Aneurysmal dilatation of the abdominal aorta is one of the most common vascular diseases in the elderly. The etiology is very complex.'A majority, but not all, of infrarenal aneurysms are consequent upon degeneration of the vessel wall secondary to atherosclerosis. Although atherosclerosis is frequently seen in the wall of AAA, much evidence suggests that other complex issues are involved. The extracellular matrix of the tunica media is one of the most important structural components of the aortic wall. It contains fibrous proteins, elastin, and collagen, which provide the structural integrity and the main mechanical properties of the aorta.'Histological examination of AAA walls reveals a deficiency of elastin fi-bers. Quantitative analysis of the elastin confirms a reduction in the normal aortic elastin concentration (12%) to significantly lower levels (l%). 3-7 In addition, urinary elastin-derived peptides (EDP), products of elastin degradation, are significantly higher in patients with AAA than in control subjects, 8 indicating increased elastolysis. Circulating neutrophils in patients with AAA have increased amounts of elastase activity compared with patients with aortic occlusive di~ ease.~ It is shown that loss of elastin is an initiating factor in the development of aneurysm in animal models. IO Aneurysms were formed by arterial infusion of elastase."." Elastin is synthesized early in life and has a long biological half-life (-70 years). There is no change in elastin synthesis in AAA compared to normal~.~-'~ Therefore, it is unlikely that the reduced elastin is due to inadequate elastin synthesis. Some of the morphological changes commonly ascribed to aging elastic tissue that are also recognized in the atherosclerotic wall concern the elastic lamellae: fragmentation, fraying, irregularity, and flattening. l4 Incubation of aorta segments with porcine pancreatic elastase is shown to produce similar effects." The elastase levels found in normal and aortic occlusive disease (AOD) are very low compared to the amounts found in AAA.'Two major groups of elastases are found to be responsible for the excess elastolysis of the aortic wall. One group of these enzymes is metal dependent with molecular masses ranging from 32 to 80 kDa. 16 The other group of elastases observed by us and others is smaller, approximately 20-30 kDa and more common in the inner aspect of the media. This group is more active in the AAA tissues than in the contr~ ls. l'-'~ Recently