Abstract
Abdominal aortic aneurysm (AAA) affects approximately 2-4% of the adult population and is the thirteenth leading cause of death in the United States. Patients are mostly asymptomatic but they can present with mild abdominal or back pain, distal embolization of thrombus, compression of ureters and hydronephrosis, pulsatile abdominal mass, as well as rupture, which is characterized by sudden-onset pain, hypotension, syncope, or sudden death. Risk factors for AAA formation and progression include cigarette smoking, hypertension, dyslipidemia, advancing age, male gender, and family history, while protective factors include African race, female gender, and diabetes mellitus. The pathophysiology of thoracic aortic aneurysms (TAA) is cystic medial degeneration, a non-inflammatory process. On the other hand, formation of AAA results from complex interactions between mural inflammation, proteolysis by matrix metalloproteinases, oxidative stress, apoptosis of smooth muscle cells, and neovascularization of the vasa vasorum. Ultrasonography is the method of choice for detection of AAA, while computerized tomography (CT) and magnetic resonance imaging (MRI) are the most frequently used methods for planning therapeutic strategies. Surgical treatment of AAA is generally reserved for larger (> 5 cm), rapidly expanding, or symptomatic aneurysms and consists of open versus endovascular aneurysm repair (EVAR). Although endovascular repair has lower short-term mortality, this does not translate into long-term survival difference. With increased understanding of the pathophysiology of AAA formation, new medications are being investigated for prevention of AAA and their progression, including angiotensin II inhibitors and statins. This review summarizes current knowledge of the incidence, pathophysiology, risk factors, natural history, and treatment of this increasingly more common pathology.
