Although treatment for heart failure inducedby cancer therapy has improved in recent years, theprevalence of cardiomyopathy due to antineoplastic therapyremains significant worldwide. In addition to traditionalmediators of myocardial damage, such as reactiveoxygen species, new pathways and target cells should beconsidered responsible for the impairment of cardiacfunction during anticancer treatment. Accordingly, thereis a need to develop novel therapeutic strategies to protectthe heart from pharmacologic injury, and improve clinicaloutcomes in cancer patients. The development of novelprotective therapies requires testing putative therapeuticstrategies in appropriate animal models of chemotherapyinducedcardiomyopathy. This Position Paper of theWorking Group on Drug Cardiotoxicity and Cardioprotectionof the Italian Society of Cardiology aims to: (1)define the distinctive etiopatogenetic features of cardiactoxicity induced by cancer therapy in humans, whichinclude new aspects of mitochondrial function andoxidative stress, neuregulin-1 modulation through theErbB receptor family, angiogenesis inhibition, and cardiacstem cell depletion and/or dysfunction; (2) review thenew, more promising therapeutic strategies for cardioprotection,aimed to increase the survival of patients withsevere antineoplastic-induced cardiotoxicity; (3) recommendthe distinctive pathological features of cardiotoxicityinduced by cancer therapy in humans that should bepresent in animal models used to identify or to test newcardioprotective therapies.
|Number of pages||11|
|Journal||Heart Failure Reviews|
|Publication status||Published - 2015|
- Cardiology and Cardiovascular Medicine