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BACKGROUND:Radiation exposure during fluoroscopically guided interventions such as endovascular aortic repair (EVAR) is a growing concern for operators. This study aimed to measure DNA damage/repair markers in operators perfoming EVAR. METHODS:Expression of the DNA damage/repair marker, γ-H2AX and DNA damage response marker, phosphorylated ataxia telangiectasia mutated (pATM), were quantified in circulating lymphocytes in operators during the peri-operative period of endovascular (infrarenal, branched, and fenestrated) and open aortic repair using flow cytometry. These markers were separately measured in the same operators but this time wearing leg lead shielding in addition to upper body protection and compared with those operating with unprotected legs. Susceptibility to radiation damage was determined by irradiating operators' blood in vitro.RESULTS: γ-H2AX and pATM levels increased significantly in operators immediately after branched endovascular aortic repair/fenestrated endovascular aortic repair (P<0.0003 for both). Only pATM levels increased after infrarenal endovascular aortic repair (P<0.04). Expression of both markers fell to baseline in operators after 24 hours (P<0.003 for both). There was no change in γ-H2AX or pATM expression after open repair. Leg protection abrogated γ-H2AX and pATM response after branched endovascular aortic repair/fenestrated endovascular aortic repair. The expression of γ-H2AX varied significantly when operators' blood was exposed to the same radiation dose in vitro (P<0.0001).CONCLUSIONS: This is the first study to detect an acute DNA damage response in operators performing fluoroscopically guided aortic procedures and highlights the protective effect of leg shielding. Defining the relationship between this response and cancer risk may better inform safe levels of chronic low-dose radiation exposure. 1,2 The growing number and complexity of procedures means that interventionists are exposed to higher amounts of radiation, a subject that is becoming increasingly topical. Radiation-Induced3-7 A recently published 15-year follow-up study of the EVAR trial, comparing endovascular and open aortic repair, reported an increased incidence of malignancy in patients treated by EVAR. 8 There is, rightly so, a significant focus currently on reducing the patients' exposure to radiation, but mounting evidence suggests that recurrent lowdose exposure to the practitioner is equally as important. Robust data collection to assess the risks posed to the interventionist is in its infancy, but a number of studies suggest a link to adverse health effects, including a higher risk of posterior subcapsular lens changes and malignancy.9-11 One recent study found a higher incidence of malignancy, including brain cancer, breast cancer, and melanoma, in interventionists who performed fluoroscopically guided procedures compared with those who had never performed these.12 A better understanding of the hazards of occupational radiation exposure requires sensitive tools to measure exposure at an individu...

The head is an unprotected area receiving a significant radiation dose during complex endovascular aortic repair. The deleterious effects of exposure to this area are not fully understood. Vascular interventionalists should be cognisant of head exposure increasing with C-arm angulation, and limit this manoeuvre.

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Introduction: Cell therapy using unselected mononuclear cell populations has had modest benefits in patients with critical limb ischemia (CLI). We hypothesized that tissue-remodeling monocytes, identified by their expression of CD16 (CD16+ Mo), may be a novel cellular therapy for CLI. Methods and Results: Flow cytometry showed that the proportion of circulating CD16+ Mo was greater in CLI patients (n=25) compared with matched controls (n=15, P<0.0001). Removal of ischemia following revascularization or amputation resulted in a fall in CD16+ Mo to control levels (P<0.05). CLI CD16+ Mo expressed higher levels of the adhesive proteins VLA, ICAM-1 and CD11c compared with controls (P<0.05). Conditioned media from these cells contained higher levels of HB-EGF, PlGF, endoglin, VEGF-C and VEGF-D (P<0.05) and induced greater endothelial cell tubule formation (P<0.05) compared with CD16- Mo from the same patients (n=9). CD16+ Mo preferentially migrated towards ischemic muscle supernatants isolated from CLI patients (n=7, P<0.02). CD16+ and CD16- Mo were isolated from 12 CLI patients and 1x10 6 cells injected into the adductor muscles of nude athymic mice following femoral artery excision. More ischemic hindlimbs were salvaged when treated with CD16+ compared with CD16- Mo (83% [10/12] vs 17% [2/12] limbs, P<0.05) and this was associated with enhanced arteriogenesis (αSMA-stained vessels, P<0.05). Conclusion: Circulating CD16+ Mo from CLI patients have increased expression of adhesion markers, are preferentially retained within ischemic muscle and promote robust arteriogenesis and limb salvage in experimental HLI. This monocyte subset may be an effective cellular therapy for CLI.

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spinal cord ischemia, respiratory and renal and insufficiency. Secondary end points included blood loss, operative time, ICU stay, the length of hospital stay. Results: Primary endpoints: 30 days mortality rate 24.1% (7.18% standard group, p ¼ 0.001), spinal cord ischemia rate 13.8% (14.1% standard group, p ¼ 0.964), respiratory failure rate 13.8% (4.95% standard group, p ¼ 0.0442) and renal failure rate 27.6% (26.2% standard group, p ¼ 0.869). Secondary endpoints: mean blood loss 7062 mL (5246 mL standard group, p ¼ 0.018), mean operative time 5,39 h (4,79 h standard group, p ¼ 0.021), mean ICU stay 3.4 days (2.7 days standard group, p ¼ 0.068), length of hospital stay 10.7 days (10.4 days standard group, p ¼ 0.852). Conclusion: Previous thoracic endovascular repair is a significant preoperative risk factor for patients requiring subsequent open TAA repair. Not only does it increase the complexity of the repair with longer operative time and blood loss but also there is a worsening in terms of both mortality and respiratory morbidity.