Cancer and cardiovascular (CV) disease are the most prevalent diseases in the developed world. Evidence increasingly shows that these conditions are interlinked through common risk factors, coincident in an ageing population, and are connected biologically through some deleterious effects of anticancer treatment on CV health. Anticancer therapies can cause a wide spectrum of short-and long-term cardiotoxic effects. An explosion of novel cancer therapies has revolutionised this field and dramatically altered cancer prognosis. Nevertheless, these new therapies have introduced unexpected CV complications beyond heart failure. Common CV toxicities related to cancer therapy are defined, along with suggested strategies for prevention, detection and treatment. This ESMO consensus article proposes to define CV toxicities related to cancer or its therapies and provide guidance regarding prevention, screening, monitoring and treatment of CV toxicity. The majority of anticancer therapies are associated with some CV toxicity, ranging from asymptomatic and transient to more clinically significant and long-lasting cardiac events. It is critical however, that concerns about potential CV damage resulting from anticancer therapies should be weighed against the potential benefits of cancer therapy, including benefits in overall survival. CV disease in patients with cancer is complex and treatment needs to be individualised. The scope of cardio-oncology is wide and includes prevention, detection, monitoring and treatment of CV toxicity related to cancer therapy, and also ensuring the safe development of future novel cancer treatments that minimise the impact on CV health. It is anticipated that the management strategies discussed herein will be suitable for the majority of patients. Nonetheless, the clinical judgment of physicians remains extremely important; hence, when using these best clinical practices to inform treatment options and decisions, practitioners should also consider the individual circumstances of their patients on a case-by-case basis.

Purpose The purpose of this study is to evaluate the effect of graft size on patient-reported outcomes and revision risk following ACL reconstruction. Methods A retrospective chart review of prospectively collected cohort data, 263 of 320 consecutive patients (82.2%) undergoing primary ACL reconstruction with hamstring autograft were evaluated. Graft size, femoral tunnel drilling technique, patient age, sex, and BMI at the time of ACL reconstruction, pre-operative and 2-year post-operative KOOS and IKDC scores, and whether each patient underwent revision ACL reconstruction during the 2 year follow-up period were recorded. Revision was used as a marker for graft failure. The relationship between graft size and patient-reported outcomes was determined by multiple linear regression. The relationship between graft size and risk of revision was determined by dichotomizing graft size at 8mm and stratifying by age. Results After controlling for age, sex, operative side, surgeon, BMI, graft choice, and femoral tunnel drilling technique, a 1 mm increased in graft size was noted to correlate with 3.3-point increase in the KOOS-pain subscale (p = 0.003), a 2.0-point increased in the KOOS activities of daily living subscale (p = 0.034), a 5.2-point increase in the KOOS-sport/recreation function subscale (p = 0.004), and a 3.4-point increase in the subjective IKDC score (p = 0.026). Revision was required in 0 of 64 patients (0.0%) with grafts greater than 8mm in diameter and 14 of 199 patients (7.0%) with 8 mm or smaller grafts (p = 0.037). Among patients age 18 and under, revision was required in 0 of 14 patients (0.0%) with grafts greater than 8mm in diameter and 13 of 71 patients (18.3 %) with 8 mm or smaller grafts. Conclusions Smaller hamstring autograft size is a predictor of poorer KOOS Sport and Recreation function 2 years following primary ACL reconstruction. Larger sample size is required to confirm the relationship between graft size and risk of revision ACL reconstruction. Level of Evidence Level 3

Adverse cardiovascular events among patients with normal findings on CCTA are rare. There are incrementally increasing future MACE with increasing CAD by CCTA.

The discipline of Cardio-Oncology has seen tremendous growth over the past decade. It is devoted to the cardiovascular (CV) care of the cancer patient, especially to the mitigation and management of CV complications or toxicities of cancer therapies, which can have profound implications on prognosis. To that effect, many studies have assessed CV toxicities in patients undergoing various types of cancer therapies; however, direct comparisons have proven difficult due to lack of uniformity in CV toxicity endpoints. Similarly, in clinical practice, there can be substantial differences in the understanding of what constitutes CV toxicity, which can lead to significant variation in patient management and outcomes. This document addresses these issues and provides consensus definitions for the most commonly reported CV toxicities, including cardiomyopathy/heart failure and myocarditis, vascular toxicity, and hypertension, as well as arrhythmias and QTc prolongation. The current document reflects a harmonizing review of the current landscape in CV toxicities and the definitions used to define these. This consensus effort aims to provide a structure for definitions of CV toxicity in the clinic and for future research. It will be important to link the definitions outlined herein to outcomes in clinical practice and CV endpoints in clinical trials. It should facilitate communication across various disciplines to improve clinical outcomes for cancer patients with CV diseases.

HIV infection and PI exposure are not strong independent risk factors for subclinical atherosclerosis. Confounding may contribute to overestimation of the risk associated with HIV and PI exposure.