International Research Journal of Oncology

Background: Modern targeted and immune cancer therapies have shifted cardiotoxicity from acute myocardial damage to a chronic, multifaceted cardiovascular risk involving vascular, metabolic, and immune-mediated mechanisms.

Aim: To delineate the emerging triad of chronic cardiovascular injury in modern cardio-oncology (vascular toxicity, metabolic toxicity, and immune-mediated toxicity) and to argue for a fundamental transition from reactive monitoring to proactive protection in cancer therapy-associated cardiotoxicity.

Methodology: Published literature was reviewed from February 24^th to April 30^th, focusing on prevalence rates, mechanistic pathways, and clinical patterns of three pillars of cancer therapy-associated cardiotoxicity: vascular toxicity, metabolic toxicity, and immune-mediated toxicity, as well as temporal patterns of cardiovascular injury across the cancer care continuum. The following electronic databases were searched for peer-reviewed articles: PubMed/MEDLINE, CINAHL, PsycINFO, Scopus, Web of Science, and Google Scholar. Included articles comprised original research, systematic reviews, meta-analyses, clinical guidelines, and consensus statements addressing cardiovascular toxicities of cytotoxic, targeted, immunotherapies, and hormonal therapies in adult populations.

Results: The review finds that modern cancer therapies produce a triad of toxicities that frequently converge: vascular toxicity (endothelial dysfunction and hypertension from VEGF/BTK inhibitors), metabolic toxicity (insulin resistance and dyslipidaemia from hormonal therapies), and immune-mediated toxicity (myocarditis from checkpoint inhibitors). These toxicities compress a decade-long atherosclerotic process into just a few years of survivorship, often progressing silently until a major adverse event.

Conclusion: The authors call for integrated and dedicated prevention clinics that systematically safeguard the long-term cardiovascular health of cancer survivors, ensuring that survival is not compromised by preventable heart disease. The proposed shift from reactive monitoring to proactive protection is essential, utilising a structured risk assessment, multimodal surveillance, and a targeted management toolkit (including endothelial protection, SGLT2 inhibitors, protocolized immunosuppression, and lifestyle medicine)