To fully understand the enlargement and rupture of aneurysms, one requires an in vivo
model. Several have been developed, including those addressing (1) atherosclerosis (2)
genetic abnormalities,(3) experimental alterations of metabolism,(4) mechanical and
chemical injury,(5) hemodynamic factors,(6) allografts and xenographs,(7) inflammation, and
(8) infusion of elastase. This review examines a variety of in vivo models, with particular
attention given to the elastase infusion model.