Aneurysm of the Abdominal Aorta

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Basics

Description

  • There are two types of aneurysms: true and false. A true aneurysm involves all three vessel wall layers. False aneurysms or pseudoaneurysms occur when the intimal and medial layers are disrupted, and the dilated segment is surrounded by the adventitia only, and possibly a perivascular clot. Ruptures are usually higher with false aneurysms due to poor support of the aneurysmal wall.
  • Abdominal aortic aneurysm (AAA) is the most common true arterial aneurysm. False aneurysms of the abdominal aorta are usually due to trauma or infection.
  • The average diameter of the infrarenal aorta is 2.0 cm; an aortic diameter of ≥3.0 cm is considered aneurysmal.
  • In men, AAA diameters are predictive of clinical events. In women, aneurysms are still defined as >3.0 cm, but the aortic scaling index (ASI; diameter [cm]/body surface area [m2]) is more predictive of clinical events.
  • System(s) affected: cardiovascular; neurologic; heme/lymphatic/immunologic
  • Synonym(s): aortic aneurysms; AAA

Geriatric Considerations
Incidence of AAA, risk of rupture, and operative morbidity and mortality all rise with age.

Pediatric Considerations
Rare in children; may be associated with umbilical artery catheters, connective tissue diseases, arteritides, or congenital abnormalities

Epidemiology

  • Estimated prevalence of AAA in developed countries is 2–8%. Age-related increase is seen more with men than women.
  • Ultrasound studies show that 4–8% of older men have an occult AAA.
  • 90% of all AAA >4 cm are related to atherosclerotic disease, with the vast majority located infrarenally.
  • Predominant sex: male > female

Incidence
  • Roughly 15,000 deaths per year and the 15th leading cause of death in United States
  • 0.4–0.67% in Western populations or 2.5 to 6.5 aneurysms per 1,000 patient-years
  • If stratified into years, the incidence of AAA is increased in the older populations. For example, the incidence increases from 55 to 298 per 100,000 patient-years if comparing men aged 65 to 74 years versus men >85 years of age.
Prevalence
  • The prevalence of AAA-associated mortality has decreased by 50% since the 1990s, likely due to the decline in cigarette smoking, increased screening for AAA detection, and early interventions.
  • With the increasing life expectancy in developed countries, the prevalence of AAA is expected to increase, but the decreased prevalence of smoking will have the opposite effect.

Etiology and Pathophysiology

  • AAAs are caused by degradations of abnormal production of elastin and collagen, the structural components of the aortic wall.
  • There are many causes of aortic aneurysms: inflammation, degenerative disorders, vasculitis, infections, and trauma. However, the vast majority of AAA are caused by inflammation with atherosclerosis as the inciting factor.
  • B-cell and T-cell lymphocytes, macrophages, inflammatory cytokines, and matrix metalloproteinases degrade elastin and collagen, thus decreasing the aortic wall strength, leading to a decreased ability to accommodate the pulsatile flow.
  • Histopathology shows elastin and collagen destruction, decreased vascular smooth muscle, ingrowth of new blood vessels, and subsequent inflammation.
  • Although most aortic aneurysms are caused by inflammatory or degenerative destruction of elastin and collagen, infections, trauma, and connective tissues disorders can also degrade elastin and collagen, leading to similar presentations.
  • The natural course of a AAA is progressive expansion, based on a variety of factors, the most important being on going smoking.

Genetics
  • Familial aggregations exist with aneurysms developing at an earlier age.
  • Familial abdominal aortic aneurysms have a variable polygenetic inheritance pattern.
  • Monogenetic inheritance patterns such as: Marfan syndrome (fibrillin-1 defect), Ehlers-Danlos syndrome (type IV collagen defect), or Loeys-Dietz syndrome are more commonly associated with thoracoabdominal aortic aneurysms.

Risk Factors

Older age, male sex, Caucasian race, family history, smoking, hypertension (HTN), hyperlipidemia, atherosclerosis, peripheral aneurysms, obesity

General Prevention

  • Address cardiovascular disease risk factors.
  • Follow screening guidelines: U.S. screening for detection of AAA in male patients, 65 to 75 years, who have ever smoked.

Commonly Associated Conditions

  • HTN, myocardial infarction (MI), heart failure, carotid artery atherosclerosis, and/or lower extremity peripheral arterial disease, tobacco abuse
  • Screening for thoracic aneurysm should also be considered.
  • 20% of patients with AAA have concurrent thoracic aneurysm (1).

