Abdominal aortic aneurysm is a potentially fatal disorder, defined as a focal dilatation exceeding 150% of the normal arterial diameter, with the risk for rupture increasing as maximum diameter increases. The prevalence of the disorder is estimated at 3% in individuals over the age of 50 years, with male dominance. 2· 1% of all men over 65 years of age die from aortic aneurysm rupture, the tenth leading cause of death in this group. However, no drug treatments are effective in prevention. It seems that patients and doctors are still waiting for aneurysms to rupture or to become large enough to justify surgical or endovascular repair. 1

Abdominal aortic aneurysm and atherosclerotic disease manifestations are characterised by acute and chronic inflammation of the vessel wall, matrix degradation, and vascular tissue remodelling. 2 Angiotensin II (ATII), the major effector peptide of the renin-angiotensin-aldosterone system, plays an important part in the perpetuation of the inflammatory response, and in animal studies consistently promotes the formation of aneurysms. Mechanisms have not been clearly defined. 3 In animal models an attenuated degradation of medial elastin and prevention of aneurysmal degeneration was seen with angiotensinconverting-enzyme (ACE) inhibitors but not with blockers of ATII receptor. 4, 5 So, although the reninangiotensin-aldosterone system is associated with a range of key events in vascular inflammation, mechanisms underlying inflammation-associated