Background and Aims: this multicenter prospective observational study defined the incidence and risk factors of surgical wound infections (Swi) after infrarenal aortic and lower limb vascular surgery procedures and evaluated the severity and costs of these infections.Methods: the study cohort comprised of 184 consecutive patients. postoperative complications were recorded. the additional costs attributable to Swi were calculated.Results: eighty-four (46%) patients had critical ischaemia, 81 (45%) patients underwent infrainguinal bypass surgery and 64 (35%) received vascular prosthesis or prosthetic patch. forty-nine (27%) patients developed Swi. Staphylococcus aureus was the leading pathogen cultured from the wound. forty-seven of the 49 infected wounds responded to and healed with the treatment. Swi was the cause of one major amputation. independent predictors for Swi were infrainguinal surgery (or 7.2, 95% cl 2.92-17.65, p < 0.001), obesity (or 6.1, 95% cl 2.44-15.16, p < 0.001) and arteriography injection site within the operative area (or 2.5, 95% cl 1.13-5.48, p = 0.02). the average cost attributable to Swi was 3320 €.Conclusion: the incidence of Swi after vascular surgery is high. the risk factors for Swi are infrainguinal surgery, obesity and arteriography injection site within the operative area. Swi increases morbidity and costs of operative treatment.

Endotension after EVAR may cause subsequent aneurysm rupture. Endotension is evidently not associated with endoleak I to III provided that the endovascular graft is maintained in appropriate position and that free endovascular flow is observed. We propose to consider a nonoperative approach in the clinically asymptomatic patient with aneurysm enlargement after EVAR if endoleak is excluded by well-performed imaging techniques.

Background Surgical wound infection (SWI) is a common complication after peripheral vascular surgery. Infections increase morbidity and costs of treatment. The aim of the present study was to test the hypothesis that supplemental postoperative oxygen decreases the incidence of SWI after lower limb revascularization.Methods This prospective, randomized, multicenter, single-blinded trial was conducted between May 2009 and February 2010 in six secondary referral hospitals in Finland. We randomly allocated 274 patients undergoing surgery for lower limb revascularization to the study group (n = 137) or a control group (n = 137). The study group received supplemental inspired oxygen for the first 2 days after surgery. The main outcome was SWI. Patients were followed up for 30 days or until the SWI was healed. Logistic regression analysis was used to assess the independent effect of supplemental oxygen on the incidence of SWI.Results Altogether 63 (23%) patients developed SWI; 47 (75%) of the infections were superficial. There were two vascular graft infections. SWI occurred in 25 patients (18.2%) in the study group and in 38 patients (27.7%) in the control group [odds ratio (OR) 0.56, 95% confidence interval (CI) 0.30-1.04; P = 0.07]. In isolated groin incisions, 3 patients of 52 (5.8%) in the study group and 12 patients of 51 (23.5%) in the control group developed SWI; OR = 0.20, 95% CI 0.04-0.95; P = 0.04. Conclusions There was an indication that supplemental inspired oxygen tended to decrease the incidence of SWI after lower limb vascular surgery. In isolated groin incisions, the decrease of SWI incidence in the supplemental oxygen group was significant.

Background Atherosclerosis is a complex disease with hundreds of genes influencing its progression. In addition, the phenotype of the disease varies significantly depending on the arterial bed. Methodology/Principal Findings We characterized the genes generally involved in human advanced atherosclerotic (AHA type V–VI) plaques in carotid and femoral arteries as well as aortas from 24 subjects of Tampere Vascular study and compared the results to non-atherosclerotic internal thoracic arteries (n=6) using genome-wide expression array and QRT-PCR. In addition we determined genes that were typical for each arterial plaque studied. To gain a comprehensive insight into the pathologic processes in the plaques we also analyzed pathways and gene sets dysregulated in this disease using gene set enrichment analysis (GSEA). According to the selection criteria used (>3.0 fold change and p-value <0.05), 235 genes were up-regulated and 68 genes down-regulated in the carotid plaques, 242 genes up-regulated and 116 down-regulated in the femoral plaques and 256 genes up-regulated and 49 genes down-regulated in the aortic plaques. Nine genes were found to be specifically induced predominantly in aortic plaques, e.g., lactoferrin, and three genes in femoral plaques, e.g., chondroadherin, whereas no gene was found to be specific for carotid plaques. In pathway analysis, a total of 28 pathways or gene sets were found to be significantly dysregulated in atherosclerotic plaques (false discovery rate [FDR] <0.25). Conclusions This study describes comprehensively the gene expression changes that generally prevail in human atherosclerotic plaques. In addition, site specific genes induced only in femoral or aortic plaques were found, reflecting that atherosclerotic process has unique features in different vascular beds.

This study compared four geographically adjacent populations with identical demographics, similar patient characteristics, and similar indications for the treatment of intact abdominal aortic aneurysms. Endovascular repair was adopted with significantly variable rates between these populations ranging from 38% to 74%. However, despite these disparities between the regions, there were no significant differences in early or late outcomes such as mortality, complications, and re-interventions. Thus, the remarkably different enthusiasm for the use of endovascular repair between these health care districts did not seem to affect the overall outcomes of these otherwise comparable patient populations. Objectives: The aim was to study outcomes of endovascular aneurysm repair (EVAR) and open surgical repair (OSR) of abdominal aortic aneurysms (AAAs) in four geographically adjacent populations with identical demographics and variable EVAR rates. Methods: This was a multicentre cohort study based on local and national registry data from an area of 815 000 inhabitants. The study involved 527 consecutive patients with an intact AAA treated with EVAR (n ¼ 327) or OSR (n ¼ 200) between 2010 and 2016. The catchment area was divided into four health care districts (populations A, B, C, and D) with one central hospital in each district. Each hospital decided independently between OSR and EVAR for patients within their population; OSR was performed in all hospitals while EVAR was centralised in one of them. Patient demographics and treatment outcomes were extracted from local registries. Population demographics, overall AAA incidence, and mortality data were retrieved from a national database. Results: The rate of new intact AAA diagnosis varied between 20 and 29 per 100 000 inhabitants/year with the highest incidence in population D (p < .001). The intact AAA repair rates were 9.8, 8.9, 9.9, and 8.7 per 100 000 inhabitants/year for populations A, B, C, and D, respectively (p ¼ .64). There were no significant differences in mean age (73.6 AE 8.0 years) or mean aortic diameter (62 AE 13 mm) between the treated patient populations. Groups A and B had high EVAR rates (74% and 72%, respectively) whereas the EVAR rates were lower in groups C and D (50% and 38%, respectively) (p < .001). The 30 day mortality rates were 2%, 2%, 4%, and 1% (p ¼ .55), and complication rates were 17%, 12%, 15%, and 11% (p ¼ .39) for A, B, C and D, respectively. There were no significant differences in mortality, complication or re-intervention rates between the groups during the mean follow up of 3.3 AE 2.0 years. Conclusions: At population level, high EVAR rates had no measurable effect compared with lower EVAR rates on the outcomes in patients with intact AAA.