A 72-year-old white man underwent a computed tomographic (CT) scan of the chest to evaluate a pulmonary nodule and incidentally found to have a 6-cm descending aortic aneurysm beginning distal to the subclavian artery and ending proximal to the celiac axis. The patient denied any chest or back pain. His past medical history was significant for hypertension, hyperlipidemia, and chronic obstructive pulmonary disease. He also relayed that his father died as a result of a ruptured aneurysm. Auscultation of the chest revealed distant lung sounds but otherwise his physical examination was unremarkable. Risks and benefits of open and endovascular repair of the aneurysm were discussed with the patient, and he elected to undergo endovascular repair.

This patient has a descending thoracic aortic aneurysm (TAA). Most patients are asymptomatic on presentation. The goal of aneurysm repair is to prevent death from rupture.

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  Aortic disease is the 12th leading cause of death in the United States.¹

  
  
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  A descending aortic aneurysm is defined as a dilatation of the thoracic aorta to at least 1.5 times its normal diameter.¹

  
  
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  Descending thoracic aneurysms are less common than abdominal aortic aneurysms (AAAs).¹

  
  
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  Incidence is approximately 5.9 cases per 100,000 person-years.¹

  
  
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  Found mostly in the elderly with a male predominance.¹

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  Genetics, cellular imbalance, and altered hemodynamics are all factors involved in the development of a TAA.

  
  
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  The loss and fragmentation of elastic fibers and smooth muscle cells within the aortic wall is referred to as medial degeneration. It is responsible for approximately 80% of thoracic aneurysms.¹

  
  
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  As people age, medial degeneration occurs, but it is accelerated by hypertension and atherosclerosis.² Patients with Marfan syndrome have accelerated medial degeneration.³

  
  
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  Dissections, connective tissue disorders, autoimmune disorders, and infections are also responsible for the development of thoracic aneurysms.¹

Thoracic aneurysms are usually asymptomatic and often discovered incidentally during the workup for unrelated conditions.¹

No laboratory test is currently available to detect the presence of a TAA. Serum chemistry including serum creatinine, complete blood count, and coagulation studies should be obtained in preparation for repair.

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  Computed tomography angiogram (CTA)—Chest or abdomen or pelvis is the primary modality utilized for preoperative planning; 64-slice CT provides excellent detailed imaging and can also be reconstructed for three-dimensional viewing.⁴

  
  
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  Arteriography—used in conjunction with the CTA to help provide additional anatomic information; invasive; usually performed at time of repair⁴ (Figure 32-1).

  
  
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  Magnetic resonance angiogram (MRA)—may be used in place of the CTA in patients with severe allergies; no radiation risk⁴ but contraindicated in those with renal failure secondary to nephrogenic systemic fibrosis.