# The Prognostic Value of High-Sensitive Troponin T Rise Within the Upper Reference Limit in Breast Cancer: A Prospective Pilot Study

**Authors:** Sergey Kozhukhov, Nataliia Dovganych

PMC · DOI: 10.3390/cancers17142412 · 2025-07-21

## TL;DR

This study shows that a rise in high-sensitive troponin T in breast cancer patients during treatment can predict early heart damage, even before symptoms appear.

## Contribution

The study identifies a specific threshold (81% increase) for troponin T rise as a novel early marker of cardiotoxicity in breast cancer patients.

## Key findings

- A troponin T increase of more than 81% was the best threshold for detecting early heart damage in breast cancer patients.
- Left ventricular ejection fraction significantly decreased after 6 months of treatment in patients with elevated troponin T.
- High-sensitive troponin T rise below the upper reference limit predicted heart function decline with 78% accuracy.

## Abstract

Anti-cancer therapy is often accompanied by adverse reactions, among which cardiovascular toxicity is the most significant. Therefore, it is very important to diagnose cardiotoxicity before myocardial systolic function decreases or symptoms of heart failure appear. In this prospective study of 60 breast cancer patients, we studied dynamic changes in high-sensitive cardiac troponin T below the upper limit of normal. We found that an increase in troponin T > 81% was determined as the optimal threshold value for detecting early biochemical cardiotoxicity. Those patients should be considered as high-risk patients for cardiotoxicity and need more precise cardiac monitoring and early preventive strategies.

Background: We investigated the role of a high-sensitive cardiac troponin T (hsTnT) increase below the upper limit of normal (ULN) in patients with breast cancer (BC). hsTnT assays accurately quantify very low plasma troponin concentrations and enable the early detection of cardiomyocyte injury before a drop in the left ventricular ejection fraction (LVEF). The increase in hsTnT below the ULN in response to chemotherapy has not previously been studied. Method: This was an open-label pilot study. Female patients with newly diagnosed BC scheduled to receive systemic cancer treatment were recruited. Blood sampling and echocardiography were performed at baseline, at 3 and 6 months of cancer treatment. hsTnT concentrations were measured using the Elecsys TnT hs assay (Roche Diagnostics). The limit of blank and 99th percentile cutoff values for the hsTnT assay were 3 and 14 ng/L. We calculated the rise in hsTnT (ΔhsTnT) by the difference (%) between its baseline level and during follow-up (FU) in each patient. Results: Among eligible subjects, we excluded 4 patients before the start of treatment and 17 patients during the follow-up with values for the hsTnT >14 ng/L. Finally, 60 women with a median age of 48.6 ± 1.3 years were included in the study. The median baseline hsTnT concentration was 5.5 ± 1.4 ng/L. During 6 months of cancer treatment, hsTnT increased in all patients by up to 10–305% from baseline, with an average of 94.2%. LV EF was normal at baseline and decreased significantly compared to the value before cancer treatment (61.9 ± 3.3% vs. 56.3 ± 7.0%; p < 0.045). We correlated the hsTnT rise with a drop in LV EF ≥ 10% from its baseline level. Logistic regression analysis showed that Δ hsTnT has a good predictive value for LV dysfunction, 0.78 (p = 0.05), 95% CI (0.67–0.90). The increase in hsTnT > 81% was determined as the optimal threshold value for detecting early biochemical cardiotoxicity. Conclusion: It was investigated that hsTnT rise within the cutoff < 14 ng/L can be used as a marker of early biochemical cardiotoxicity and is valuable for predicting LV drop in 6 months of FU. We conclude that BC patients with increased hsTnT plasma concentration > 81% from the baseline value should be considered as high-risk patients for cardiotoxicity and need more precise cardiac monitoring and early preventive medical intervention strategies.

## Linked entities

- **Proteins:** TNNT3 (troponin T3, fast skeletal type)
- **Diseases:** breast cancer (MONDO:0004989), heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** TNNT1 (troponin T1, slow skeletal type) [NCBI Gene 7138] {aka ANM, NEM5, STNT, TNT, TNTS}
- **Diseases:** cardiomyocyte injury (MESH:D014947), cancer (MESH:D009369), BC (MESH:D001943), LV EF (MESH:D018487), cardiotoxicity (MESH:D066126)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12294006/full.md

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Source: https://tomesphere.com/paper/PMC12294006