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Soluble suppression of tumorigenicity-2 changes during cardiotoxic cancer treatment: a systematic review and
Luca Fazzini1, Simone Angius1, Nicola Campana1
1Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Background:
Soluble suppression of tumorigenicity-2 (sST2) is a promising biomarker of cardiovascular disease and heart failure. Data about the changes in sST2 concentrations during cancer treatment and the relationship with cancer treatment-related cardiotoxicity are sparse.
Methods:
We conducted a systematic review and meta-analysis to explore longitudinal changes in sST2 levels at three time points (T0 baseline, T1 post-chemotherapy, and T2 follow-up) in cancer patients treated with cardiotoxic therapies and compared these changes to traditional biomarkers of cardiac injury, i.e., troponin and NT-proBNP. Using random-effects models, mean differences (MD), and standardized MD (SMD), we analyzed (i) ST2 longitudinal changes, (ii) the association between ST2 and cardiotoxicity [defined through left ventricular ejection fraction (LVEF)] providing pooled estimates of correlations, and (iii) the SMD variations among biomarkers.
Results:
Eight studies were included, comprising 433 patients treated with anthracycline and/or HER2-directed antibodies. There was a trend toward increased sST2 levels from T0 to T2 (MD 1.86, 95% CI -0.97 to 4.68, p = 0.200) and decreased levels from T1 to T2 (MD -1.96, 95% CI -4.28 to 0.37, p = 0.100). A pooled analysis showed a negative correlation between sST2 levels and LVEF (r -0.29, 95% CI, -0.49- -0.05, p < 0.010). Comparisons with Troponin and NT-proBNP showed a significantly higher Troponin SMD at T0-T1 (p = 0.027), while no significant differences were observed for NT-proBNP.
Conclusion:
sST2 showed dynamic changes during cardiotoxic therapy correlating with cardiotoxicity. Troponin was demonstrated to have greater longitudinal variations. Further research is needed to evaluate longitudinal sST2 levels in patients who develop cardiotoxicity vs. those who do not.
Insights
Soluble suppression of tumorigenicity-2 (sST2) levels change during cancer treatment and correlate with cardiotoxicity. While troponin shows greater longitudinal variation, sST2 offers insights into cardiac injury during cancer therapy.
Area of Science:
- Cardiology
- Oncology
- Biomarker Research
Background:
- Soluble suppression of tumorigenicity-2 (sST2) is recognized as a biomarker for cardiovascular disease and heart failure.
- Limited data exists on sST2 concentration changes during cancer treatment and its association with cardiotoxicity.
Purpose of the Study:
- To systematically review and meta-analyze longitudinal changes in sST2 levels during cardiotoxic cancer therapies.
- To compare sST2 dynamics with traditional cardiac injury biomarkers like troponin and NT-proBNP.
- To assess the correlation between sST2 levels and cardiotoxicity, defined by left ventricular ejection fraction (LVEF).
Main Methods:
- Systematic review and meta-analysis of eight studies involving 433 patients undergoing anthracycline and/or HER2-directed therapies.
- Analysis of sST2 levels at baseline (T0), post-chemotherapy (T1), and follow-up (T2).
- Utilized random-effects models to calculate mean differences (MD) and standardized mean differences (SMD) for biomarker variations and correlations.
Main Results:
- A trend towards increased sST2 from T0 to T2 (MD 1.86) and decreased levels from T1 to T2 (MD -1.96) was observed, though not statistically significant.
- A significant negative correlation was found between sST2 levels and LVEF (r -0.29, p < 0.010), indicating higher sST2 with reduced cardiac function.
- Troponin exhibited significantly greater longitudinal variations (SMD) from T0 to T1 compared to sST2.
Conclusions:
- sST2 demonstrates dynamic changes during cardiotoxic cancer therapy and correlates with cardiotoxicity.
- Troponin shows more pronounced longitudinal variations compared to sST2.
- Further research is warranted to investigate longitudinal sST2 levels in patients who develop versus those who do not develop cardiotoxicity.
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