Abdominal aortic aneurysm pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Pathophysiology & Etiology

The exact causes of the degenerative process remain unclear. There are, however, some theories and risk factors defined.

• Genetic influences: The influence of genetic factors is highly probable. The high familial prevalence rate is most notable in male individuals. There are many theories 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, some experimental works favored the theory of X-linked mutation, which would explain the lower incidence in heterozygous females. Other theories of genetic etiology were also formulated.

• Hemodynamic influences: Abdominal aortic aneurysm is a focal degenerative process with predilection for the subrenal aorta. The histological structure and mechanical characteristics of subrenal aorta differ from those of the thoracic aorta. The diameter decreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a lesser proportion of elastin. The mechanical tension in abdominal aortic wall is therefore higher than in the thoracic aortic wall. The elasticity and distensibility also decline with age, which can result in gradual dilatation of the segment. Higher intraluminal pressure in patients with arterial hypertension markedly contributes to the progression of the pathological process.

• Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA are frequently affected heavily. However, this theory cannot be used to explain the initial defect and the development of occlusion, which is observed in the process.

• Other causes: Other causes of the development of AAA include: infection, trauma, arteritis, cystic medial necrosis (m. Erdheim) and connective tissue disorders (e.g. Marfan syndrome, Ehlers-Danlos syndrome).

The most striking histopathological changes of aneurysmatic aorta are seen in tunica media and intima. These include accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, ulcerations and ruptures of the layers and thrombosis. There is an adventitial inflammatory infiltrate. However, the degradation of tunica media by means of proteolytic process seems to be the basic pathophysiologic mechanism of the AAA development. Some researchers report increased expression and activity of matrix metalloproteinases in individuals with AAA. This leads to elimination of elastine from the media, rendering the aortic wall more susceptible to the influence of the blood pressure. Other pathophysiological cause for development of the AAA is inflammation.

• The aortic wall has a specific arrangement of structural proteins that give it both strength and elasticity.
• The composition of the extracellular matrix protein in the media may change with age or in reponse to other conditions, therefore resulting in subsequent destruction of the elastic lamella, rendering the aorta less able to withstand the force of systolic pressure.
• The infrarenal aorta is more prone to develop aneurysms than other segments for the following reasons:

  • It is the segment that must expand the most during systole and contract the most during diastole.
  • It has a thinner wall, and has fewer vasa vasora than the thoracic aorta
  • It is more prone to atherosclerosis, a proposed nidus for aneurysmal dilatation.

• Patients with abdominal aortic aneurysms (AAA) also have atherosclerosis in the aorta and other arteries, suggesting that aneurysmal disease may be part of a larger spectrum of vascular disease, and that atherosclerosis actually promotes AAA formation.
• In atherosclerotic AAA, inflammatory cells infiltrate into the vessel wall and may secrete specific matrix metalloproteinases (MMPs)

  • The different types of MMPs play diverse roles via complex interactions that eventually lead to degradation of the structural media proteins, and subsequently to aneurysmal dilatation.

• There are significantly fewer smooth muscle cells in human AAA tissues than in normal or atherosclerotic nonaneurysmal aortic tissue.

  • This decrease in smooth muscle cells in suspected to be secondary to apoptosis, therefore suggesting a role for focal cell apoptosis in the pathogenesis of AAA.

Acknowledgements

The content on this page was first contributed by: C. Michael Gibson M.S., M.D. Template:WH Template:WS