Background 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. Methods 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. Results Comparing biopsies in non-ruptured AAA versus a non-rupture site biopsy from ruptured AAA; there was no significant difference in IL-6, IL-1β, 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-1β and lymphocytes were lower at the rupture site compared to the non-rupture site (IL-1β 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). Conclusions These findings suggest the biological events leading to AAA rupture may not be dependent on an up-regulation in the inflammatory process.