Assessment of anthracycline-induced cardiotoxicity with biochemical markers.

Aim: Assessment of acute and chronic cardiotoxicity of anthracyclines in patients treated for acute leukemia (AL) with biochemical markers - "N-terminal pro brain natriuretic peptide" (NT-proBNP), cardiac troponin T (cTnT), creatine kinase MB (CK-MB mass), and echocardiography.

Methods: Twenty-six adult AL patients (mean age 46.2 +/- 12.4 years, 15 males) treated with 2-6 cycles of chemotherapy (CT) containing anthracyclines in the total cumulative dose of 464.3 +/- 117.5 mg/m2 were studied. Cardiac evaluation was performed at baseline, after first and last CT with anthracyclines and 6 months after CT.

Results: Mean baseline NT-proBNP concentration was 117.7 +/- 46.4 ng/L (slightly elevated in 3 patients). After first and last CT, NT-proBNP elevations to 299.7 +/- 176.2 ng/L and 287.1 +/- 147.4 ng/L were observed, respectively. Six months after CT, mean NT-proBNP concentration was 362.5 +/- 304.9 ng/L (elevated in 16 patients). Changes in NT-proBNP were significant in comparison with the baseline values (p < 0.001). Six months after CT, two patients with marked NT-proBNP elevations during CT developed treatment-related cardiomyopathy with symptoms of heart failure. NT-proBNP correlated with systolic and diastolic LV dysfunction on echocardiography (r = 0.514; p < 0.01) and (r = 0.587; p < 0.01). CTnT concentrations were negative (bellow 0.01 microg/L) during CT in all patients. Six months after CT, delayed cTnT positivity occurred in 3 patients. CK-MB mass remained within the reference range in all patients.

Conclusion: Our study shows that anthracycline treatment is associated with acute and chronic neurohumoral activation of cardiac dysfunction that is manifested by a significant increase in NT-proBNP. It seems that NT-proBNP could be useful in the early detection of anthracycline cardiotoxicity. CTnT negativity during anthracycline treatment suggests that anthracyclines, even in higher cumulative doses, do not cause detectable acute injury to cardiomyocyte structure. Further studies using more sensitive markers of cardiac damage will be needed in this context.