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Hypereosinophilic syndrome (HES) is a rare disorder characterized by persistent marked eosinophilia combined with eosinophil-mediated organ damage. Myeloproliferative variants are associated with a high prevalence of cardiac involvement, which is very unusual in lymphocytic variants. Imatinib mesylate (Gleevec(R)) is a small molecule with tyrosine kinase activity that has shown marked effects in some individuals with HES. In this case report, we present a patient with a hypereosinophilic syndrome (lymphocytic variant) that first manifested as hypereosinophilia and heart failure secondary mainly to right ventricle systolic dysfunction. A week after imatinib therapy instauration the eosinophil count was within normal range but the patient suffered a severely left ventricular dysfunction that was restablished after early drug withdrawal. Surgical removal of a new onset mass in right atrium was required because of progressively growth despite anticoagulant therapy. Clinicians should be aware of the variable heart manifestations in patients with HES and the potential cardiotoxicity of imatinib.

Background Chagas' disease is becoming a public health problem in Europe because of migratory movements. Cardiac magnetic resonance (CMR) has emerged as a non-invasive tool to assess cardiac tissue characteristics. There is scarce data available on CMR in patients with Chagas' disease. Objective To describe CMR findings in patients with Chagas' disease living in a non-endemic area focusing on differentiation from other cardiomyopathies and relation with clinical status. Methods and results Sixty-seven Chagas' disease patients divided into 3 groups—group 1 (indeterminate form: positive serology without ECG or 2D-echocardiographic abnormalities; N =27), group 2 (ECG abnormalities of Chagas' disease but normal 2D-echocardiography; N =19), and group 3 (regional wall motion abnormalities, LV end-diastolic diameter >55mm or LV ejection fraction N =21)—were studied. The presence of wall motion abnormalities and delayed enhancement (DE) by CMR was more frequent in the inferolateral and apical segments. DE distribution in the myocardial wall was heterogeneous (subendocardial 26.8%, midwall 14.0%, subepicardial 22.6%, and transmural 36.0% of total segments with DE) and related to larger cardiac chambers and worse systolic function. Conclusion Pattern of DE in Chagas' disease may mimic that of both ischemic and nonischemic cardiomyopathies, with especial predilection for the apical and inferolateral segments of the left ventricle. These findings support that myocardial involvement in chronic Chagas' cardiomyopathy (CCC) may be due to both microvascular disturbances and chronic myocarditis and may favor CCC in the differential diagnosis of patients with compatible epidemiological history and heart failure of uncertain etiology.