Introduction. Ruptured abdominal aortic aneurysm (rAAA) causes a significant inflammatory response. The study aims to investigate this response following endovascular and open repair of ruptured AAA. Patients and Methods. Consecutive rAAA patients had either endovascular aneurysm repair (EVAR) or open repair (OR). Blood samples were taken for cytokines, lipid hydroperoxides (LOOH), antioxidants, and neutrophil elastase/α1-anti-trypsin complexes (NE/AAT) before surgery, 6 hours after clamp release and 1, 3, 5 days postoperatively. Results. 30 patients were included in the study, with 14 undergoing eEVAR and 16 eOR, with comparable baseline comorbidities, age, and parameters. IL-6 peaked higher in eOR patients ( ), while p75TNFr was similar between groups except at day 5 ( ). The NE/AAT concentrations were higher in eOR patients ( ), particularly in the first postoperative day, and correlated with blood ( , ) and platelet ( , ) volume transfused. C-reactive protein rose and lipid hydroperoxide fell in both groups without significant intergroup difference. Vitamins C and E, lycopene, and β-carotene levels were similar between groups. Conclusion. EVAR is associated with lower systemic inflammatory response compared to OR. Its increased future use may thereby improve outcomes for patients. 1. Introduction Ischaemia-reperfusion injury plays an important role in the development of multiorgan failure following abdominal aortic aneurysm (AAA) repair. Shock in ruptured aneurysm (rAAA) results in global ischemia, and reestablishing the blood supply can cause further tissue injury due to the generation of oxygen-derived free radicals [1]. Normally the reactive oxygen species (ROS) are produced in small amounts via aerobic metabolic pathways, with a fine balance between the prooxidants and antioxidants. ROS damage cellular molecules leading to DNA fragmentation, membrane damage and lipid peroxidation, and consequently to cell death [2, 3]. Lipid peroxidation produces lipid hydroperoxide (LOOH), thus damaging the vascular endothelium, with increased capillary permeability to protein and consequently tissue oedema and renal albumin excretion [4, 5]. Activation of the arachidonic acid cascade leads to the generation of thromboxanes, prostaglandins, and leukotrienes. These are potent platelet and neutrophil activators, and vasoconstrictors [6, 7]. Neutrophil-dependent injury, important in the genesis of SIRS and MODS, is characterised by the adhesion of activated polymorphonuclear neutrophils (PMNs) to endothelium and their release of metabolites, resulting in capillary
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