Anthracyclines, such as doxorubicin and epirubicin, are highly effective and frequently used antineoplastic drugs prescribed for a variety of malignancies, including breast cancer [
1,
2]. These drugs inhibit the enzyme topoisomerase II, leading to disruption in DNA replication and transcription, which in turn impedes multiplication of cancer cells. Furthermore, they promote the production of Reactive Oxygen Species (ROS) which damage proteins, DNA and cell membranes of the fastest-dividing human cancer cells [
2]. Anthracycline-based chemotherapy for the treatment of breast cancer is very effective, reducing the annual mortality in women with breast cancer by 20–38%; nevertheless, the increased risk of cardiotoxicity in patients from anthracycline use has been very well described and analyzed in the medical literature [
1‐
3]. The use of anthracyclines as chemotherapeutic agents involves an evident risk for development of cardiac toxicity generating restrictive and dilated cardiomyopathy resulting in congestive heart failure in approximately 16–20% of the treated patients [
4]. The current assumptions indicate that anthracycline-induced cardiomyopathy is the result of complex multifactorial processes affecting cardiomyocytes such as inhibition of protein and nucleic acid synthesis, the generation of ROS, through interactions with topoisomerase-IIβ present in cardiomyocytes, changes in adrenergic function and adenylate cyclase, increased membrane lipid peroxidation, abnormalities in calcium ion handling, impairment of membrane binding, enzymatic activity and assembly of mitochondrial creatine kinase, induction of nitric oxide synthase enzyme, leading to nitric oxide and peroxynitrite and converse nitration/inactivation of myofibrillar creatine kinase or nitration/activation of metalloproteinases, accumulation of anthracyclines metabolites in the cardiomyocytes, and the development of apoptosis [
2,
5]. The main potential risk factors described for anthracycline-induced cardiotoxicity includes cumulative and individual anthracyclines dose, age extremes, female sex, previous history of cardiovascular disease, pulmonary disease, pregnancy, infection, reduced infusion time, concomitant radiation therapy, and concomitant cardiotoxic chemotherapies (e.g her-2 anatgonists) [
2]. The damage upon the heart may occur months or years after chemotherapeutic treatment at or near usual maximum doses [
2,
6,
7]. Although genome-wide association investigations performed have discovered correlations between anthracycline cardiotoxicity and specific genetic mutations, there is not currently enough evidence to recommend screening patients for variants to guide clinical decision-making for cancer patients.