Key result
Cycle 3 hs-cTnI elevation linked to ~15.4-fold higher odds of anthracycline-induced cardiotoxicity.
Why the study?
The study was conducted to investigate the clinical value of high-sensitivity cardiac troponin I in evaluating chemotherapy-related cardiac dysfunction induced by anthracyclines in postoperative breast cancer patients.
Does dynamic monitoring of serum high-sensitivity cardiac troponin I (hs-cTnI) accurately predict anthracycline-induced chemotherapy-related cardiac dysfunction (CTRCD) compared to NT-proBNP in postoperative breast cancer patients receiving CEF chemotherapy?
Cohort (n=180)
Single-blind (cardiologist measuring LVEF blinded to biomarker results)
No
Does dynamic monitoring of serum high-sensitivity cardiac troponin I (hs-cTnI) accurately predict anthracycline-induced chemotherapy-related cardiac dysfunction (CTRCD) compared to NT-proBNP in postoperative breast cancer patients receiving CEF chemotherapy?
Serum hs-cTnI measured at the third cycle of anthracycline chemotherapy provides superior predictive accuracy (AUC 0.957) over NT-proBNP for identifying breast cancer patients who will develop chemotherapy-related cardiac dysfunction.
Answers are grounded in this paper and cite their sources.
hs-cTnI at cycle 3 may aid risk stratification; leaves open prospective validation before changing practice in anthracycline-treated breast cancer.
Objective To investigate the clinical value of high-sensitivity cardiac troponin I (hs-cTnI) in evaluating chemotherapy-related cardiac dysfunction (CTRCD) induced by anthracyclines in postoperative breast cancer patients. Methods A retrospective study was conducted including 180 postoperative breast cancer patients treated at our hospital from August 2021 to August 2024. All patients completed six cycles of the cyclophosphamide–epirubicin–fluorouracil (CEF) regimen. According to the Chinese Society of Clinical Oncology (CSCO) guideline criteria, patients were divided into a cardiotoxicity group (n = 50) and a non-cardiotoxicity group (n = 130). Serum hs-cTnI and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, as well as left ventricular ejection fraction (LVEF) measured by echocardiography, were dynamically monitored before chemotherapy (T0) and after each chemotherapy cycle (T1–T6). The predictive value of each marker for CTRCD was evaluated using receiver operating characteristic (ROC) curves. Results Compared with the non-cardiotoxicity group, the cardiotoxicity group showed significantly higher serum hs-cTnI and NT-proBNP levels from T1 onward, with progressive increases over chemotherapy cycles (P < 0.01), while LVEF progressively decreased (P < 0.01). ROC analysis indicated that serum hs-cTnI at the third chemotherapy cycle (T3) had an area under the curve (AUC) of 0.957 (95% CI: 0.905–0.988) for predicting CTRCD, with an optimal cutoff value of >1358.5 pg/mL, yielding a sensitivity of 92.00% and specificity of 91.54%. Its predictive performance was significantly superior to that of NT-proBNP at the same time point [AUC = 0.684 (95% CI: 0.590–0.763)]. Conclusion Serum hs-cTnI is a highly sensitive and specific biomarker for the early and dynamic monitoring of anthracycline-induced cardiotoxicity. The hs-cTnI level at mid-chemotherapy (third cycle) has excellent predictive value for CTRCD, facilitating early identification of high-risk patients and timely clinical intervention.
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Li et al. (2026) conducted a cohort in Postoperative invasive breast cancer receiving adjuvant anthracycline-based chemotherapy (n=180). Serum hs-cTnI >1358.5 pg/mL at the third chemotherapy cycle (T3) vs. Serum hs-cTnI <=1358.5 pg/mL at the third chemotherapy cycle (T3) was evaluated on Anthracycline-induced cardiotoxicity (chemotherapy-related cardiac dysfunction, defined as symptomatic LVEF decline >=5% or asymptomatic decline >=10% to <55%) (OR 15.42, 95% CI 6.78-35.08, p=<0.001). Serum hs-cTnI >1358.5 pg/mL at cycle 3 independently predicted anthracycline-induced cardiotoxicity (aOR 15.42, 95% CI 6.78-35.08; AUC 0.957) in postoperative breast cancer patients.
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