Abdominal aortic aneurysm (AAA) is a late-age onset disorder that affects a high percentage of the population in industrialized countries, and rupture of AAA is associated with high mortality rates ( 1 ). The etiology of AAA is complex with a relevant contribution of genetic factors ( 2 ). Although much effort has been made to clarify the mechanism of AAA development, currently the only effective approach to prevent aneurysm rupture is surgical repair by conventional or endovascular techniques.Evidence has been established for a relationship between atherosclerosis and AAA, both disorders being characterized by an underlying chronic infl ammation . However, there are marked differences between atherosclerotic lesions and AAA. Whereas atherosclerotic plaque is characterized by leukocyte infi ltration at the lumen site and hyperproliferation of vascular smooth muscle cells (VSMCs) causing neointimal hyperplasia, AAA is characterized by leukocyte infi ltration into adventitia and depletion of VSMCs in the media. Other relevant features of AAA are the wall tension strength breakdown caused by proteolytic enzymes progressively destructing elastic fi bers ( 3 ) and hypervascularization of aortic tissue. It has been proposed that this vascularization might contribute to the development and rupture of aneurysms ( 4, 5 ).
Abstract We investigated the prostaglandin (PG)E