It is still unclear what initiates aneurysmal dilatation and what determines whether or not an aneurysm will continue to expand and rupture. Early detection and operative repair of an abdominal aortic aneurysm (AAA) still remains the only effective means of reducing the high mortality rate associated with the condition. Endovascular techniques are being developed in an attempt to reduce the mortality rate associated with elective repair. A variety of animal models and experimental techniques have been described in the investigation of the pathophysiology of AAA and in the development of improved endovascular surgical and pharmacological therapies. This article discusses these models and techniques, their advantages and some of the problems encountered in extrapolating experimental findings to the human condition.

This review is based on a search of the Medline database from 1966 to March 1998 using recognized key words and text words. A further search was then conducted on references quoted within selected relevant publications.

Treatment of rodent aortas with intraluminal elastase or periaortic calcium chloride creates reproducible aneurysms that have certain similarities to the human pathology; such aneurysms have been favoured in the investigation of the pathophysiology of aneurysm expansion. However, these models lack several of the prominent features of the human lesion, such as atherosclerosis and intraluminal thrombosis. The development of gene knockout mice may lead to a more analogous aneurysm formation, with associated atherosclerosis. Many large animal models have been used in the development of endovascular techniques but, in general, these do not mimic the human pathophysiology and fail to predict medium‐ and long‐term complications. © 1999 British Journal of Surgery Society Ltd