RESUMO
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 = 327) or OSR (n = 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 = .64). There were no significant differences in mean age (73.6 ± 8.0 years) or mean aortic diameter (62 ± 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 = .55), and complication rates were 17%, 12%, 15%, and 11% (p = .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 ± 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.
Assuntos
Aneurisma da Aorta Abdominal/cirurgia , Implante de Prótese Vascular , Procedimentos Endovasculares , Complicações Pós-Operatórias/mortalidade , Idoso , Aneurisma da Aorta Abdominal/epidemiologia , Implante de Prótese Vascular/efeitos adversos , Implante de Prótese Vascular/métodos , Implante de Prótese Vascular/estatística & dados numéricos , Estudos de Coortes , Procedimentos Endovasculares/efeitos adversos , Procedimentos Endovasculares/métodos , Procedimentos Endovasculares/estatística & dados numéricos , Feminino , Finlândia/epidemiologia , Humanos , Incidência , Masculino , Avaliação de Resultados em Cuidados de Saúde , Utilização de Procedimentos e Técnicas/estatística & dados numéricos , Sistema de Registros/estatística & dados numéricos , Análise de SobrevidaRESUMO
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.
Assuntos
Artérias/patologia , Perfilação da Expressão Gênica , Placa Aterosclerótica/genética , Idoso , Artérias/metabolismo , Artérias/fisiopatologia , Estudos de Casos e Controles , Feminino , Finlândia , Genômica , Humanos , Masculino , Especificidade de Órgãos , Placa Aterosclerótica/patologia , Placa Aterosclerótica/fisiopatologiaRESUMO
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.
Assuntos
Oxigenoterapia/métodos , Doenças Vasculares Periféricas/cirurgia , Infecção da Ferida Cirúrgica/terapia , Procedimentos Cirúrgicos Vasculares/efeitos adversos , Cicatrização/fisiologia , Idoso , Idoso de 80 Anos ou mais , Intervalos de Confiança , Feminino , Finlândia , Seguimentos , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Doenças Vasculares Periféricas/diagnóstico , Cuidados Pós-Operatórios/métodos , Estudos Prospectivos , Valores de Referência , Medição de Risco , Método Simples-Cego , Estatísticas não Paramétricas , Infecção da Ferida Cirúrgica/prevenção & controle , Resultado do Tratamento , Procedimentos Cirúrgicos Vasculares/métodosRESUMO
OBJECTIVE: The necessity of operative treatment of endotension after endovascular grafting of abdominal aortic aneurysms (endovascular aneurysm repair; EVAR) is under debate. The proposed causes of endotension and related treatment protocols are controversial. We report the outcome of a nonoperative approach to five patients with endotension after EVAR. METHODS: From February 1997 to August 2004, 160 patients who underwent EVAR of an infrarenal abdominal aortic aneurysm were evaluated for the incidence of endotension. According to the endovascular protocol, plain radiographs, spiral computed tomography, and angiography were performed before and after surgery for follow-up. To detect endotension, spiral computed tomography was performed by using a delayed imaging technique after the infusion of contrast medium. Endotension was defined as an aneurysm sac enlargement after EVAR without evidence of endoleak. Aneurysm sac rupture was defined as discontinuity of the calcific rim of the aneurysmal sac and the presence of intra-aneurysmal fluid outside the sac. RESULTS: We found five (3.1%) patients with endotension. Three of these experienced aneurysmal sac rupture. Only one of the three was underwent operation on experiencing sudden intestinal occlusion due to intra-abdominal adhesions. This patient had no intra-abdominal or retroperitoneal bleeding or hematoma but died after intensive care as a result of non-aneurysm-related problems. Four patients with endotension are still being closely followed up according to our surveillance protocol, and they are doing clinically well. After rupture, clear shrinking of the aneurysm sac was seen in two patients. CONCLUSIONS: 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.