['Evidence is emerging that abdominal aortic aneurysm (AAA) formation cannot completely be explained by systemic atherosclerosis and is in part due to other pathophysiological mechanisms such as local immune reactions. The aim of the present study was to study variance in AAA wall inflammation, and relate that to clinical patient characteristics.', 'Ventral walls from 201 patients with intact AAAs undergoing open repair were prospectively collected and processed for histology and protein measurements. Patients were monitored for 3 years postoperatively.', 'The amount of lymphocytic infiltrate was used to distinguish 96 lymphocyte-poor AAAs from 105 lymphocyte-rich AAAs. The walls of lymphocyte-rich AAAs had higher concentrations of various inflammatory markers, including interleukin (IL) 6, IL8, matrix metalloproteinase (MMP) 8; however, MMP9 levels were comparable. Patients with lymphocyte-poor AAAs had more atherosclerotic risk factors: type 2 diabetes (22% vs. 9%, P\xa0=\xa0.008), hypertension (81% vs 66%, P\xa0=\xa0.019), and serum cholesterol levels (mean[SD] 5.2[2.5] vs. 4.2[1.0] mmol/L, P\xa0=\xa0.023). Intimal lesions in the AAAs revealed more frequently an extracellular lipid pool in lymphocyte-poor AAAs (66% vs. 52%, P\xa0=\xa0.026). Lymphocyte poor AAAs were associated with a worse survival during 3 years of follow-up, although this association did not reach statistical significance when correcting for other cardiovascular predictors (24% vs. 14%; HR 1.9-2.3).'] Are atherosclerotic risk factors and atherosclerotic postoperative events associated with low inflammation in abdominal aortic aneurysms?