Use of N-Terminal Pro-Brain Natriuretic Peptide to Assess Left Ventricular Function after Adjuvant Doxorubicin Therapy in Early Breast Cancer Patients A Prospective Series

Background and objective: Anthracyclines are well established and highly efficacious antineoplastic agents for various haematopoietic and solid tumours, such as breast cancer. The main adverse effect of anthracycline therapy is cardiotoxicity. The aim of this prospective study was to determine the role of plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) in assessing left ventricular function in early breast cancer patients receiving adjuvant anthracycline treatment. Methods: Thirty-three newly diagnosed breast cancer patients who received a total doxorubicin dosage of 240 mg/m(2) over four treatment cycles as part of adjuvant chemotherapy after curative breast surgery were included in this study. Venous NT-proBNP levels were measured before and at the end of doxorubicin therapy. Left ventricular function was measured by echocardiography conducted 3 weeks after surgery and at the end of doxorubicin therapy. Results: NT-proBNP levels were significantly higher in patients (n = 10) with decreased left ventricular ejection fraction (LVEF) [p = 0.02]. There was no difference in LVEF (p = 0.164) or NT-proBNP levels (p = 0.844) between the patients who had high NT-proBNP levels and those who had normal NT-proBNP levels before doxorubicin chemotherapy. None of the factors studied (breast cancer grade, estrogen receptor status, progesterone receptor status, human epidermal growth factor receptor 2 status, age) was found to be significantly related to NT-proBNP. Conclusion: The association between higher NT-proBNP levels and reduced LVEF in asymptomatic breast cancer patients after doxorubicin administration could be an early indication of subclinical acute anthracycline cardiotoxicity. Furthermore, breast cancer patients experiencing a progressive increase in NT-proBNP levels might be in a higher risk group for acute anthracycline cardiotoxicity.