Aortic Aneurysm

Aortic aneurysms involve a dilation of the aortic wall and are categorized into true and false types. True aortic aneurysms involve all layers of the vessel wall—intima, media, and adventitia—while false aneurysms only involve the adventitia. The majority of abdominal aortic aneurysms (AAA) form below the renal arteries; involvement of these arteries can lead to renal injury and even failure. Many patients with AAA also have atherosclerosis, particularly within the aneurysm itself. Risk factors for AAA include age (especially >60 years), smoking, and family history.

In contrast, thoracic aortic aneurysms (TAA) often share risk factors with atherosclerosis, most notably hypertension, which is present in 60% of cases. TAAs are also associated with conditions like Marfan syndrome, due to a mutation in fibrillin that decreases aortic distensibility, and Turner syndrome, which is often associated with bicuspid aortic valves that lead to dilation of the aortic root. The aortic arch is the second most common site for aneurysm formation in many patients who also have AAA.

Cystic medial degeneration is a common pathology in aortic aneurysms. It features inflammatory cell infiltrate, smooth muscle apoptosis and necrosis leading to accumulation of mucopolysaccharide, degradation of elastic lamina, and degradation of the extracellular matrix by metalloproteinases.

Screening for AAA is crucial and involves an abdominal ultrasound, particularly in men over 65 who have a history of smoking. AAA may present on physical examination as a palpable, pulsatile abdominal mass. Complications of AAA can include acute limb ischemia due to distal embolization of thrombus or postrenal kidney injury if the aneurysm obstructs the ureters. The risk of rupture correlates with the vessel's diameter; increased vessel radius leads to elevated wall tension and hemodynamic stress. A ruptured AAA can result in severe retroperitoneal hemorrhage, presenting as acute, severe flank pain and is associated with a 50% mortality rate due to hypovolemic shock.

TAAs can also present with unique complications such as tracheal compression leading to cough, wheezing, or dyspnea. They may compress the left recurrent laryngeal nerve causing hoarseness or the esophagus leading to dysphagia. If extending proximally, they can cause dilation of the aortic root leading to aortic regurgitation, characterized by a diastolic decrescendo murmur, or even ischemic heart disease by blocking coronary artery ostia. They can also cause embolism of thrombus into the cerebral circulation leading stroke.

Various underlying conditions can exacerbate aortic aneurysm formation. These include inflammatory vasculitides like Takayasu arteritis and temporal arteritis, and infections like tertiary syphilis, which leads to syphilitic aortitis. This is characterized by destruction of the vasa vasorum in the aortic arch, leading to cystic medial degeneration and aneurysm formation. The aorta may show a ‘tree bark’ appearance due to extensive fibrosis and linear calcification of the aortic arch visible on CXR.