Key Takeaways
- Troponin and GLS detect subclinical myocardial injury before overt HF, providing a therapeutically actionable window to manage CTRCD during active cancer treatment. [1-4]
- Persistent troponin elevation during chemotherapy predicts subsequent LVEF decline and adverse cardiac events, functioning as a high-sensitivity indicator for cardiac risk. [5-7]
- A multimarker strategy using troponin for rule-out and NT-proBNP for global cardiovascular stress improves predictive performance for short- and long-term CTRCD.[7-9]
- Biomarker elevation identifies a pre-HF phenotype (Stage A/B) that justifies selective cardioprotection to prevent symptomatic decline and maintain cancer therapy continuity. [10]
This section presents a concise, high-yield summary of the video’s core content, designed as a quick reference for Healthcare Professionals (HCPs).
Note: This content was developed by our editorial team and was not reviewed or endorsed by the video speaker.
Q1. What makes CTRCD a clinically important phenotype in cardio-oncology?
As the most critical toxicity in cardio-oncology, CTRCD directly compromises long-term survival, increases heart failure risk, and jeopardizes the delivery of life-saving cancer treatment.[11,12]
Q2. How do troponin and GLS contribute to early detection?
Both detect subclinical myocardial injury before symptoms or overt HF develop. This early signal may precede the therapeutic inflection point at which intervention may alter long-term cardiac outcomes. [1,2,3]
Q3. What is the prognostic value of troponin elevation during chemotherapy?
Troponin elevation correlates with subsequent declines in LVEF and a higher risk of adverse cardiac events, particularly when elevations persist beyond treatment completion. [2,6,7]
Q4. How do troponin and natriuretic peptides differ in their biomarker roles?
Troponin has a strong negative predictive value for excluding short-term CTRCD, whereas NT-proBNP reflects global cardiovascular stress and carries prognostic information even when not directly associated with CTRCD. [7,8,9]
Q5. Why is a multi-marker approach advantageous?
Integration of troponin with additional biomarkers such as MPO and NT-proBNP increases predictive granularity, and dynamic percentile-based thresholds may better capture individual variability than absolute cut-offs. [7,13]
Q6. How does CTRCD map onto the heart failure staging continuum?
CTRCD aligns with Stage A/B HF in the universal HF definition, suggesting that biomarker-defined injury may justify selective cardioprotective strategies prior to symptomatic decline.[5,10]
Q7. What do recent biomarker-guided cardioprotection trials indicate?
Therapeutic response appears phenotype- and agent-specific: carvedilol + candesartan did not improve outcomes in troponin-positive patients (Cardiac CARE), whereas sacubitril/valsartan showed signals of GLS and LVEF preservation (SARAH). [14,15]
Q8. Are new biomarkers emerging beyond troponin and NT-proBNP?
Chromogranin A (CgA) correlated with GLS/LVEF impairment and predicted non-recovery of LV function in single-center cohorts, suggesting potential utility in future multi-marker models. [16]
References
- Cardinale D, Sandri MT, Martinoni A, et al. Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy. J Am Coll Cardiol. 2000;36(2):517-522. doi:10.1016/s0735-1097(00)00748-8
- Cardinale D, Sandri MT, Colombo A, et al. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004;109(22):2749-2754. doi:10.1161/01.CIR.0000130926.51766.CC
- Alvarez-Cardona JA, Zhang KW, Mitchell JD, Zaha VG, Fisch MJ, Lenihan DJ. Cardiac Biomarkers During Cancer Therapy: Practical Applications for Cardio-Oncology. JACC CardioOncol. 2020;2(5):791-794. Published 2020 Dec 15. doi:10.1016/j.jaccao.2020.08.014
- Cardinale D, Colombo A, Lamantia G, et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010;55(3):213-220. doi:10.1016/j.jacc.2009.03.095
- Cardinale D, Colombo A, Sandri MT, et al. Prevention of high-dose chemotherapy-induced cardiotoxicity in high-risk patients by angiotensin-converting enzyme inhibition. Circulation. 2006;114(23):2474-2481. doi:10.1161/CIRCULATIONAHA.106.635144
- Cardinale D, Colombo A, Torrisi R, et al. Trastuzumab-induced cardiotoxicity: clinical and prognostic implications of troponin I evaluation. J Clin Oncol. 2010;28(25):3910-3916. doi:10.1200/JCO.2009.27.3615
- Demissei BG, Hubbard RA, Zhang L, et al. Changes in Cardiovascular Biomarkers With Breast Cancer Therapy and Associations With Cardiac Dysfunction. J Am Heart Assoc. 2020;9(2):e014708. doi:10.1161/JAHA.119.014708
- Michel L, Mincu RI, Mahabadi AA, et al. Troponins and brain natriuretic peptides for the prediction of cardiotoxicity in cancer patients: a meta-analysis. Eur J Heart Fail. 2020;22(2):350-361. doi:10.1002/ejhf.1631
- Park H, Lee N, Yoon HJ. Reply: Withdrawal of Cardioprotective Therapy Following Improvement in Cancer Therapeutics-Related Cardiac Dysfunction. JACC CardioOncol. 2025;7(2):190. doi:10.1016/j.jaccao.2024.12.006
- Bloom MW, Vo JB, Rodgers JE, et al. Cardio-Oncology and Heart Failure: a Scientific Statement From the Heart Failure Society of America. J Card Fail. 2025;31(2):415-455. doi:10.1016/j.cardfail.2024.08.045
- Anand K, Ensor J, Trachtenberg B, Bernicker EH. Osimertinib-Induced Cardiotoxicity: A Retrospective Review of the FDA Adverse Events Reporting System (FAERS). JACC CardioOncol. 2019;1(2):172-178. Published 2019 Dec 17. doi:10.1016/j.jaccao.2019.10.006
- Bak M, Park H, Lee SH, et al. The Risk and Reversibility of Osimertinib-Related Cardiotoxicity in a Real-World Population. J Thorac Oncol. 2025;20(2):167-176. doi:10.1016/j.jtho.2024.10.003
- Ky B, Putt M, Sawaya H, et al. Early increases in multiple biomarkers predict subsequent cardiotoxicity in patients with breast cancer treated with doxorubicin, taxanes, and trastuzumab. J Am Coll Cardiol. 2014;63(8):809-816. doi:10.1016/j.jacc.2013.10.061
- Henriksen PA, Hall P, MacPherson IR, et al. Multicenter, Prospective, Randomized Controlled Trial of High-Sensitivity Cardiac Troponin I-Guided Combination Angiotensin Receptor Blockade and Beta-Blocker Therapy to Prevent Anthracycline Cardiotoxicity: The Cardiac CARE Trial. Circulation. 2023;148(21):1680-1690. doi:10.1161/CIRCULATIONAHA.123.064274
- Bonatto MG, Avila MS, Ayub Ferreira SM, et al. Sacubitril-Valsartan for the Prevention of Anthracycline Cardiotoxicity in Patients With Elevated Cardiac Troponin I Concentration During Chemotherapy: A Double-Blind Randomized Placebo-Controlled Clinical Trial: The SARAH Trial. Circulation. 2025;152(25):1742-1755. doi:10.1161/CIRCULATIONAHA.125.073322
- Data on file. Chonnam National University Hwasun Hospital, 2020–2023.