Objectives Daunorubicin causes cardiac injury in acute nonlymphocytic leukemia. Early identifying caridotoxicity induced by daunorubicin might help individualise cardiac protect treatment. Dexrazoxane can reduce cardiac damage. In this study, we assess the left ventricular function in patients with acute nonlymphocytic leukemia who had daunorubicin treatment with or without in combination with dexrazoxane.
Methods Patients with acute nonlymphocytic leukemia, undergoing three-cycle chemotherapy regimen, were randomly assigned to receive daunorubicin alone (n = 22) or daunorubicin with dexrazoxane (n = 20). Echocardiograms and serial measurements of cardiac troponin T (cTnT), N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hsCRP) were obtained before, during and after treatment.
Results There were no significant differences in left ventricle ejection faction (LVEF), diastolic mitral wave ratio E/A throughout all phases of the treatment between two groups. Tissue Doppler index e’/a’ in daunorubicin group before treatment was 1.08 ± 0.05 and 0.98 ± 0.24 after treatment (P = 0.04), however, in daunorubicin-dexrazoxane group was 1.11 ± 0.07 to 1.09 ± 0.10 (P = 0.57). Tei index in daunorubicin group before treatment was 0.32 ± 0.03 and 0.49 ± 0.11 after treatment (P = 0.001), in daunorubicin-dexrazoxane group was 0.33 ± 0.03 to 0.34 ± 0.04 (P = 0.07). After treatment, cTnT levels were increased 52% in daunorubicin group and 14% in doxorubicin-dexrazoxane group, (P = 0.003). NT-proBNP levels were increased 48% and 16%, respectively, after treatment (P = 0.04). The percentage of hsCRP levels did not differ between groups at any time. During the treatment, e’/a’, Tei index were associated with abnormally increased cTnT and NT-proBNP levels (P <0.05).
Conclusions Cardiac diastolic dysfunction index e’/a’ and Tei index showed better performance in the group received dexrazoxane, and they were related to abnormal changes in cardiac biomarkers too. It shows that e’/a’ and Tei index would be potential applicable markers for detecting early daunorubicin–induced cardiac damage.