Values of high sensitive troponin T in long-term survivors of childhood cancer treated with anthracyclines

• High sensitive cardiac troponin T is measured in survivors of childhood cancer.
• It is not a good biomarker in late subclinical anthracycline induced cardiotoxicity.
• Its role in early-onset anthracycline-induced cardiotoxicity should be investigated.

BackgroundCardiac biomarkers can play an important role in the early detection of subclinical heart failure. Our aims are to 1) obtain values of high sensitive cardiac troponin T (hs-cTnT) in long-term survivors of childhood cancer and 2) investigate the potential role of hs-cTnT in the detection of subclinical late-onset cardiotoxicity.MethodsHs-cTnT and N-terminal-pro-brain natriuretic peptide (NT-pro-BNP) were measured in 64 survivors. Electrocardiography and echocardiography were performed to evaluate cardiac function.ResultsMean follow-up period was 8.3 years (range of 4.5 to 34.1). All survivors were clinically asymptomatic and had no history of clinical heart failure during or immediately after anthracycline treatment. Electrocardiography (available in 59 of 64 survivors) showed no signs of myocardial injury related to ischemia or abnormal QTc. Echocardiography was performed in all survivors. Mean left ventricular shortening fraction (SF) was 34% (range of 28 to 43%); mean ejection fraction (EF) was 61% (range of 48 to 74%). Seven survivors had a mildly decreased EF between 48% and 55%. Normal hs-cTnT levels were found in all 64 survivors (range of 3 to 13 ng/L) and did not differ among different anthracycline dosage groups: ≤ 120, 120–300 and ≥ 300 mg/m2. Yet, 5/64 survivors had elevated NT-pro-BNP levels (range of 7 to 25 pg/ml) with normal SF and ECG findings and only one mildly abnormal EF of 51%.ConclusionsHs-cTnT concentrations are normal in long-term survivors of childhood cancer, even in the subpopulations with elevated NT-pro-BNP and/or a mildly decreased EF, indicating that it is not a sensitive marker for late onset subclinical anthracycline induced cardiotoxicity.