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The field of cardio-oncology is challenged to address an ever greater spectrum of cardiotoxicity associated with combination chemotherapy, greater dose intensity, extremes of age, and enhanced patient survival which exposes more protracted risk of developing congestive heart failure (CHF). Recent reports of chemotherapy-induced hypertension as a common adverse effect of angiogenesis inhibitors and immunosuppressants clarify the need for routine blood pressure (BP) monitoring and guideline-based management of hypertension as an integral strategy to preserve LV function. Serial monitoring of radionuclide left ventricular ejection fraction (LVEF) in adults and echocardiography in children continues to provide outcome based, cost-effective prevention of CHF in high risk patients receiving chemotherapy. To optimize treatment and monitoring strategies to eliminate late-onset LV dysfunction and CHF, traditional and novel candidate methods for assessment of chemotherapy-induced LV dysfunction are reviewed. These include serial assessment of LV volume indices by gated SPECT ERNA and gated SPECT MPI, 3D echocardiography and contrast 2D echocardiography; longitudinal strain imaging, diastolic functional parameters, 123I-MIBG, 111In-Antimyosin antibody imaging, and 99mTc-Annexin V apoptosis imaging, biomarkers including troponins and BNP; genetic markers, and both functional and tissue characterization techniques with T1 weighted and T2 weighted images with cardiac magnetic resonance imaging (CMR). In our quest to optimize strategies for long-term cancer survival and prevention of CHF for patients receiving chemotherapy, rigorous modality and guideline-specific clinical outcome trials are required. A new multi-modality monitoring approach is proposed, which integrates evidence-based strengths of CMR, echocardiography, ERNA, biomarkers, and BP management for surveillance and validation of cardiotoxicity and prevention of clinical heart failure in patients receiving a broad spectrum of cancer therapies.

With the increasing number of individuals living with a current or prior diagnosis of cancer, it is important for the cardiovascular specialist to recognize the various complications of cancer and its therapy on the cardiovascular system. This is true not only for established cancer therapies, such as anthracyclines, that have well established cardiovascular toxicities, but also for the new targeted therapies that can have “off target” effects in the heart and vessels. The purpose of this informational statement is to provide cardiologists, cardiac imaging specialists, cardio-oncologists, and oncologists an understanding of how multimodality imaging may be used in the diagnosis and management of the cardiovascular complications of cancer therapy. In addition, this document is meant to provide useful general information concerning the cardiovascular complications of cancer and cancer therapy as well as established recommendations for the monitoring of specific cardiotoxic therapies.

Pharmacologic reversal of serious or intolerable side effects (SISE) from vasodilator stress is an important safety and comfort measure for patients experiencing such effects. While typically performed using intravenous aminophylline, recurrent shortages of this agent have led to a greater need to limit its use and consider alternative agents. This information statement provides background and recommendations addressing indications for vasodilator reversal, timing of a reversal agent, incidence of observed SISE with vasodilator stress, clinical and logistical considerations for aminophylline-based reversal, and alternative non-aminophylline based reversal protocols.

Although ionizing radiation is a known carcinogen, the long-term risk from relatively higher-dose diagnostic procedures during childhood is less well known. We evaluated this risk indirectly by assessing thyroid cancer incidence in a cohort treated with “lower-dose” chest radiotherapy more than 55 years ago. Between 2004 and 2008, we re-surveyed a population-based cohort of subjects treated with radiation for an enlarged thymus during infancy between 1926 and 1957 and their unexposed siblings. Thyroid cancer occurred in 50 irradiated subjects (mean thyroid dose, 1.29 Gy) and in 13 nonirradiated siblings during 334,347 person-years of follow-up. After adjusting for attained age, Jewish religion, sex and history of goiter, the rate ratio for thyroid cancer was 5.6 (95% CI: 3.1–10.8). The adjusted excess relative risk per gray was 3.2 (95% CI: 1.5–6.6). The adjusted excess absolute risk per gray was 2.2 cases (95% CI: 1.4–3.2) per 10,000 person-years. Cumulative thyroid cancer incidence remains elevated in this cohort after a median 57.5 years of follow-up and is dose-dependent. Although the incidence appeared to decrease after 40 years, increased risk remains a lifelong concern in those exposed to lower doses of medical radiation during early childhood.

Background Studies of cancer survivors treated with older radiotherapy (RT) techniques (pre-1990s) strongly suggest that ionizing radiation to the chest increases the risk of coronary heart disease (CHD). Our goal was to evaluate the impact of more modern cardiac shielding techniques of RT on the magnitude and timing of CHD risk by studying a cohort exposed to similar levels of cardiac irradiation years ago. Methods Between 2004 and 2008, we re-established a population-based, longitudinal cohort of 2657 subjects exposed to irradiation for an enlarged thymus during infancy between 1926 and 1957 and 4388 of their non-irradiated siblings. CHD events were assessed using a mailed survey and from causes of death listed in the National Death Index. We used Poisson regression methods to compare incidence rates by irradiation status and cardiac radiation dose. Results were adjusted for the CHD risk factors of attained-age, sex, diabetes, dyslipidemia hypertension and smoking. Results Median age at time of follow-up was 57.5 years (range 41.2–88.8 yrs) for irradiated and non-irradiated siblings. The mean estimated cardiac dose amongst the irradiated was 1.45 Gray (range 0.17–20.20 Gy), with 91% receiving < 3.00 Gy. During a combined 339,924 person-years of follow-up, 213 myocardial infarctions (MI) and 350 CHD events (MI, bypass surgery and angioplasty) occurred. After adjustment for attained age, gender, and other CHD risk factors, the rate ratio for MI incidence in the irradiated group was 0.98 (95%CI, 0.74–1.30), and for any CHD event was 1.07 (95%CI, 0.86–1.32). Higher radiation doses were not associated with more MIs or CHD events in this dose range, in either the crude or the adjusted analyses. Conclusions Radiation to the heart during childhood of < 3 Gy, the exposure in most of our cohort, does not increase the lifelong risk of CHD. Reducing cardiac radiation to this amount without increasing other cardiotoxic therapies may eliminate the increased CHD risk associated with radiotherapy for childhood cancer. By extension there is unlikely to be increased CHD risk from relatively higher dose imaging techniques, such as CT, because such techniques use much smaller radiation doses than received by our cohort.