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Whereas anthracycline\u2010based and human epidermal growth receptor 2 (HER2)\u2010targeted therapies remain the most extensively studied causes, newer targeted agents and immune\u2010based therapies introduce additional, mechanistically distinct cardiotoxic phenotypes, including endothelial dysfunction and afterload\u2010driven heart failure (vascular endothelial growth factor [VEGF]\u2010pathway inhibitors, proteasome inhibitors), arrhythmia\u2010associated cardiac dysfunction (Bruton tyrosine kinase inhibitors) and inflammation\u2010mediated myocardial depression in the context of cytokine release syndromes (chimeric antigen receptor T [CAR\u2010T] 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. 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