Abdominal aortic aneurysm (AAA) rupture is the 13th commonest cause of death in the Western World. Although considerable research has been applied to the aetiology and mechanism of aneurysm expansion, little is known about the mechanism of rupture. Aneurysm rupture was historically considered to be a simple physical process that occurred when the aortic wall could no longer contain the haemodynamic stress of the circulation. However, AAAs do not conform to the law of Laplace and there is growing evidence that aneurysm rupture involves a complex series of biological changes in the aortic wall. This paper reviews the available data on patient variables associated with aneurysm rupture and presents the evidence implicating biological factors in AAA rupture.

Objective-Matrix metalloproteinase (MMP) activity has been linked to abdominal aortic aneurysm (AAA) rupture.Medial neovascularization (MNV), a histopathologic characteristic of AAAs, involves proteolytic degradation of extracellular matrix by MMPs to facilitate endothelial cell migration. The role of MNV in aneurysm rupture is unknown. This study investigated whether MNV is increased in aneurysm rupture. Methods and Results-Biopsy samples from aneurysm rupture edge were compared with control biopsy samples from aneurysm wall at the level of rupture and from anterior sac in 12 ruptured AAAs. Further controls were obtained from anterior sac of 10 nonruptured AAAs. MNV, microvessel diameter, maturity index, and inflammatory infiltrate were quantified using morphometric analyses following immunohistochemistry. Expression of proangiogenic mediators was quantified using quantitative real-time-polymerase chain reaction. is expansion and rupture. Recent insights into the biological processes causing aneurysm expansion have led to translational research investigating the use of novel pharmacotherapeutic agents aimed at retarding aneurysm growth. [1][2][3] Any medical treatment of AAA must address aneurysm rupture as well as expansion. In contrast to the expansion of AAA, the biological processes causing aneurysm rupture have received little attention and current knowledge relating exclusively to the vascular biology of AAA rupture is lacking. Prospects for the development of pharmacological inhibition of aneurysm rupture therefore remain poor.Aneurysm rupture was historically considered to be a simple physical process that occurred when wall stress from the circulation exceeded the tensile strength of the aortic wall. 4 Focusing on aortic wall stress as the cause of rupture has led to the view that aneurysm rupture was regulated solely by mechanical factors. Just as the complexity of the atherosclerotic plaque has become apparent, it is now recognized that AAA rupture is a multifaceted biological process involving biochemical, cellular, and proteolytic influences in addition to biomechanical factors. 5 Proteolytic activities of MMPs have been implicated in aneurysm wall weakening and rupture. [5][6][7] Previous work have demonstrated that high levels of MMPs-8 and MMP-9 were localized to aneurysm rupture edge in humans 5 and experimental studies in rats have shown that inhibition of MMP activity by tissue inhibitor of MMP (TIMP)-1 prevented aneurysm rupture. 6 The MMP family is closely involved in the process of neovascularization 8 and play key proangiogenic roles such as the proteolytic degradation of extracellular matrix (ECM) to facilitate endothelial cell migration during angiogenesis, 9 detachment of pericytes from microvessels undergoing angiogenesis, release of ECMsequestered angiogenic growth factors, 10 exposure of cryptic proangiogenic integrin binding sites in the ECM, cleavage of vascular endothelial-cadherin endothelial cell-cell adhesions and generation of promigratory ECM fragments. 11 The medial layer o...

Aortic aneurysms account for 10,000 deaths annually in the UK, due to rupture. At present the only effective therapeutic strategy to treat abdominal aortic aneurysms is to surgically repair them; this carries an elective mortality of up to 10%. Recent advances in vascular biology have led to a greater understanding of the pathophysiological process that causes aortic aneurysms to expand and rupture. Key pathological processes include widespread aortic inflammation, proteolytic degradation of the extracellular matrix, neovascularisation and generation of reactive oxygen species. Identification of these processes has lead to pharmacological strategies to prevent aneurysm expansion and rupture. Many of these strategies have undergone proof of concept in animal models and some have now entered clinical trials. This review outlines current thinking regarding the molecular events leading to aneurysm expansion and explains how these processes may be inhibited. Experimental data on agents retarding aneurysm expansion in animal models are discussed. A significant proportion of the review details pharmacological agents that have undergone or are undergoing clinical trials. Pharmacological treatment for abdominal aneurysms is urgently required given the number of small aneurysms being diagnosed by screening programmes. This is a rapidly evolving field and one in which translation from experimental research to clinical practice is anticipated within 5 years.

The purpose was to review outcome data following endovascular repair of the descending thoracic aorta from reports published between 1994 and 2004. To accomplish this task, 1,518 patients underwent endovascular repair for thoracic aortic disease; 810 thoracic aortic aneurysms, 500 type B thoracic aortic dissections, and 106 traumatic ruptures. The 30-day mortality rate was 5.5% and 6% for late postoperative deaths. The primary technical success rate was 97%, with only 15 patients requiring open conversion. Neurologic deficits occurred in 29 patients. In total, 118 endoleaks were reported; 29 were restented, and the remainder required surgical intervention. Graft infection occurred in 6 cases, and migrations were detected in 10. The conclusion reached is that endovascular repair of descending thoracic aortic disease is feasible and can be achieved with low rates of perioperative morbidity and mortality. As few long-term data exist on the durability of thoracic stent grafts, lifelong surveillance remains necessary.