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Abdominal Aortic Aneurysm - Etiology

Ngày 26/07/2016 07:43 | Lượt xem: 2471

AAA is thought to be a degenerative process of the aorta, the cause of which remains unclear. It is often attributed to atherosclerosis because these changes are observed in the aneurysm at the time of surgery. 

However, a study by Blanchard et al found that the risk factors for AAA differ from those for atherosclerosis, with no association between cholesterol and AAA. In addition, atherosclerosis fails to explain the development of occlusion, which is observed in the disease process.

Patients at greatest risk for AAA are men who are older than 65 years and have peripheral atherosclerotic vascular disease. A history of smoking often is elicited. Accordingly, in 2005, the US Preventive Services Task Force (USPSTF) recommended ultrasonography screening in men aged 65-75 years who had ever smoked. As of June 2014, these recommendations were being updated on the basis of evidence from a 2014 study by Guirguis-Blake et al.

A 2011 Swedish study showed that instances of AAA in elderly men have been decreasing, A phenomenon that can be attributed to a nationwide decline in smoking for the past 30 years, as well as the significantly improved longevity of the elderly population. A one-time ultrasound scan is recommended for men once they reach age 65 years to detect and prevent possible occurrences of AAA.

Other risk factors for AAA include the following:

-Chronic obstructive pulmonary disease (COPD)

-Previous aneurysm repair or peripheral aneurysm (popliteal or femoral)

-Coronary artery disease

-Hypertension (1-15% of cases)

Less frequent causes of AAA include Marfan syndrome, Ehlers-Danlos syndrome, and collagen-vascular diseases. In fewer than 5% of cases, AAA is caused by mycotic aneurysm of hematogenous origin. In these cases, local invasion of the intima and media gives rise to abscess formation and aneurysmal dilation of the vessel. Gram-positive organisms most commonly cause mycotic aneurysms. Other uncommon causes include cystic medial necrosis, arteritis, trauma, and anastomotic disruption producing pseudoaneurysms.

Persons who have first-degree relatives with AAA are at increased risk for AAA. The familial prevalence rate of AAA has been estimated at 15-25%. Studies by Majumder et al suggest that the genetic predisposition is isolated to a single dominant gene with low penetrance that increases with age.

Tilson et al described the potential for an autoimmune basis for the development of AAA involving the DRB1 major histocompatibility locus. This locus has been identified as a basis for inflammatory AAA.

Risk factors for rupture

Aneurysm diameter is an important risk factor for rupture. In general, AAAs gradually enlarge (0.2-0.8 mm/year) and eventually rupture. Hemodynamic factors play an important role. Areas of high stress have been found in AAAs and appear to correlate with the site of rupture. Computer-generated geometric models have demonstrated that aneurysm volume is a better predictor of areas of peak wall stress than aneurysm diameter. This may have implications for determining which AAAs require surgical repair.

AAA rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue. Wall tension can be calculated by applying Laplace’s law, as follows:

P × R/W

where P is the mean arterial pressure (MAP), R is the radius of the vessel, and W is the thickness of the vessel wall. AAA wall tension is a significant predictor of pending rupture. The actual tension in the AAA wall appears to be a more sensitive predictor of rupture than aneurysm diameter alone. For these reasons, the clinician may wish to achieve acute blood pressure control in patients with AAA and elevated blood pressure.

Source emedicine.com

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