Abstract Background Endovascular aortic repair (EVAR) uses a significant dose of radiation. Studies have suggested a higher incidence of cancer in EVAR patients, but evidence is insufficient. We investigated biological sequalae of radiation exposure, including markers of genomic instability, in patients after complex EVAR. Methods Lymphocytes were isolated from patients after complex (branched/fenestrated) EVAR and non-irradiated controls. Dicentric chromosomes (DC), chromosomal aberrations caused by irradiation were enumerated. γ-H2AX, a marker of acute DNA damage/repair, was measured by immunofluorescence after ex vivo irradiation of 0.2 and 1 Gy. Expression of radiation-responsive genes (FDXR, CCNG1, P21 and PHPT1) was measured by qPCR following irradiation of blood samples. Results Seventeen patients (82% male, age 73 range 59–85 years) and sixteen controls (56% male, age 68 range 53–83 years) were recruited. The mean incidence of DC was 3.782, 95% c.i.3.13, 4.43 and 0.898, 95% c.i.0.48, 1.32 per 1000 cells for patients and controls, respectively (P 0.0001). Patients had higher background of γ-H2AX foci than controls, (0.7056, 95% c.i.0.3163, 1.095 versus 0.2413, 95% c.i.0.0774, 0.4051) per cell, (P 0.05). FDXR was the most radio-responsive gene (P 0.0001), but no statistically significant difference was found between the two groups. Conclusions We have shown an increased frequency of chromosomal aberrations in patients after complex EVAR. A higher background DNA damage/repair activity was also found in this cohort, observed as an increased baseline expression of γ-H2AX. The link between DNA damage and clinical effects remains unclear, further work is required to understand the radiation risk in this cohort.
Yeong et al. (Sun,) studied this question.