title: Endovascular AAA repair attenuates the inflammatory and renal responses associated with conventional surgery.
abstract: OBJECTIVE
  To quantify the inflammatory and renal parameters in comparative cohorts of patients undergoing surgical or endovascular repair of abdominal aortic aneurysms (AAAs).
  
  
  METHODS
  Forty-three patients (41 men; ages 58-81 years) underwent endovascular or conventional aneurysm surgery according to aortic morphology. All patients received a standard general anesthetic and had 12 serial blood and urine samples collected during the perioperative period. Samples underwent analysis for the cytokines interleukin (IL) 1beta tumor necrosis factor-alpha (TNF-alpha), and IL-6. White cell and platelet activation were estimated indirectly by measuring sL-selectin and 11-dehydrothromboxane B2, respectively. The urinary albumin:creatinine ratio (ACR) and N-acetyl-beta-D-glucosaminidase (NAG) activity were estimated to assess renal injury. Fibrinogen and fibrinogen degradation products were calculated to assess activation of the clotting cascade.
  
  
  RESULTS
  Twenty-three patients underwent endovascular AAA repair and 20 had conventional surgery. Concentrations of IL-6 (p < 0.002) and TNF-alpha (p < 0.0004) were significantly higher in the conventional group. The ACR (p < 0.002) and urinary NAGs (p < 0.0009) were also significantly higher in this group, suggesting greater renal injury. Platelet activity was significantly greater in the endovascular group (p < 0.01), perhaps indicating thrombus organization within the aneurysm sac.
  
  
  CONCLUSIONS
  These data suggest that the inflammatory response associated with conventional aneurysm repair is largely obviated by endovascular techniques. This may potentially translate to a lower incidence of multiple organ failure after endovascular surgery.
authors.affiliation: Department of Surgery, University of Leicester, Leicester Royal Infirmary, England, UK. jonboyle@dial.pipex.com
authors.forename: J R
authors.initials: JR
authors.lastname: Boyle
authors.forename: S
authors.initials: S
authors.lastname: Goodall
authors.forename: J P
authors.initials: JP
authors.lastname: Thompson
authors.forename: P R
authors.initials: PR
authors.lastname: Bell
authors.forename: M M
authors.initials: MM
authors.lastname: Thompson
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine; D000368:Aged; D000369:Aged, 80 and over; D000419:Albuminuria / Q000652:urine; D017544:Aortic Aneurysm, Abdominal / Q000601:surgery*; D001792:Blood Platelets / Q000502:physiology; D003404:Creatinine / Q000652:urine; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D007375:Interleukin-1 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007668:Kidney / Q000502:physiology*; D019041:L-Selectin / Q000032:analysis; D008297:Male; D008875:Middle Aged; D019060:Minimally Invasive Surgical Procedures / Q000009:adverse effects / Q000379:methods*; D011446:Prospective Studies; D013929:Thromboxane B2 / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019041:L-Selectin; D013929:Thromboxane B2; D003404:Creatinine; D000118:Acetylglucosaminidase