Heart failure medication to prevent cancer therapy-related cardiac dysfunction: A narrative review

Advances in oncological therapies have improved cancer survival but also have increased the clinical incidence of cancer therapy-related cardiac dysfunction (CTRCD), a spectrum of conditions ranging from subclinical biomarker or strain abnormalities to progressive heart failure and cardiogenic shock. Whereas anthracycline-based and human epidermal growth receptor 2 (HER2)-targeted therapies remain the most extensively studied causes, newer targeted agents and immune-based therapies introduce additional, mechanistically distinct cardiotoxic phenotypes, including endothelial dysfunction and afterload-driven heart failure (vascular endothelial growth factor [VEGF]-pathway inhibitors, proteasome inhibitors), arrhythmia-associated cardiac dysfunction (Bruton tyrosine kinase inhibitors) and inflammation-mediated myocardial depression in the context of cytokine release syndromes (chimeric antigen receptor T [CAR-T] cells and bispecific antibodies). This narrative review summarises the rationale and available evidence for the preventive use of conventional heart failure therapies across this evolving landscape. It further highlights current gaps in knowledge, especially regarding modern heart failure therapies and modern immune-mediated oncological therapies.