Elizabeth Hutchins

Permissive cardiotoxicity is an evolving clinical practice pattern that balances the management of cancer treatment‐associated cardiotoxicities with the risk of interrupting lifesaving or life‐extending cancer treatments. This paradigm shift has been catalyzed by advancements in the diagnostic and therapeutic tools available to treating clinicians, as well as a recognition of the consequences of withholding or delaying cancer therapy. Permissive cardiotoxicity has become a central tenet in the practice of cardio‐oncologists; however, recognition and confidence in managing cardiotoxicity is also crucial for the general cardiologist and oncologist due to the growing population of patients with cancer. This review aims to (1) highlight the philosophy of permissive cardiotoxicity, (2) provide a framework for risk stratification of cardiovascular toxicities, (3) describe systems of care considerations for successful implementation of permissive cardiotoxicity, and (4) review the existing literature and guideline recommendations for specific cardiovascular toxicity mitigation.

Immune checkpoint inhibitor (ICI) therapy is a class of immune‐activating therapies that has revolutionized the treatment of various cancers over the past decade. With expanding clinical indications of this drug class, understanding the short‐term and long‐term implications of checkpoint inhibitor therapy has grown in importance. Numerous reports have highlighted potential inflammatory adverse effects, including cardiotoxicity. Efforts to characterize cardiovascular adverse events, however, have largely focused on myocarditis with emerging evidence demonstrating the association between ICI therapies and atherosclerotic cardiovascular disease. Given the inherently higher risk of thrombosis and bleeding in patients with cancer, the safe and effective management of ICI‐associated acute coronary syndrome remains a therapeutic challenge requiring a tailored and multidisciplinary approach. In this review, we discuss the pathophysiology of ICI‐associated atherosclerosis, the complexities of acute coronary syndrome management in patients with cancer, and the opportunities for risk prevention in patients receiving ICI therapies.

A 50-year-old woman presented to an outpatient cardiology clinic with a chief complaint of chest pain and dyspnoea on exertion. Physical exam was unrevealing. Chest radiograph showed prominence of the right pulmonary vasculature system in a characteristic curvilinear pattern suspicious for scimitar syndrome (Figure 1). Given this finding, electrocardiogram-gated coronary computed tomography angiography was obtained and demonstrated a large right pulmonary vein draining into the inferior vena cava (IVC), confirming the diagnosis of scimitar syndrome (Figure 1). Given her symptoms and a pulmonary-to-systemic flow > 2.14, the patient underwent surgical repair with creation of intra-atrial baffle to connect the anomalous right pulmonary vein to the left atrium. In the 9 years since her surgery, she reports complete resolution of her symptoms.

HIV infection has been associated with diastolic heart failure and atrial fibrillation. The purpose of this study is to determine whether HIV infection is associated with differences in left ventricular mass (LVM), left ventricular end-diastolic volume (LVEDV), and left atrial volume (LAV) indexed to body surface area (left ventricular mass index, left ventricular end-diastolic volume index [LVEDVI], and left atrial volume index [LAVI], respectively). Cross-sectional study of 721 men [425 HIV-infected (HIV+), 296 HIV-uninfected (HIV−) enrolled in the cardiovascular substudy of the Multicenter AIDS Cohort Study (MACS). Participants underwent cardiac computed tomography imaging. A blinded reader measured LVM, LVEDV, and LAV. We used multivariable linear regression models to evaluate whether LVEDVI, left ventricular mass index (LVMI), and LAVI differed by HIV serostatus, adjusting for demographics and cardiovascular disease risk factors. LVMI was significantly greater in HIV+ compared with HIV− men, with adjusted difference of 2.65 g/m ² (95% confidence interval 0.53–4.77, p < .001). Left ventricular end-diastolic index and LAVI did not differ significantly between the two groups. HIV-related factors (nadir CD4 count, clinical AIDS diagnosis, cumulative antiretroviral therapy use, and cumulative protease inhibitor use) were not significantly associated with LVMI, LVEDVI, or LAVI. LVM was significantly higher in HIV+ than HIV− men, which may contribute to the observed increased risk for diastolic heart failure associated with HIV infection. Although HIV infection has been associated with an increased risk for atrial fibrillation, we did not find any difference in LAV by HIV serostatus.