This study postulated that antihypertensive therapy with renin-angiotensin-aldosterone system (RAAS) inhibition may mitigate vascular endothelial growth factor inhibitor (VEGFi)–mediated increases in blood pressure more effectively than other antihypertensive medications in patients receiving VEGFi therapy. VEGFi therapy is commonly used in the treatment of cancer. One common side effect of VEGFi therapy is elevated blood pressure. Evidence suggests that the RAAS may be involved in VEGFi-mediated increases in blood pressure. This retrospective cohort analysis was performed using a de-identified version of the electronic health record at Vanderbilt University Medical Center in Nashville, Tennessee. Subjects with cancer who were exposed to VEGFi therapy were identified, and blood pressure and medication data were extracted. Changes in mean systolic and diastolic blood pressure in response to VEGFi therapy in patients receiving RAAS inhibitor (RAASi) therapy before VEGFi initiation were compared with changes in mean systolic and diastolic blood pressure in patients not receiving RAASi therapy before VEGFi initiation. Mean systolic and diastolic blood pressure rose in both groups after VEGFi use; however, patients who had RAASi therapy before VEGFi initiation had a significantly lower increase in systolic blood pressure as compared with patients with no RAASi therapy (2.46 mm Hg [95% confidence interval: 0.7 to 4.2] compared with 4.56 mm Hg [95% confidence interval: 3.5 to 5.6], respectively; p = 0.034). In a real-world clinical population, RAASi therapy before VEGFi initiation may ameliorate VEGFi-mediated increases in blood pressure. Randomized clinical trials are needed to further our understanding of the role of RAASi therapy in VEGFi-mediated increases in blood pressure. (J Am Coll Cardiol CardioOnc 2019;1:14–23)

Five-year survival for childhood cancer now exceeds 85%. However, for many patients, treatment requires the use of intensive anthracycline-based chemotherapy and radiotherapy, both of which are associated with significant long-term cardiovascular toxicity. As such, late cardiovascular disease is now one of the leading causes of premature morbidity and mortality among childhood cancer survivors. Recent advances over the past decade have refined the cardiotoxic potential of various chemotherapeutics, and ongoing work seeks to determine the efficacy of various cardioprotective strategies in children receiving active cancer therapy. The development of risk prediction models offers an additional strategy to define risk for both newly treated and long-term survivors. Current screening strategies are primarily based on echocardiography, although there is active research investigating methods to further optimize screening through myocardial strain, cardiac magnetic resonance imaging, blood biomarkers, and genetics, along with the cost-effectiveness of different screening strategies. Active research is also underway investigating the efficacy of prevention strategies for childhood cancer survivors who have completed cancer therapy. This ranges from the use of medications to mitigate potential pathologic ventricular remodeling to reducing adverse and modifiable cardiovascular risk factors (eg, hypertension, dyslipidemia, insulin resistance, physical inactivity, tobacco exposure), many of which may be more common in cancer survivors vs the general population and are often underrecognized and undertreated in relatively young adult-aged survivors of childhood cancer.

Background: Cardiovascular disease (CVD) is a leading cause of morbidity and mortality among cancer survivors. Hypertension, which is common among cancer survivors with a prevalence of greater than 70% by age 50, potentiates the risk for CVD in a more than additive fashion. For example, childhood cancer survivors who develop hypertension may have up to a 12 times higher risk for heart failure than survivors who remain normotensive. Studies have shown that mild valvular disease (28% incidence), cardiomyopathy (7.4%), arrhythmias (4.6%), and coronary artery disease (3.8%) are among the most common CVDs in childhood cancer survivors. Among adolescent and young adult cancer survivors, the most common reasons for cardiovascular-related hospital admission are venous/lymphatic disease (absolute excess risk 19%), cardiomyopathy and arrhythmia (15%), hypertension (13%), and ischemic heart disease (12%). In addition, cancer therapies can increase the risk for hypertension and CVD. Therefore, early detection and treatment of hypertension is essential to reducing cardiovascular morbidity and mortality among survivors. Methods: We present a literature review, which identified over 20 clinical trials, systemic reviews, and meta-analyses (13 clinical trials, 8 systemic reviews or meta-analyses) by searching PubMed, Google Scholar, and the Cochrane Library for relevant articles addressing hypertension in cancer survivors. Results: Although our understanding of the complex relationship between cancer therapies and CVD has grown significantly over the past 2 decades, there remain several gaps in knowledge when specifically addressing CVD in the survivor population. This review provides an up-to-date survivor-centered approach to the screening and treatment of hypertension, which considers survivor-specific cardiovascular risk, applies guideline directed therapies when appropriate, screens for survivor-specific factors that may influence antihypertensive medication selection, and finally considers the prohypertensive mechanisms of antineoplastic agents as a potential target for antihypertensive medications. Conclusions: Screening for and treating hypertension among survivors can promote cardiovascular health in this vulnerable population.