Abdominal Aortic Aneurysm

Abstract

Abstract-Abdominal aortic aneurysm (AAA) affects approximately 5% of elderly men and is responsible for a significant number of deaths in Western Countries. At present surgery by open or endovascular means is the only widely used therapy for this condition. In this review we examine the risk factors, serum, and genetic associations of AAA. Epidemiology studies suggest that smoking cessation and control of cholesterol and blood pressure should reduce the number of patients developing AAA. Natural history studies suggest that smoking cessation should reduce the rate of progression of AAA. Clear level 1 evidence for drug treatments of AAA are presently lacking; however, animal and human in vitro studies suggest that medication targeted at reducing inflammation and proteolysis are most likely to be beneficial, with limited data to support the use of statins, Angiotensin II inhibitors, and macrolides. Work has commenced in understanding which patients, identified by clinical, serum, and genotype, are more at risk of AAA progression and thus should be selected out for aggressive treatment.Well designed large multicenter randomized controlled trials are required to examine the medical treatment of AAA.

A single nucleotide polymorphism in exon 3 of the kallikrein 1 gene is associated with large but not small abdominal aortic aneurysm

“…Progressive aortic wall dilatation is associated with cycles of extracellular matrix degradation [30] and inflammation, involving proteolytic enzymes produced by invading inflammatory cells [31,2]. Our findings suggest a role of the KLK1 gene in large but not small AAA.…”

“…Important risk factors for AAA include age, smoking, coronary heart disease, hypertension and family history [2]. Subjects with a first degree relative with a history of AAA have a approximately 2-fold increased risk of developing the condition [3].…”

Associations of IGF1 and its binding proteins with abdominal aortic aneurysm and aortic diameter in older men

“…However, AAA and CVD may develop in parallel through different pathogenic mechanisms, with weakening of the aortic wall playing a key role in aortic dilation and AAA formation (7). Changes in the walls of aneurysmal aortas are characterised by up-regulation of proteolytic pathways, the loss of matrix, inflammation and, to a variable extent, atherosclerosis (22). In a study involving 115 cases of AAA, Lindholt et al (23) recently showed that IGF1 levels are correlated with aneurysmal diameter and rate of progression.…”

Plasma concentrations of growth arrest specific protein 6 and the soluble form of its tyrosine kinase receptor Axl as markers of large abdominal aortic aneurysms

“…Inflammation, as reflected by increased plasma concentrations of fibrinogen, IL-6, Creactive protein 3 , and elevation of matrix metalloproteinases 4 has also been suggested to be involved in the pathogenesis of AAA 5 . Biomarkers that could differentiate between stable aneurysms and aneurysms prone to growth and subsequent rupture have been extensively sought for, as they would be of great clinical relevance 1 .…”