Aneurysms are congenital or acquired, Localized, abnormal dilations of blood vessels or the heart.


Aneurysms are classified by origin, location, gross appearance, composition of vessel wall, and etiology.

1. Origin:

It can be congenital or acquired.

2. Location:

It refers to the type of vessel involved

  • Artery
  • Vein
  • Heart.

3. Depending on gross appearance (shape and size) :

  • Fusiform aneurysm: It is ovoid or fusiform dilation of vessel wall that is parallel to the long axis.
  • Saccular aneurysm: It is a localized spherical outpouchings from the portion of the vessel wall.
  • Arterial dissection/dissecting hematoma: It develops when blood enters/dissects between the layers of the arterial wall. Just like a hematoma it separates the layers of the arterial wall.
  • Arteriovenous aneurysm: It is a direct communication between an artery and a vein.

4. Depending on the composition of the wall of the aneurysm:

  • True aneurysm is composed of all the layers of thinned arterial wall (intima, media and adeventia) or attenuated ventricular wall of the heart.
  • False aneurysm (or pseudoaneurysm) is a defect in the vascular wall with a hematoma (blood-filled space forms around a blood vessel) which freely communicates with the intravascular space (pulsating hematoma). It usually develops after traumatic rupture or a perforating injury.
  • Arterial dissection is characterized by entry of blood into the arterial wall through an intimal defect, which separates the underlying layers.

5. Depending on the etiology:

  • Atherosclerotic aneurysm • Syphilitic aneurysm • Dissecting hematoma • Mycotic aneurysm • Berry aneurysm.


The loss of balance between connective tissue synthesis and degradation of the vascular wall may produce aneurysm.

1. Inadequate or abnormal synthesis of connective tissue of the vascular wall:

  • TGF-β regulates smooth muscle cell proliferation and synthesis of connective tissue matrix. Mutations in TGF-β receptors or downstream signaling pathways → defective synthesis of elastin and collagen → aneurysm.
  • Vitamin C (ascorbate) deficiency → altered collagen cross-linking.

2. Increased degradation of connective tissue:

  • Increased production of MMP enzymes (e.g. by macrophages in atherosclerosis) can degrade the ECM in the arterial wall may cause aneurysm formation. This may be seen in atherosclerotic plaque or in vasculitis.
  • Loss of smooth muscle cells: It may occur due to ischemia of the inner media as in atherosclerosis or ischemia of the outer media as in systemic hypertension.
Predisposing Factors
  • Atherosclerosis
  • Hypertension
  • Trauma
  • Vasculitis
  • Congenital defects (e.g. berry aneurysms in the circle of Willis)
  • Tertiary syphilis
  • Infections (mycotic aneurysms)

Abdominal Aortic Aneurysm

Gender and age:

Abdominal aortic aneurysm (AAA) is more common in men, in smokers, and rare before the age of 50 yeras.

1. Atherosclerotic AAA:

  • a. Atherosclerotic plaque in the intima causes thinning of media and reduces the diffusion of nutrient and waste from the lumen of vessel into the arterial wall. The media undergoes necrosis and cause weakness and thinning of arterial wall.
  • b. The excessive degradation of ECM by MMP secreted from inflammatory cell infiltrates mainly macrophages present in the plaque.

2. Inflammatory AAA: It is characterized by dense periaortic fibrosis accompanied by inflammatory cells (lymphocytes, plasma cells and macrophages).

3. Mycotic AAA: It is due to infection of the aortic wall by circulating microorganisms (e.g. bacteremia from a primary Salmonella gastroenteritis). The suppurative process destroys the media → aneurysm → rupture.


Abdominal aortic aneurysms typically occur between the renal  arteries and the aortic bifurcation, they can be saccular or fusiform and up to 15 cm in diameter and 25 cm in length.

  • In the vast majority of cases, extensive atherosclerosis is present, with thinning and focal destruction of the underlying  media. The aneurysm sac usually contains bland, laminated, poorly organized mural thrombus.
  • Inflammatory AAAs are a distinct subtype characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic inflammation with many macrophages and giant cells.
  • A subset of inflammatory AAAs may be a vascular manifestation of a recently recognized entity called immunoglobulin G4 (IgG4) related disease. This disorder is marked by tissue fibrosis associated with frequent infiltrating IgG4expressing plasma cells.
  • Mycotic AAAs occur when circulating microorganisms (as in bacteremia from infective endocarditis) seed the aneurysm wall or the associated thrombus the resulting suppuration accelerates the medial destruction and may lead to rapid dilation and rupture.

Thoracic Aortic Aneurysm

  • Thoracic aortic aneurysms most commonly are associated with hypertension, bicuspid aortic valves, and Marfan syndrome.
  • Less commonly, disorders caused by mutations in the TGF-β signaling pathway are causative.

These aneurysms manifest with the following signs and symptoms:

  •  Respiratory or feeding difficulties due to airway or esophageal compression, respectively, because of encroachment on mediastinal structures
  • Persistent cough from irritation of the recurrent laryngeal nerves
  • Pain caused by erosion of bone (i.e., ribs and vertebral bodies)
  • Cardiac disease due to valvular insufficiency or narrowing of the coronary ostia, heart failure induced by aortic valvular incompetence
  • Aortic dissection or rupture

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