The aim of this study was to determine: (i) the biological consequences of radiation exposure to both patients and operators after EVAR, (ii) whether this differs according to the case complexity; and (iii) whether there are inter-individual sensitivities to radiation exposure as evidenced by markers of DNA damage in circulating lymphocytes.
Methods: Temporal changes in peri-operative lymphocyte count were measured in patients following EVAR and open AAA repair. The expression of markers of DNA damage and repair, gamma-H2AX (ɣH2AX), phosphoATM (pATM) were measured in circulating CD3+ lymphocytes in patients before, during and 24 h after infrarenal EVAR (IEVAR), complex (branched/fenestrated [BEVAR/FEVAR]) and open aortic cases using multi-colour flow cytometry and immunofluorescence staining. For operators, ɣH2AX and pATM were measured in circulating lymphocytes before and 24 h after open and endovascular repair. Individual susceptibility to radiation damage was determined by irradiating operators' blood samples in vitro.Results: There was a greater fall in patient lymphocyte count following endovascular (n = 118) compared with open (n = 35) aortic repair (66.6 ± 3.5 vs 43.6 ± 4.1% respectively, P < 0.0001). Recovery of lymphocyte count was significantly reduced after EVAR (P < 0.007). In patients, there was a 5-fold increase in lymphocyte expression of ɣH2AX and pATM immediately after standard (P < 0.001, n = 25) and complex (P < 0.001, n = 32) EVAR compared with open repair (n = 13) and the induction of ɣH2AX correlated with DAP (P < 0.02, r = 0.2). Delivery of contrast did not induce ɣH2AX or pATM in lymphocytes in vitro.In operators, there was a significant increase in lymphocyte ɣH2AX and pATM expression after complex (P < 0.005, n = 15), but not standard EVAR (n = 14), or open AAA repair (n = 14). There was a significant difference in operator (n = 6) sensitivity to radiation exposure (P < 0.0001 by 2way ANOVA). In both patients and operators, ɣH2AX/pATM levels returned to normal 24 h after all endovascular repairs.
Conclusion: Our studies show that DNA damage occurs in both patients and operators as a consequence of radiation exposure during endovascular aneurysm repair. Such biodosimetry, aimed at measuring circulating markers of DNA damage, may be a more appropriate guide to the true biological consequences of radiation exposure than current dosimetry methods used to dictate “safe” exposure levels. A better understanding of the processes that result in ɣH2AX/pATM expression during endovascular interventions, as well as the long term consequence of this raised expression, may allow a better estimation of the increased lifetime-attributable risk of cancer for both patients and operators.