Abdominal aortic aneurysm (AAA) ranks as the 13th leading cause of death in the USA, being responsible for 0.8 per cent of all deaths. The pathogenesis of an AAA is complex and multifactorial. The common feature of both AAA and atherosclerosis is inflammation. However, atherosclerosis is primarily found within the intima and media, whereas AAA typically affects the media and adventitia. Four mechanisms relevant to AAA formation have been identified; 1) Proteolytic degradation of aortic wall connective tissue. Matrix metalloproteinases (MMPs) and other proteases, derived from macrophages and aortic smooth muscle cells, are secreted into the extracellular matrix, causing destruction of the aortic media and supporting lamina through the degradation of elastin and collagen. 2) Inflammation and immune responses. Autoimmunization and infection can cause infiltration of macrophages and lymphocytes. The reactive oxygen species can cause matrix degradation and apoptosis. 3) Biochemical wall stress. A decreased elastin-collagen ratio and an increased wall tension at infrarenal sites cause preferential sites for AAA. 4) Molecular genetics. Certain phenotypes have been associated with AAA, but no single genetic defect or polymorphism has been identified as a common denominator for AAA.