Biological Responses to Endovascular Treatment of Abdominal Aortic Aneurysms
- 1 May 1997
- journal article
- review article
- Published by SAGE Publications in Journal of Endovascular Therapy
- Vol. 4 (2) , 169-173
- https://doi.org/10.1177/152660289700400208
Abstract
Purpose: To review the findings of two studies investigating the apparent differences in inflammatory responses demonstrated in patients undergoing endovascular as opposed to classic surgical treatment of abdominal aortic aneurysms (AAAs). Methods: The clinical course of seven patients treated with an endoluminal procedure (AAA-E) and seven patients undergoing conventional surgery (AAA-C) were compared (all men; ages 52 to 80 years). Blood samples were taken pre-, intra-, and postoperatively for up to 7 days. Inflammatory responses were assessed from measurement of interleukins (IL)-1 β, IL-6, IL-8, and tumor necrosis factor (TNF-α); complement proteins C1q, C4, C5a, and terminal complement complexes, C5b-C9; and C-reactive proteins. Granulocyte and monocyte surface adhesion molecule expression was determined indirectly using a panel of monoclonal antibodies against CD11a, CD11b, CD11c, CD18, and L-selectin in donor white blood cells exposed to patient plasma. Results: In six of the AAA-E patients, blood pressure decreases were recorded during the introduction of the device. Elevated body temperature was sustained for 2 to 5 days postoperatively in the AAA-E group. IL-6 levels were significantly higher in AAA-C patients (p < 0.0005), while TNF-α release was recorded in the AAA-E group only. CD11b, CD11c, and CD18 molecules on both granulocytes and monocytes were significantly upregulated 60 minutes after the endovascular procedure compared to conventional surgery. Conclusions: Endovascular aortic aneurysm repair apparently induces a significant inflammatory response, mainly involving TNF-α release, which differs from open AAA repair. These inflammatory responses, which may be related to the observed intraprocedural blood pressure decreases, could be caused by cell activation arising from intra-aneurysmal device manipulation.Keywords
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