Aortic response to cancer therapy: a narrative review of the radiotherapy paradox and clinical implications

Abstract Background Cancer treatments such as chemotherapy and radiotherapy significantly impact the cardiovascular system. While cardiac toxicity is well characterized, the effects on the aorta, the body’s largest artery, remain less understood. Given that aortic weakening may lead to life-threatening conditions such as aneurysm formation and rupture, understanding these effects is crucial for improving long-term vascular health in cancer survivors. Methods This narrative review synthesizes findings from six selected studies comprising clinical investigations and reviews. It examines the impact of radiotherapy, chemotherapy, cancer-related systemic factors, and incidental aortic findings from radiotherapy planning computed tomography scans, analysing their roles in aortic pathology progression or stabilization. Results In this narrative review of six selected studies, radiotherapy was consistently associated with slower aneurysm expansion (~ 1.1 mm/year vs. 2.7 mm/year), suggesting a paradox wherein radiation-induced fibrosis and modulation of inflammatory processes may stabilize the aortic wall. Chemotherapy showed no significant effect on aneurysm growth, with rates comparable between treated patients and controls (~ 2.3 vs. 2.4 mm/year). Cancer-induced sarcopenia and inflammation contributed to adverse aortic remodelling within one year. Additionally, a high prevalence (9.3%) of thoracic aortic dilatation was identified via opportunistic screening on radiotherapy planning CTs, emphasizing an opportunity for earlier detection and intervention. Conclusions The complex interplay between cancer therapies and aortic biology reveals a potentially counterintuitive stabilization of aortic pathology following radiotherapy, in contrast to the neutral effects of chemotherapy and the deleterious influence of cancer-related systemic changes. Radiotherapy planning CT offers an underutilized avenue for vascular screening. Future prospective studies are essential to disentangle these paradoxes and translate mechanistic insights into strategies that protect vascular integrity while optimizing cancer treatment outcomes.