Why the study?
The prognostic value of SCORE2/SCORE2-OP scales and cardiac biomarkers (NT-proBNP and hs-TnI) for short-term fluoropyrimidine-induced cardiotoxicity needed evaluation.
Do baseline SCORE2/SCORE2-OP risk stratification and cardiac biomarkers (NT-proBNP, hs-TnI) predict fluoropyrimidine-induced cardiotoxicity in patients with colorectal cancer?
Do baseline SCORE2/SCORE2-OP risk stratification and cardiac biomarkers (NT-proBNP, hs-TnI) predict fluoropyrimidine-induced cardiotoxicity in patients with colorectal cancer?
Traditional cardiovascular risk scores and baseline cardiac biomarkers do not predict fluoropyrimidine-induced cardiotoxicity in the short term, suggesting a distinct pathophysiological mechanism from atherosclerotic events.
No association of SCORE2 or biomarkers with FIC observed; leaves open identification of reliable short-term predictors in colorectal cancer patients.
Aim. To evaluate the prognostic value of the SCORE2/SCORE2-OP scales and the level of cardiac biomarkers (N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity troponin I (hs-TnI)) for fluoropyrimidine-induced cardiotoxicity (FIC) in the short term. Material and methods. This prospective, single-center cohort study included 133 patients with colorectal cancer (stages II-IV) receiving fluoropyrimidine therapy. Before treatment, the risk of cardiovascular events (CVEs) was stratified using the SCORE2/SCORE2-OP scales and NT-proBNP and hs-TnI levels were determined. CVEs were assessed during a 6-month follow-up. Results. One hundred and three (77,4%) patients were classified as having high/very high cardiovascular risk. CVEs developed in thirty-nine patients (29,3%), the most common of which were thromboembolic events (9,8%) and blood pressure destabilization (9,8%). No significant associations were found between SCORE2/SCORE2-OP risk stratification, NT-proBNP, or hs-TnI levels, and FIC. Conclusion. Traditional cardiovascular risk factors and cardiac biomarkers do not demonstrate prognostic value for FIC in the short term. This supports the hypothesis of fundamentally different mechanisms for FIC compared to atherosclerotic events.
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Yusupova et al. (2026) studied this question.
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