Abdominal Aortic Aneurysm - Pathophysiology

Pathophysiology

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, thrombosis, and ulcerations and ruptures of the layers. 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 elastin from the media, rendering the aortic wall more susceptible to the influence of the blood pressure. There is also a reduced amount of vasa vasorum in the abdominal aorta (compared to the thoracic aorta); consequently, the tunica media must rely mostly on diffusion for nutrition which makes it more susceptible to damage.

Hemodynamics affect the development of AAA. It has a predilection for the infrarenal aorta. The histological structure and mechanical characteristics of infrarenal 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. Suitable hemodynamics conditions may be linked to specific Intraluminal Thrombus (ILT) patterns along the aortic lumen, which in turn may affect AAA's development.