Key result
Elevated cardiac troponin I during anthracycline therapy independently predicted elevated BNP levels with 90% sensitivity and 63% specificity.
Why the study?
Anthracycline cardiotoxicity negatively affects prognosis, leading investigators to evaluate serial changes in cardiac troponin I and BNP levels during therapy.
Does elevated cardiac troponin I predict elevated B-type natriuretic peptide and cardiac dysfunction in cancer patients treated with anthracycline-containing chemotherapy?
Cohort (n=91)
Does elevated cardiac troponin I predict elevated B-type natriuretic peptide and cardiac dysfunction in cancer patients treated with anthracycline-containing chemotherapy?
Elevated cardiac troponin I is an independent predictor of subsequent B-type natriuretic peptide elevation and cardiac dysfunction in patients receiving anthracycline chemotherapy.
Answers are grounded in this paper and cite their sources.
May inform troponin-based risk stratification during anthracycline therapy; leaves open whether it improves cardiac outcomes.
BACKGROUND: Anthracycline is used to treat various types of cancer; however, cardiotoxicity negatively affects patient prognosis. OBJECTIVES: The aim of the present study was to investigate serial changes in levels of cardiac troponin I (TnI) and B-type natriuretic peptide (BNP) in patients treated with anthracycline-containing therapy. METHODS: 91 consecutive cancer patients planned for anthracycline treatment were enrolled and followed up for 12 months. All patients underwent echocardiography and blood sampling at baseline, 3, 6, and 12 months. RESULTS: The patients were divided into two groups based on their TnI level during the follow-up period: the elevated TnI group (TnI ≥0.03 ng/mL; n = 37) and the normal TnI group (n = 54). In the elevated TnI group, the TnI levels increased at 3 and 6 months, but they returned to within normal range at 12 months after anthracycline administration. Unlike TnI, the BNP levels began to increase after 6 months, and remained increased at 12 months. The occurrence of cancer therapeutics-related cardiac dysfunction was higher in the elevated TnI group than in the normal TnI group. When we set the cut-off value of TnI at 0.029 ng/mL, sensitivity and specificity to predict an elevated BNP level of more than 100 pg/mL were 90 and 63%, respectively. Multivariate logistic regression analysis revealed that elevated TnI was an independent predictor of elevated BNP levels. CONCLUSION: Elevated TnI was an independent predictor for the development of BNP increase. The different characteristics of TnI and BNP should be considered when managing patients treated with anthracycline-containing therapy.
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Oikawa et al. (2020) conducted a cohort in Cancer (n=91). Elevated cardiac troponin I (TnI) vs. Normal TnI was evaluated on Elevated BNP level (>100 pg/mL). Elevated cardiac troponin I during anthracycline therapy independently predicted elevated BNP levels with 90% sensitivity and 63% specificity.
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