Deficiencies of total collagen, type III collagen, and elastin have been proposed to explain aneurysm formation. Infrarenal aortas were collected from 19 patients (age 70 ± 7 years) undergoing operative repair of abdominal aortic aneurysms (diameter 7 ± 2 cm) and from 13 autopsies (age 63 ± 17 years) of patients without aneurysm disease (controls). Wall thickness and collagen and elastin concentration were determined in full-thickness aorta. Collagen types I and III were measured after digestion with cyanogen bromide, which solubilized nearly 90% of total collagen for typing. Cyanogen bromide peptides were separated by sequential carboxymethylcellulose and agarose chromatography and quantified by peak area measurement with computerized image analysis. Histologic examination revealed prominent inflammatory cell infiltration and deficient, fragmented elastin in the aneurysms. Aortic wall thickness was similar in aneurysms and in control specimens. In the aneurysms, collagen was increased (37% ± 16% vs 24% ± 5%; p < 0.05) and elastin was decreased (1% ± 1% vs 12% ± 7%; p < 0.001), expressed as a percentage of delipidized, decalcified dry weight. Collagen type I accounted for 74% ± 4% of aneurysm and 73% ± 4% of control collagen solubilized for typing, and collagen type III accounted for 26% ± 4% of aneurysm and 27% ± 4% of control collagen solubilized for typing. Neither patients with a family history of aneurysms nor those without a history of aneurysms had collagen type III deficiency. Atherosclerotic abdominal aortic aneurysms are associated with an inflammatory process and may result from elastin degradation and not a deficiency of type III collagen. (J Vasc Surg 1989;10:365–73.)