High-sensitive cardiac troponin-I facilitates timely detection of subclinical anthracycline-mediated cardiac injury.

Background Anthracycline drugs are effective anticancer agents, but their optimal use is limited in many patients by the associated cardiotoxicity, even at designated safe doses. As conventionally sensitive cardiac troponin-I assays fail to reliably quantify concentrations of cardiac troponin-I below 30 ng/L, we investigated the potential role of high-sensitive cardiac troponin-I in the detection of subclinical cardiomyocyte injury in patients treated with anthracycline agents. Methods Serial high-sensitive cardiac troponin-I concentrations were assessed in 84 patients, receiving anthracycline-containing ( n = 38) and non-anthracycline-containing ( n = 46) regimens. Results were assessed for change from pretreatment levels and evaluated according to unisex and gender-specific 99th percentiles (25 ng/L and M: 34 ng/L, F: 16 ng/L, respectively). Results A significant increase in high-sensitive cardiac troponin-I was observed in the anthracycline cohort following five cycles of treatment, with the greatest change correlating to an absolute δ increase of 30.7 ng/L in the early-dose group (early-dose group: P < 0.0001, late-dose group: P < 0.01 and continuous-dose group: P < 0.0001). Doxorubicin dose did not correlate directly with high-sensitive cardiac troponin-I concentrations (Spearman r < -0.22). No significant changes in high-sensitive cardiac troponin-I were reported among the non-anthracycline cohort with all measurements below the 99th percentiles. Conclusions Treatment with anthracycline-based chemotherapeutic regimen demonstrated significant elevations of high-sensitive cardiac troponin-I, indicative of subclinical cardiomyocyte damage. This study demonstrates a role for high-sensitive cardiac troponin-I in evaluating those patients where cardiotoxicity is a concern and a potential future role as a biomarker in optimizing cardioprotective treatments in patients receiving anthracycline therapy.