Advancements in diagnostic tools and curative-intent therapies have improved cancerspecific survival. With prolonged survival, patients are now subject to increased aging and development of cardiovascular risk factors such that further improvements in cancerspecific mortality are at risk of being offset by increased cardiovascular mortality. Moreover, established and novel adjuvant therapies used in cancer treatment are associated with unique and varying degrees of direct as well as indirect myocardial and cardiovascular injury (i.e., cardiotoxicity). Current approaches for evaluating anticancer therapy-induced injury have limitations, particularly lack of sensitivity for early detection of subclinical cardiac and cardiovascular dysfunction. With emerging evidence suggesting early prevention and treatment can mitigate the degree of cardiotoxicity and limit interruption of life-saving cancer therapy, the importance of early detection is increasingly paramount. Newer imaging modalities, functional capacity testing and blood biomarkers have the potential to improve early detection of cardiotoxicity and reduce cardiovascular morbidity and mortality.
KeywordsMortality rates from cancer have declined over the past 30 years as more effective methods of early detection, pharmacologic treatments and surgical approaches have resulted in significant cancerrelated survival gains [1][2][3]. Long-term survivors with cancer are expected to increase by approximately 30% in the next decade to an estimated 18 million by 2022 in the USA alone [4]. With prolonged survival, cancer patients are now subject to the effects of aging and to the development of other risk factors that determine the long-term risk of cardiovascular disease (CVD) [5][6][7]. In this setting, CVD may limit the survival gains of oncology and is already the predominant cause of mortality in breast cancer patients over 50 years of age [5,6,8] and a more common contributor than cancer to mortality among older survivors [9,10].The cardiovascular effects of a prolonged survival are also compounded by those of standard modern cancer therapy. Current anticancer therapies are associated with unique and varying degrees of direct (e.g., myocardial toxicity, ischemia, hypertension, arrhythmias) [11][12][13][14] as well as indirect (e.g., unfavorable lifestyle changes) sequential and progressive cardiovascular insults [11]. The most well known direct cardiotoxic effects of cancer therapy historically occur with anthracyclinecontaining regimens (i.e., doxorubicin, epirubicin). Anthracyclines are still widely used in solid tumors (i.e., breast cancer, osteosarcoma etc.) and hematologic malignancies (Hodgkin's/nonHodgkin's lymphoma, acute lymphoblastic leukemia etc.) and are well recognized to trigger dosedependent, cumulative, progressive cardiac dysfunction [15,16] manifest as decreased left ventricular ejection fraction (LVEF) [17][18][19], and ultimately, symptomatic heart failure (HF) in up to 5% of patients [20]. Newer, targeted agents have dramatically improved the a...