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]

Overview

The underlying pathophysiology of abdominal aortic aneurysm involves genetic influences, smoking, hypertension, hemodynamic influences and underlying atherosclerosis. In rare instances infection, arteritis, and connective tissue disorders may play a role.

Genetic Influences

There is likely a genetic component to the development of an abdominal aortic aneurysm. A familial pattern of inheritance is most notable in males.[1] It has been postulated that a variant of alpha 1-antitrypsin deficiency may play a small role. It has also been postulated that there is a pattern of X-linked mutation, which would explain the lower incidence in heterozygous females.

Environmental Influences

Smoking appears to be a critical environmental influence on the development of an abdominal aortic aneurysm.

Hemodynamic Influences

Abdominal aortic aneurysm is a focal degenerative process with a predilection for the infrarenal aorta. More than 90 % of abdominal aortic aneurysms occur in the infrarenal location. The higher incidence of abdominal aortic aneurysms in the infrarenal region may be due to differences between the infrarenal and the thoracic aorta with respect to histologic and mechanical characteristics. The diameter progressively decreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a smaller proportion of elastin. The mechanical tension in the 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

Although abdominal aortic aneurysms are frequently involved with atherosclerosis, the exact role of atherosclerosis in the pathophysiology of abdominal aortic aneurysms remains unclear at this time.

Other Causes

Other causes of the development of abdominal aortic aneurysm include:

Associated Diseases

Abdominal aortic aneurysms are associated with a high prevalence of systemic atherosclerosis:

Pathology

The most striking histopathological changes of aneurysmatic aorta are seen in tunica media and intima. These changes include an accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, ulcerations, 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.

Pathological Findings

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology






















References

  1. Clifton, MA: Familial abdominal aortic aneurysms. Br. J. Surg., 64, 1977, p. 765-766


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