aortic aneurysm

Pathophysiology: Aneurysms result from weakening of the aortic wall due to degradation of elastin and collagen in the media layer. AAA is most often caused by atherosclerosis, which leads to inflammation, proteolytic enzyme release (MMPs), and destruction of the vessel wall, typically in the infrarenal aorta due to relatively lower vasa vasorum density there. TAA is often due to cystic medial necrosis (degeneration of smooth muscle and elastic fibers), seen classically in Marfan syndrome (FBN1 mutation), Loeys-Dietz syndrome, and bicuspid aortic valve. Tertiary syphilis causes obliterative endarteritis of the vasa vasorum, leading to ischemic medial damage and a characteristic 'tree bark' appearance of the ascending aorta.

Clinical significance: Most AAAs are asymptomatic and discovered incidentally or via screening (one-time ultrasound recommended for men 65-75 who have ever smoked). Symptomatic AAAs may present with abdominal/back pain and a pulsatile abdominal mass. Rupture is a surgical emergency presenting with the classic triad of hypotension, back/abdominal pain, and pulsatile mass, with high mortality. TAAs may cause chest pain, hoarseness (recurrent laryngeal nerve compression), dysphagia, or be found incidentally on chest imaging.

Management: Surveillance imaging for small aneurysms; surgical repair (open or endovascular/EVAR) indicated for AAA ≥5.5 cm (or ≥5 cm in women), rapid growth (>0.5 cm/year), or symptomatic aneurysms. TAA repair typically considered at ≥5.5 cm (lower threshold in Marfan syndrome, ~4.5-5 cm).

Key associations: AAA - atherosclerosis, smoking, hypertension, male sex, age >65, family history. TAA - Marfan syndrome, Loeys-Dietz syndrome, bicuspid aortic valve, tertiary syphilis (ascending aorta), hypertension.