Abstract
Background
Cardiac damage is a significant risk of chemotherapy. Elevated circulating cardiac troponin I was suggested as a marker for early detection of cardiac damage.
Objective
We aim to assess the predictive value of cardiac troponin I for chemotherapy-induced cardiotoxicity in cancer patients.
Methods
We searched PubMed, Web of Science, Embase, and CNKI. Nine prospective studies involving 2033 cancer patients (pts) were included in the meta-analysis. Troponin I (TnI) levels in patients who underwent chemotherapy were categorized into cardiac troponin I (cTnI) positive and negative groups based on the cutoff concentrations described in the included studies. The cumulative effects of chemotherapy-induced cardiotoxicity between the cTnI-positive and cTnI-negative patients were represented as a summarized risk difference (RD) value with a 95% confidence interval. Subgroup analysis and sensitivity analysis were employed to address heterogeneities. Stata software (version 12.0) was utilized for the analysis.
Results
cTnI-positive pts represented significant cardiotoxicity compared to cTnI-negative pts, as a decline in left ventricular ejection fraction (LVEF): RD = 0.279 [95% CI (0.248–0.311), p = 0.000, I2 = 81.3%, 8 trials], heart failure (HF): RD = 0.117, [95% CI (0.090–0.144), p = 0.000, I2 = 77.8%, 6 trials], arrhythmias: RD = 0.057 [95% CI (0.028–0.086), p = 0.000, I2 = 0.0%, 3 trials], and cumulative events: RD = 0.318 [95% CI (0.272–0.364), p = 0.000, I2 = 73.5%, 3 trials]. No statistically significant difference in cardiac death, acute pulmonary edema, and acute coronary syndromes between cTnI-positive pts and cTnI-negative pts was identified.
Conclusions
An increase in circulating troponin I serve as a potential biomarker that reflecting the high risk of early cardiotoxicity in cancer patients who have undergone chemotherapy. The presence of intrinsic unadjusted confounding factors in the reports suggests the need for further study to address this question.
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Supplementary Material
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