To the editorWith the recent interest in monoclonal antibody therapy in hypereosinophilic syndromes, we present the case of a 53-year-old lady admitted complaining of acute central chest pain and dyspnoea. This was a previously well patient with no significant ischaemic risk factors; however, admission electrocardiogram ( Fig. 1) showed lateral T-wave inversion together with an elevated troponin T of 2.18 ng/ml, leading to a provisional diagnosis of a first presentation myocardial infarction. Therefore, dual antiplatelet therapy and low molecular weight heparin were commenced with resolution of the chest discomfort. A transthoracic echocardiogram demonstrated a localized pericardial effusion and moderate global impairment of left ventricular (LV) systolic function rather than the expected regional wall deficit, which raised the possibility of an inflammatory as opposed to infarctive process. Elevated inflammatory indices included a total white cell count of 20 Â 10 9 /l with a predominant eosinophilia (65%) and these findings, together with subsequently normal coronary angiography, resulted in the assumed diagnosis of infarction being amended to that of eosinophilic myocarditis. This was confirmed on endomyocardial biopsy (Fig. 2) with concurrent bone marrow (Fig. 3) and gastric involvement seen on histopathology. In the absence of a secondary cause, a diagnosis of idiopathic hypereosinophilic syndrome was made according to the criteria outlined by Chusid et al. (Fig. 4). 1 Consequently, dual antiplatelet therapy was discontinued and the patient commenced on interferon-alpha, prednisolone and trandolapril with good clinical effect and complete resolution of the peripheral eosinophilia. Despite the initial moderate LV impairment with an ejection fraction of less than 35%, there was full recovery of LV systolic function within a few months of presentation and the initial acute ECG changes that had contributed to the assumption of ischaemia also improved progressively (Figs 5 and 6).