Anticancer Chemotherapy-Induced Atherosclerotic Cardiovascular Disease: A Comprehensive Review

The introduction of anticancer agents has transformed oncology, significantly improving survival rates. However, these therapies have introduced unintended cardiovascular risks, with atherosclerovascular disease (ASCVD) emerging as a leading cause of morbidity and mortality among cancer survivors. The development of ASCVD in this population involves multifactorial mechanisms, including endothelial dysfunction, oxidative stress, systemic inflammation, and disrupted lipid metabolism. This review examines the various mechanisms through which anticancer chemotherapy contributes to ASCVD and highlights strategies for risk assessment and management. Each class of anticancer agents presents distinct cardiovascular challenges: anthracyclines induce oxidative stress and endothelial damage, promoting foam cell formation and plaque progression; taxanes and vascular endothelial growth factor (VEGF) inhibitors impair lipid metabolism and vascular stability; anti-metabolites exacerbate endothelial injury through reactive oxygen species; and mTOR inhibitors, hormonal therapies, tyrosine kinase inhibitors, and immune checkpoint inhibitors disrupt lipid profiles and inflammatory pathways, increasing the risk of plaque rupture and thrombosis. Mitigating chemotherapy-induced ASCVD necessitates a comprehensive, multidisciplinary approach. Detailed pre-treatment cardiovascular risk assessments must address traditional and cancer-specific risk factors, including demographics, pre-existing conditions, and modifiable behaviors such as smoking and inactivity. Pharmacological interventions like statins and angiotensin-converting enzyme (ACE) inhibitors, paired with lifestyle modifications, are essential to reducing ASCVD risk. In resource-limited settings, cost-effective strategies should be prioritized to enhance accessibility. Establishing cardio-oncology units facilitates care coordination, while long-term surveillance enables timely detection and intervention. These strategies collectively improve cardiovascular outcomes and survivorship in diverse patient populations.