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.

Aortic aneurysm rupture after EVAR secondary to an isolated type II endoleak is rare (less than 1 per cent), but over a third occur in the absence of sac expansion. Translumbar embolization had a higher success rate with a lower risk of complications.

Background: Any possible long-term benefit from endovascular (EVAR) versus open surgical repair for abdominal aortic aneurysm (AAA) remains unproven. Long-term data from the Open Versus Endovascular Repair (OVER) trial add to the debate regarding long-term all-cause and aneurysm-related mortality. The aim of this study was to investigate 30-day and long-term mortality, reintervention, rupture and morbidity after EVAR and open repair for AAA in a systematic review.Methods: Standard PRISMA guidelines were followed. Random-effects Mantel-Haenszel meta-analysis was performed to evaluate mortality and morbidity outcomes. Results: The existing published randomized trials, together with information from Medicare and SwedVasc databases, were included in a meta-analysis. This included 25 078 patients undergoing EVAR and 27 142 undergoing open repair for AAA. Patients who had EVAR had a significantly lower 30-day or in-hospital mortality rate (1·3 per cent versus 4·7 per cent for open repair; odds ratio (OR) 0·36, 95 per cent confidence interval 0·21 to 0·61; P < 0·001). By 2-year follow-up there was no difference in all-cause mortality (14·3 versus 15·2 per cent; OR 0·87, 0·72 to 1·06; P = 0·17), which was maintained after at least 4 years of follow-up (34·7 versus 33·8 per cent; OR 1·11, 0·91 to 1·35; P = 0·30). There was no significant difference in aneurysm-related mortality by 2 years or longer follow-up. A significantly higher proportion of patients undergoing EVAR required reintervention (P = 0·003) and suffered aneurysm rupture (P < 0·001). Conclusion:There is no long-term survival benefit for patients who have EVAR compared with open repair for AAA. There are also significantly higher risks of reintervention and aneurysm rupture after EVAR. The aim of this systematic review and meta-analysis was to investigate short-, medium-and long-term outcomes, including morbidity, reintervention and mortality, associated with EVAR and open aneurysm repair. MethodsStandard reporting guidelines set by the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) Group 7 were followed to identify RCTs and other high-level evidence reporting comparative outcomes of endovascular and open repair of AAA. Study titles and abstracts were searched using MEDLINE, Embase, and Health and Psychosocial Instruments databases, using Ovid Online (version: OvidSP_UI03.04.02.112) in July 2012, with the most recent search carried out on 31 December 2012, separately by two researchers. No language restrictions or filters used to restrict study designs were applied. Reference lists were searched for further studies to be included. Eligibility criteria and study selectionA comprehensive literature search was performed using the search terms 'endovascular AND open AND repair AND abdominal AND aortic AND aneurysm' AND 'randomised OR randomized' AND 'trial' NOT 'thoracic'. Two reviewers individually reviewed potential studies according to a set of eligibility criteria, with discussion of discrepancies. Inclusion criteria were that t...

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...