Cardiovascular disease (CVD) remains the leading cause of mortality in women, yet many people perceive breast cancer to be the number one threat to women's health. CVD and breast cancer have several overlapping risk factors, such as obesity and smoking. Additionally, current breast cancer treatments can have a negative impact on cardiovascular health (eg, left ventricular dysfunction, accelerated CVD), and for women with pre-existing CVD, this might influence cancer treatment decisions by both the patient and the provider. Improvements in early detection and treatment of breast cancer have led to an increasing number of breast cancer survivors who are at risk of long-term cardiac complications from cancer treatments. For older women, CVD poses a greater mortality threat than breast cancer itself. This is the first scientific statement from the American Heart Association on CVD and breast cancer. This document will provide a comprehensive overview of the prevalence of these diseases, shared risk factors, the cardiotoxic effects of therapy, and the prevention and treatment of CVD in breast cancer patients. The number one cause of mortality in US women is cardiovascular disease (CVD), 1 yet the general public awareness of this remains suboptimal despite large-scale public education campaigns. Awareness is particularly low in racial and ethnic minority communities.2,3 CVD and breast cancer have individually received significant publicity with media campaigns (such as the Red Dress and Pink Ribbon campaigns); however, there is inadequate public awareness of the coexistence of common risk factors associated with these 2 conditions.Although cardiology and oncology are often considered separate medical fields, they are frequently intertwined. Multidisciplinary care is critical in the management of cancer patients. Cancer outcomes can be influenced by cardiovascular health: antecedent cardiovascular health can affect cancer treatment selection, and furthermore, cancer care can result in cardiovascular toxicities that could impact ongoing cancer treatment. Finally, latent effects of CVD from cancer treatment can alter cancer survivorship. Much of the intersection between CVD and breast cancer pertains to similarities in predisposing risk factors such as age, tobacco use, diet, obesity, and sedentary lifestyle. CVD risk factors are increased in long-term cancer survivors; however, discussion of CVD prevention and modification of these risk factors during and after cancer treatment is limited. 4 The risk of CVD (heart failure [HF], myocardial ischemia, hypertension) is high, and development of CVD risk factors (obesity and dyslipidemia) is higher in older breast cancer survivors than the risk of tumor recurrence. In addition, with advancements

Modern cancer therapy has successfully cured many cancers and converted a terminal illness to chronic disease. Because cancer patients often have co-existing heart diseases, expert advice from the cardiologists will improve clinical outcome. In addition, cancer therapy can also cause myocardial damage, induce endothelial dysfunction, and alter cardiac conduction. Thus, it is important for practicing cardiologists to be knowledgeable about the diagnosis, prevention, and management of cardiovascular complications of cancer therapy. In this first part of a 2-part review, we will review cancer therapy-induced cardiomyopathy and ischemia. This review is based on MEDLINE literature search, published clinical guidelines, and best practices in major cancer centers. With the number of cancer survivors expanding quickly, the time has come for cardiologists to work closely with cancer specialists to prevent and treat cancer therapy-induced cardiovascular complications.

In this second part of a 2-part review, we will review cancer or cancer-therapy associated systemic and pulmonary hypertension, QT-prolongation, arrhythmias, pericardial disease, and radiation-induced cardiotoxicity. This review is based on MEDLINE literature search, published clinical guidelines, and best practices in major cancer centers. Newly developed targeted therapy can exert off-target effects causing hypertension, thromboembolism, QT-prolongation and atrial fibrillation. Radiation therapy often accelerates atherosclerosis. Furthermore, radiation can damage the heart valves, the conduction system, and pericardium that may take years to manifest clinically. Management of pericardial disease in cancer patients also posed clinical challenges. This review highlights the unique opportunity of caring for cancer patients with heart problems caused by cancer or cancer therapy. It is an invitation to action for cardiologists to become familiar with this emerging subspecialty.

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Background: Doxorubicin remains one of the most common causes of cardiotoxicity in patients with lymphoma, leading to significant morbidity and mortality. Early decline in left ventricular (LV) ejection fraction predicts chemotherapy-induced cardiotoxicity and mortality, but limited data exist on doxorubicin-induced subclinical right ventricular (RV) dysfunction. We investigated dose-dependent subclinical doxorubicin-induced RV dysfunction in lymphoma patients. Methods: Thirty-five patients with adult lymphoma treated with doxorubicin were studied. All patients had normal baseline LV ejection fraction (LVEF > 55%), and no known cardiopulmonary disease. We studied the dosedependent effect of doxorubicin on RV strain by 2D speckle-tracking echocardiography (STE) using a vendorindependent software (TomTec). Images were analyzed offline by two independent observers blinded to the clinical characteristics of the study population. Baseline LVEF, RV fractional area change (RV FAC), RV free wall strain (RV FWS), and RV global longitudinal strain (RV GLS) were measured prior to chemotherapy initiation and compared with echo studies obtained at a 6-month follow-up interval. Patients served as their own controls. Comparisons between pre-and post-therapy were achieved using paired Student's t-tests or Chi-Square test. Results: The Interobserver Intraclass Correlation Coefficient for RV GLS, RV FAC and RV FWS, was 0.87, 0.81 and 0.79, respectively. The mean age was 51 ± 13 years, 40% women, 60% white. The mean cumulative doxorubicin dose was 239 ± 104 mg m − 2. There was there was significant decline in RV FAC (47.3 ± 4.4% vs. 43.7 ± 3.9%), RV FWS (− 24.9 ± 3.3 vs.-22.2 ± 2.9), and RV GLS (− 22.4 ± 4.1 vs.-20.6 ± 3.4) (all p < 0.01); but no significant decline in LVEF during the 6-month follow up (63.3 ± 6.2% vs. 61.6 ± 11.1%, p = 0.374). At cumulative doxorubicin dose ≥200 mg m − 2 we found a significant decline in RV FAC (47.0 ± 4.7% vs. 42.2 ± 3.1%, p < 0.01), RV FWS (− 24.6 ± 3.6 vs.-21.5 ± 2.4, p < 0.01), and RV GLS (− 22.3 ± 4.5 vs.-20.1 ± 2.9, p = 0.03). Conclusion: In this cohort of adult lymphoma patients, doxorubicin-based therapy was associated with subclinical RV dysfunction, but not LV dysfunction, at a cumulative dose ≥200 mg m − 2. Additional studies evaluating the longterm prognostic implications of RV dysfunction in this population are essential.