Although treatment for
heart failure induced by
cancer therapy has improved in recent years, the prevalence of
cardiomyopathy due to
antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as
reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in
cancer patients. The development of novel protective
therapies requires testing putative therapeutic strategies in appropriate animal models of
chemotherapy-induced
cardiomyopathy. This Position Paper of the Working Group on
Drug Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology aims to: (1) define the distinctive etiopatogenetic features of
cardiac toxicity induced by
cancer therapy in humans, which include new aspects of mitochondrial function and oxidative stress,
neuregulin-1 modulation through the
ErbB receptor family, angiogenesis inhibition, and cardiac stem cell depletion and/or dysfunction; (2) review the new, more promising therapeutic strategies for cardioprotection, aimed to increase the survival of patients with severe
antineoplastic-induced
cardiotoxicity; (3) recommend the distinctive pathological features of
cardiotoxicity induced by
cancer therapy in humans that should be present in animal models used to identify or to test new cardioprotective
therapies.