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Onco-cardiology is a fast-growing medical subspecialty focused on the management of heart diseases in patients with cancer. Although cancer remains a leading cause of morbidity and mortality worldwide, the survival rate of patients with cancer has increased in the last 25 years. In the United States, the 5-year relative survival rate of patients diagnosed with cancer between 1975 and 1977 was 50%; it increased to 68% between 1999 and 2005. The US National Cancer Institute estimates that at least 13.7 million cancer survivors were alive in the United States in 2012 (1). With the survival improvement, the long-term adverse treatment effects have also become more apparent. A survey of 1,807 cancer survivors with a 7-year follow-up found that 33% died of heart diseases and 51% died of cancer (2). Historically, since the late 1970s, the interest in chemotherapy-induced cardiotoxicity was focused on cardiomyopathy related to few chemotherapeutic agents. As the field of cancer therapies has expanded, so has the finding of other cardiovascular side effects such as transient left ventricular dysfunction, hypertension (HTN), cardiac arrhythmias, pericardial effusions, and arterial ischemia. Patients with known or subclinical cardiac disease are more susceptible to the cardiotoxic side effects of cancer therapy, and those with known cardiac disease often need to alter their cardiac management to allow for the treatment of cancer. This can be associated with significant cardiovascular risks. Onco-cardiology has evolved to address the cardiovascular needs of patients whose optimal outcome mandates close and collaborative efforts between cardiologists and oncologists in a multidisciplinary approach. Involvement of cardiologists in cancer patients’ care has changed from focusing on management of the cardiovascular complications of therapy to an overall assistance in the care of these patients from the initial cancer diagnosis to survivorship as outlined in Fig. 54-1.
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Clinical knowledge and basic science discoveries in onco-cardiology have grown over the last decade. There is better understanding of molecular mechanisms of cardiac toxicity of several cancer drugs. An example is the observation that the Bruton tyrosine kinase receptor is expressed in the atria of human heart tissue (3). This tyrosine kinase receptor is the target of a novel drug, ibrutinib, used in certain hematologic malignancies including chronic lymphocytic leukemia. Ibrutinib has been associated with a significant incidence of atrial arrhythmias, potentially mediated by its on-target effect and more specifically by inhibiting the PI3K-Akt signaling pathway (3). Similarly, trastuzumab targets ErbB2 in breast cancer cells and has been shown to improve outcome and prolong survival in HER2+/ErbB2 breast cancer. The same receptors within the cardiac myocyte are responsible for normal cell function and myocyte repair. When affected by ErbB2 inhibitors like trastuzumab, secondary mitochondrial dysfunction can be observed (...