Use of biomarkers for the assessment of chemotherapy-induced cardiac toxicity.

Background Spontaneous progression of severe congestive heart failure is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The cardiac muscle isoform of troponin I is uniquely expressed in the adult human myocardium, and an increase in its circulating levels is highly indicative of myocardial injury. Accordingly, we addressed the usefulness of cardiac troponin I as a sensitive and specific molecular marker of congestive heart failure in patients with severely reduced left ventricular performance. Methods and Results A new generation single-step immunoenzymoluminometric assay with high analytical sensitivity was used to assess cardiac troponin I in patients with severe congestive heart failure, healthy blood donors, and hospitalized control subjects without known cardiac disease. The cardiac troponin I concentration (mean±SEM) was 72.1±15.8 pg/mL in heart failure patients and 20.4±3.2 and 36.5±5.5 pg/mL in healthy and hospitalized control subjects, respectively...

Circulating Cardiac Troponin I in Severe Congestive Heart Failure

It is difficult to draw conclusions about the effectiveness of technologies for reducing or preventing cardiotoxicity and about the use of cardiac markers in children as the evidence is limited in quantity and quality. The lack of standardisation for monitoring and reporting cardiac performance is problematic. Not all studies report effectiveness in terms of cardiac outcomes and event-free survival with supporting statistical analyses. Studies are mostly small and of short duration, making generalisation difficult. Increasing numbers of survivors of childhood cancer treated with anthracyclines will experience cardiac damage and require long-term surveillance and management. This will have an impact on cardiac services and costs. Diverse medical problems and other late sequelae that affect cardiac outcome will have an impact on other specialist services. Mechanisms to reduce or prevent cardiotoxicity from anthracycline therapy and cardiac markers to improve monitoring could alter the extent of this impact on service provision. RCTs of the different methods for reducing or preventing cardiotoxicity in children treated with anthracyclines for cancer with long-term follow-up are needed to determine whether the technologies influence the development of cardiac damage. Cost-effectiveness research is also required

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Cardioprotection against the toxic effects of anthracyclines given to children with cancer: a systematic review

Anthracycline-induced cardiotoxicity can cause serious health problems for an increasing number of children surviving childhood malignancies. Early detection of cardiac failure is critically important for the prevention and management of anthracycline-induced cardiotoxicity. The aim of this research was to determine the role of biomarkers in the early detection of anthracycline-induced cardiotoxicity in children. A literature review is presented of studies regarding the use of the biomarkers B-type natriuretic peptide (BNP), N-terminal pro-BNP (NT-pro-BNP), cardiac troponin T (cTnT), and cardiac troponin I (cTnI) in relation with anthracycline-induced cardiotoxicity in children. Six of 14 studies in children showed a significant relation between elevated biomarkers BNP, NT-pro-BNP, and cTnT and cardiac dysfunction. Six studies, although small, suggest that BNP, NT-pro-BNP, and cTnT might be useful markers in the early detection of anthracycline-induced cardiotoxicity.

The role of biomarkers in the early detection of anthracycline-induced cardiotoxicity in children: a review of the literature.

Objective: Assessing a diverse biomarker panel (NT-proBNP, TNF-α, galectin-3, IL-6, Troponin I, ST2 and sFlt-1) to detect subclinical cardiotoxicity after treatment with anthracyclines.Methods: Of 55 breast cancer patients biomarkers were assessed and echocardiography was performed one year after treatment with anthracyclines.Results: 29.1% of patients showed abnormal biomarker levels: NT-proBNP in 18.2%, TNF-α and Galectin-3 in 7.3%. IL-6, troponin I, ST2 and sFlt-1 were normal in all patients. A correlation between left ventricular ejection fraction (LVEF) and NT-proBNP was observed (r = −0.564, p ≤ 0.01).Conclusion: The evaluated biomarkers do not contribute to early detection. Future research should focus on NT-proBNP.

New biomarkers for early detection of cardiotoxicity after treatment with docetaxel, doxorubicin and cyclophosphamide

Doxorubicin has been used in the the treatment of malignant tumors in children. Its use is limited by cardiotoxic effects beyond a cumulative dose of 450 mg/m2. To detect cardiotoxicity at an early stage and identify patients at risk for development of cardiotoxicity are matters of concern. Recently, cardiac troponin I (cTnI) has been reported to be useful for detecting minor myocardial damage. In the present study, we investigated whether cumulative doxorubicin-related myocardial cell damage can potentially increase cTnI levels above the expected values in 22 patients treated with cumulative doxorubicin doses of 120 to 450 mg/m2. Impaired cardiac functions were found in three patients by echocardiography, but serum CTnI levels were within the ranges expected in healthy individuals both in patients with cumulative doxorubicin doses > or = 400 mg/m2 and in patients with disturbed cardiac functions. We found no relationship between serum cTnI, cumulative dose of doxorubicin, and echocardiographical findings.

Semha Berberoğlu

Papers

Cardiac troponin I: is it a marker to detect cardiotoxicity in children treated with doxorubicin?