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* Increased activity of certain enzymes causes degradation of [[elastin]] and [[collagen]] in the arteries. This leads to loss of elasticity, weakens the aortic wall and causes it to dilate.
* Increased activity of certain enzymes causes degradation of [[elastin]] and [[collagen]] in the arteries. This leads to loss of elasticity, weakens the aortic wall and causes it to dilate.
* Moreover, the part of aorta below the origin of renal arteries has less amount of [[elastin]] compared to [[collagen]], accounting for increased frequency of aneurysms in this area.
* Moreover, the part of aorta below the origin of renal arteries has less amount of [[elastin]] compared to [[collagen]], accounting for increased frequency of aneurysms in this area.
*In patients with Marfan syndrome there is a defect on chromosome 15 that is associated with impaired [[fibrillin]] synthesis, which is the core protein of [[microfibrils]]. Frequently among patients with [[Marfan's syndrome]] there is [[cystic medial degeneration]].


===Hemodynamic factors===
===Hemodynamic factors===

Revision as of 19:57, 21 October 2012

Thoracic aortic aneurysm Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]

Overview

An aneurysm occurs when a part or entire circumference of the vessel is pathologically dilated. A true aneurysm involves all three layers of the vessel, whereas pseudoaneurysm is characterized by disruption of the intima and media, and the dilated segment of the aorta is lined by adventitia alone.

Pathophysiology

  • The clinical manifestations of thoracic aortic aneurysms depends on hemo-dynamic factors as well as factors intrinsic to individual arterial components.
  • Cystic medial necrosis is the most common pathology associated with ascending aortic aneurysms, whereas atherosclerosis is most frequently involved in the arch and descending aorta.
  • The aortic aneurysms associated with Marfan syndrome grow at a faster rate and are more prone to rupture.
  • Most thoracic aneurysms are asymptomatic. However, the enlarging aorta can compress adjacent organs and cause symptoms like chest pain, dyspnea, hoarseness of voice, cough and dysphagia. Also symptoms of congestive heart failure can occur from severe aortic regurgitation and congestion of head, neck and upper extremities from superior vena cava compression.

Elastin and collagen

  • Increased activity of certain enzymes causes degradation of elastin and collagen in the arteries. This leads to loss of elasticity, weakens the aortic wall and causes it to dilate.
  • Moreover, the part of aorta below the origin of renal arteries has less amount of elastin compared to collagen, accounting for increased frequency of aneurysms in this area.
  • In patients with Marfan syndrome there is a defect on chromosome 15 that is associated with impaired fibrillin synthesis, which is the core protein of microfibrils. Frequently among patients with Marfan's syndrome there is cystic medial degeneration.

Hemodynamic factors

  • The aorta being a low resistance circuit, repeated trauma from a reflected wave results in dilatation.
  • Systemic hypertension accelerates the process of dilatation of aorta and contributes to the formation of aneurysms.

Gross Pathology

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

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