Abstract Purpose This article evaluates and summarizes mechanisms, clinical presentations, comparative assessments, and treatments of cardiotoxicity associated with select classes of anticancer agents, including (1) anthracyclines; (2) arsenic trioxide; (3) HER2-directed therapies; (4) fluoropyrimidines; (5) immunomodulatory drugs (IMiDs); (6) oral kinase inhibitors targeting BTK, the fusion kinase encoded by BCR-ABL1, and the VEGF signaling pathway; and (7) immune checkpoint inhibitors (ICIs). Specific examples of oral kinase inhibitors are also discussed. Together, the evidence highlights and illustrates important breakthroughs and/or opportunities for pharmacists to advance cardio-oncology pharmacy practice. Summary Cardiotoxicity associated with anticancer agents is a common complication in many patients with cancer. The improvement in the life expectancy of patients with cancer has led to a heightened awareness and demand for mitigation strategies in patients at risk of developing long-term anticancer treatment–related adverse effects. Advances in understanding of the pathogenesis associated with drug-induced cardiotoxicity have led to improved surveillance, risk de-escalation for specific therapies (eg, arsenic trioxide), optimization of cardioprotection and harmonization strategies (eg, for anthracyclines), and specific treatment plan modifications or supportive care (eg, for oral kinase inhibitors, fluoropyrimidines, ICIs, and IMiDs), among other approaches. Non–treatment-related factors such as aging, genetic predisposition, and cardiovascular disease contribute to cardiotoxicities; however, some of the mechanisms of drug-induced cardiotoxicity remain poorly characterized. Conclusion Strategies to mitigate the cardiotoxicity of anticancer therapies and identify patients who may require time-sensitive interventions or long-term follow-up represent promising opportunities to improve the quality and safety of care in the emerging field of cardio-oncology pharmacy.
Chung et al. (Sun,) studied this question.