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Basics

Description

  • There are two types of aneurysms: true and false. A true aneurysm involves all three vessel wall layers. False aneurysms or pseudoaneurysms occur when the intimal and medial layers are disrupted, and the dilated segment is surrounded by the adventitia only, and possibly a perivascular clot. Ruptures are usually higher with false aneurysms due to poor support of the aneurysmal wall.
  • Abdominal aortic aneurysm (AAA) is the most common true arterial aneurysm. False aneurysms of the abdominal aorta are usually due to trauma or infection.
  • The average diameter of the infrarenal aorta is 2.0 cm; an aortic diameter of ≥3.0 cm is considered aneurysmal.
  • In men, AAA diameters are predictive of clinical events. In women, aneurysms are still defined as >3.0 cm, but the aortic scaling index (ASI; diameter [cm]/body surface area [m2]) is more predictive of clinical events.
  • System(s) affected: cardiovascular; neurologic; heme/lymphatic/immunologic
  • Synonym(s): aortic aneurysms; AAA

Geriatric Considerations
Incidence of AAA, risk of rupture, and operative morbidity and mortality all rise with age.

Pediatric Considerations
Rare in children; may be associated with umbilical artery catheters, connective tissue diseases, arteritides, or congenital abnormalities

Epidemiology

  • Estimated prevalence of AAA in developed countries is 2–8%. Age-related increase is seen more with men than women.
  • Ultrasound studies show that 4–8% of older men have an occult AAA.
  • 90% of all AAA >4 cm are related to atherosclerotic disease, with the vast majority located infrarenally.
  • Predominant sex: male > female

Incidence
  • Roughly 15,000 deaths per year and the 15th leading cause of death in United States
  • 0.4–0.67% in Western populations or 2.5 to 6.5 aneurysms per 1,000 patient-years
  • If stratified into years, the incidence of AAA is increased in the older populations. For example, the incidence increases from 55 to 298 per 100,000 patient-years if comparing men aged 65 to 74 years versus men >85 years of age.
Prevalence
  • The prevalence of AAA-associated mortality has decreased by 50% since the 1990s, likely due to the decline in cigarette smoking, increased screening for AAA detection, and early interventions.
  • With the increasing life expectancy in developed countries, the prevalence of AAA is expected to increase, but the decreased prevalence of smoking will have the opposite effect.

Etiology and Pathophysiology

  • AAAs are caused by degradations of abnormal production of elastin and collagen, the structural components of the aortic wall.
  • There are many causes of aortic aneurysms: inflammation, degenerative disorders, vasculitis, infections, and trauma. However, the vast majority of AAA are caused by inflammation with atherosclerosis as the inciting factor.
  • B-cell and T-cell lymphocytes, macrophages, inflammatory cytokines, and matrix metalloproteinases degrade elastin and collagen, thus decreasing the aortic wall strength, leading to a decreased ability to accommodate the pulsatile flow.
  • Histopathology shows elastin and collagen destruction, decreased vascular smooth muscle, ingrowth of new blood vessels, and subsequent inflammation.
  • Although most aortic aneurysms are caused by inflammatory or degenerative destruction of elastin and collagen, infections, trauma, and connective tissues disorders can also degrade elastin and collagen, leading to similar presentations.
  • The natural course of a AAA is progressive expansion, based on a variety of factors, the most important being on going smoking.

Genetics
  • Familial aggregations exist with aneurysms developing at an earlier age.
  • Familial abdominal aortic aneurysms have a variable polygenetic inheritance pattern.
  • Monogenetic inheritance patterns such as: Marfan syndrome (fibrillin-1 defect), Ehlers-Danlos syndrome (type IV collagen defect), or Loeys-Dietz syndrome are more commonly associated with thoracoabdominal aortic aneurysms.

Risk Factors

Older age, male sex, Caucasian race, family history, smoking, hypertension (HTN), hyperlipidemia, atherosclerosis, peripheral aneurysms, obesity

General Prevention

  • Address cardiovascular disease risk factors.
  • Follow screening guidelines: U.S. screening for detection of AAA in male patients, 65 to 75 years, who have ever smoked.

Commonly Associated Conditions

  • HTN, myocardial infarction (MI), heart failure, carotid artery atherosclerosis, and/or lower extremity peripheral arterial disease, tobacco abuse
  • Screening for thoracic aneurysm should also be considered.
  • 20% of patients with AAA have concurrent thoracic aneurysm (1).

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