Imatinib treatment–induced cardiomyopathy in hypereosinophilic syndrome

35%, and serum cTnT concentrations decreased to less than 0.02 ng/mL after 15 days. The remaining 3 pts showed no echocardiographic and/or cTnT changes after treatment with imatinib and at the follow-up checks (Table 1). In an idiopathic hypereosinophilic syndrome a major source of the morbidity and mortality is associated with cardiac involvement due to infiltrating eosinophils and based on an activation process involving surface molecules with release of eosinophilic cationic proteins that are known to be cytotoxic and to cause endothelial damage.3 Several reports have focused on the echocardiographic assessment of cardiovascular abnormalities associated with HES even if microscopic evidence of eosinophilic infiltration of the endomyocardium without echocardiographic evidence of abnormality occurs in at least a subset of patients with HES in percutaneous right ventricular biopsy samples.2 Cardiac Troponin T is a structural protein that attaches the troponin-tropomyosin complex to the thin filament of actin.4 Measurement of serum concentrations of cTnT in HES seems to indicate myocyte degeneration and may be helpful as a sensitive noninvasive marker of cardiac disorder.5 In our experience the rise of cTnT before starting imatinib and the evaluation of cTnT soon after imatinib have accurately predicted the development of acute left ventricular (LV) depression (cases 1 and 2). The mechanism of myocyte degeneration in HES during therapy with imatinib is not fully understood. However, the time course of development of acute LV dysfunction after starting imatinib and the rapid response to corticosteroid therapy suggest that an inflammatory response to degranulation of infiltrating eosinophils is responsible for the acute cardiogenic shock. Thus, it is necessary to recognize this potentially life-threatening complication promptly so as to start corticosteroid therapy at once. A larger study is warranted to investigate the value of cTnT and serial echocardiograms in predicting cardiac dysfunction in pts with HES treated with imatinib.