Lenihan, Daniel J.

Cancer therapy has dramatically changed over the past many decades, not only in efficacy but also complexity, with targeted therapeutics that have novel mechanisms of action. As a direct result of these remarkable treatments that have extended the lives of many patients, the increased recognition of cancer therapy-related cardiac dysfunction as well as the broader description of cancer therapy-related cardiovascular toxicity (CTR-CVT) has become obvious. The discipline of cardio-oncology has accepted the challenge to provide excellent cardiovascular (CV) protection for our patients being treated for cancer in order to achieve the best overall outcomes. The successful application of optimal CV protection by cardio-oncology needs to incorporate basic principles to realise these improved overall outcomes. Critical paradigm principles include: (1) using effective CV therapy; (2) targeting the likely mechanisms of action responsible for CTR-CVT; and (3) documenting cancers and cancer therapies associated with high CTR-CVT. Such a CV protection paradigm is likely to have the biggest impact and confirm an improved overall outcome. In addition, it is important to emphasise that knowing those cancers with high CTR-CVT risk requires careful comparative study of CV endpoints during exploratory cancer trials. Furthermore, astute clinical observations of specific CTR-CVT should be routinely reported to allow the development of strategies that minimise the negative impact of CTR-CVT. Lastly, coordinated efforts that allow realistic goals of cancer treatment while minimising the impact of CTR-CVT are the end goal in order to eliminate CV disease as a barrier to effective cancer treatment.

Abstract 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.