Abstract
Anthracycline (ANT) is a topoisomerase-interacting agent that is used in most malignancy treatments. We investigated the efficacy of enalapril (angiotensin-converting enzyme inhibitor) in the prevention of ANT-induced cardiomyopathy. In this randomized, single-blind, and placebo-controlled study, 69 patients with a newly diagnosed malignancy for which ANT therapy was planned were randomly assigned to either a group receiving enalapril (n = 34) or placebo (n = 35). Echocardiography studies were performed before chemotherapy and at 6 months after randomization. Additionally, troponin I and creatinine kinase-MB (CK-MB) were measured 1 month after the initiation of chemotherapy. In the enalapril group, the mean left ventricular ejection fraction (LVEF) (p = 0.58) was the same at baseline and 6 months after randomization. Conversely, LVEF significantly decreased in the control group (p < 0.001). Additionally, LV end systolic volume and left atrial diameter were significantly increased compared with the baseline measures in the control group. According to the tissue Doppler study, the mitral annuli early diastolic (e′) and peak systolic (s′) velocities were significantly reduced, and the E (the peak early diastolic velocity)/e′ ratio was significantly increased in the control group. Furthermore, the TnI and CK-MB levels were significantly higher in the control group than in the enalapril group. Enalapril appears efficacious in preserving systolic and diastolic function in cancer patients treated with ANTs.





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Acknowledgments
This study was Dr. Mohsen Faghihinia’s postgraduate thesis. The authors would like to thank all the patients who enrolled in this study and the staff at the Toba Oncology Department, Sari, Iran. Financial support was obtained from the Research Council of the Mazandaran University of Medical Sciences to Dr. Maryam Nabati, Assistant Professor, Fellowship of Echocardiography.
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Janbabai, G., Nabati, M., Faghihinia, M. et al. Effect of Enalapril on Preventing Anthracycline-Induced Cardiomyopathy. Cardiovasc Toxicol 17, 130–139 (2017). https://doi.org/10.1007/s12012-016-9365-z
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DOI: https://doi.org/10.1007/s12012-016-9365-z