LAUSR

A growing number of cancer patients survive of cancer and one third of them will eventually die of heart disease that is at least partly related to cancer and its therapy.1,2 The recognition of this association has recently given rise to a new field in cardiovascular medicine, that of cardio-oncology. In fact, over the previous few years, the number of publications on cardiovascular complications of cancer patients increased impressively, dedicated cardio-oncology clinics begun to arise in heart centres throughout the US and Europe, and the European Society of Cardiology published a position paper on the cardiotoxicity of cancer therapy.3 Cardiac disease in cancer results from the interaction of three main factors: (i) the underlying cardiovascular status of the patient, including pre-existing heart disease and cardiovascular risk factors, (ii) cancer itself that may affect directly and mostly indirectly the cardiovascular system, and (iii) cancer therapy, including classical chemotherapy, targeted agents and radiotherapy, that may damage the heart and vessels through several mechanisms4 (Figure 1). Among cancer therapies, anthracyclines constitute traditionally the typical model of chemotherapy-induced cardiotoxicity. The classical knowledge dictates that anthracyclines represent the main class of anticancer drugs causing cardiomyopathy in a dose-dependent manner, resulting from irreversible oxidative cardiomyocyte damage, usually manifested as ventricular dysfunction and heart failure a long time after patient’s exposure.5 However, recent advances in our understanding of cardiomyopathy caused by cancer therapies have challenged the above long-standing statements. First, although anthracyclines are top in the list of anticancer agents causing cardiomyopathy, with an incidence ranging between 3% and 48% depending on anthracycline type and total dose, other