Abdominal aortic aneurysm rupture is not associated with an up-regulation of inflammation within the aneurysm wall.

Abstract

The nature of the inflammatory change within ruptured AAA has not been extensively reported. The aim of this study was to compare the inflammatory response in non-ruptured and ruptured aneurysms with emphasis on the site of rupture. Non-rupture site biopsies were taken from the anterior aneurysm sac of non-ruptured (n=31) and ruptured AAA (n=20). In 12 ruptured AAA, a further biopsy was taken from the rupture site. Enzyme-linked immunosorbent assay was used to quantify IL-6, IL-1beta and TNF-alpha. Quantitative immunohistochemistry was undertaken for generic lymphocytes, T-cells, and B-cells. Comparing biopsies in non-ruptured AAA versus a non-rupture site biopsy from ruptured AAA; there was no significant difference in IL-6, IL-1beta, TNF-alpha, generic lymphocytes, T-cell or B-cell content. Comparing ruptured AAA--non-rupture site with rupture site; IL-6 and TNF-alpha were unchanged. By contrast IL-1beta and lymphocytes were lower at the rupture site compared to the non-rupture site (IL-1beta 1.39 ng/mg [0.97-2.29] vs. 1.92 ng/mg [1.46-2.57], p=0.027; generic lymphocytes 2.89% [0.51-5.51] vs. 4.73% [2.27-12.40], p=0.018; T-cells 0.28% [0.04-1.18] vs. 0.82% [0.40-1.36], p=0.027; B-cells 0.16% [0.04-1.14] vs. 1.30% [0.32-5.40], p=0.021). These findings suggest the biological events leading to AAA rupture may not be dependent on an up-regulation in the inflammatory process.