syndrome [2, 3]. Magnetic resonance imaging showed multiple little cerebral infarctions probably due to embolism from thrombotic material in the left ventricle [3, 4].
Figure 1.
Figure 2.
Figure 3.
References
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