The use of potent chemotherapeutic agents and radiotherapy to target cancer cells has certainly improved outcomes for oncology patients. However, there is increasing recognition of the importance of cardiotoxic side effects of such therapy in both specialties, affecting not just patient survival but also quality of life. Consequently, there is an increasing need for cardiologists to work in close collaboration with oncologists to not only develop methods of predicting patient susceptibility to cardiotoxicity, but also to provide long term follow-up for these patients after the cessation of chemotherapy. The impact of cancer therapy upon cardiac status should be part of the knowledge base for all cardiologists and this new interdisciplinary specialty has become known as cardioncology.

It has been suggested that the effects should be classified as non-reversible (type I) and reversible (type II), with the former associated with ultrastructural changes on myocardial biopsy.1 This distinction is especially important given the potential for cure or prolonged survival for oncology patients after some treatment regimens, in whom such end-organ disease may affect not only the prognosis but also quality of life. Yet the dysfunction caused by ‘type II’ agents is not always reversible, the distinction not always binary, and the clinical presentation is perhaps just as relevant when identifying causative agents and initiating appropriate therapy. As such we have classified the cardiac complications of the effects of the potentially cardiotoxic agents used in the treatment of oncological disease and their presenting syndrome (heart failure (HF), cardiac ischaemia, arrhythmias, and hypertension). We then consider the current approaches to the diagnosis of cardiotoxicity (especially chemotherapy induced cardiomyopathy) and the contemporary evidence and guidance on patient management.

Heart failure