Cardiotoxicity evaluation in pediatric patients with acute lymphoblastic leukemia – results of prospective study

The harmful effect of chemotherapy on the heart muscle is well known, the most impugned being the anthracyclines (AC) class [4], which triggers the prototype for type I chemotherapy-induced cardiotoxicity (CIC), characterized by dose-dependent irreversible myocardial cell death [5]. Alongside cardiac troponins and natriuretic peptides, novel biomarkers emerge, such as high-sensitivity Creactive protein and fatty acid binding protein [12]. The aim of our study was to assess the early-onset CIC after low-dose doxorubicin-based treatment in children diagnosed with ALL, in a single pediatric hematologyoncology center, by monitoring the changes of troponin I (TnI) and heart-type binding protein (HFABP) levels and the parameters of conventional and TDI echocardiography over a period of one year after diagnosis. The following measurements were performed: left ventricle ejection fraction (LVEF) with the M mode Teichholz method, LV outflow tract time-velocity integral (TVI), tricuspid annular plane systolic excursion (TAPSE), peak systolic septal mitral annulus velocity (SS), peak systolic lateral mitral annulus velocity (SL) and right ventricle (RV)-peak systolic tricuspid annulus velocity (RVS), early filling transmitral flow velocity (E), late filling transmitral flow velocity (A), E-wave deceleration time (EDT), isovolumic relaxation time (IVRT), E/A.