The high familial prevalence rate is most notable in male individuals. There are many hypotheses about the exact genetic disorder that could cause higher incidence of AAA among male members of the affected families. Some presumed that the influence of alpha 1-antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis of X-linked mutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated. Connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA. Both relapsing polychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm. Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot be used to explain the initial defect and the development of occlusion, which is observed in the process. Other causes of the development of AAA include: infection, trauma, arteritis, and cystic medial necrosis. Pathophysiology
The most striking histopathological changes of the aneurysmatic aorta are seen in the tunica media and intima layers. These changes include the accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, thrombosis, and ulcerations and ruptures of the layers. Adventitial inflammatory infiltrate is present. However, the degradation of the tunica media by means of a proteolytic process seems to be the basic pathophysiologic mechanism of AAA development. Some researchers report increased expression and activity of matrix metalloproteinases in individuals with AAA.
Recent reports have shown that these stress distributions have been shown to correlate to the overall geometry of the AAA rather than solely to the maximum diameter. It is also known that wall stress alone does not completely govern failure as an AAA will usually rupture when the wall stress exceeds the wall strength. In light of this, rupture assessment may be more accurate if both the patient-specific wall stress is coupled together with patient-specific wall strength. A noninvasive method of determining patient-dependent wall strength was recently reported, with more traditional approaches to strength determination via tensile testing performed by other researchers in the field. Some of the more recently proposed AAA rupture-risk assessment methods include: AAA wall stress; AAA expansion rate; degree of asymmetry; presence of intraluminal thrombus (ILT); a rupture potential index (RPI); a finite element analysis rupture index (FEARI); biomechanical factors coupled with computer analysis; growth of ILT; geometrical parameters of the AAA; and also a method of determining AAA growth and rupture based on mathematical models.The postoperative mortality for an already ruptured AAA has slowly decreased over several decades but remains higher than 40%. However, if the AAA is surgically repaired before rupture, the postoperative mortality rate is substantially lower, approximately 1-6%. Epidemiology
The occurrence of AAA varies by ethnicity. In the United Kingdom, the rate of AAA in Caucasian men older than 65 years is about 4.7%, while in Asian men it is 0.45%. It is also less common in individuals of African, and Hispanic heritage.