Clinical meaning
An abdominal aortic aneurysm (AAA) is defined as a focal dilation of the abdominal aorta to ≥3.0 cm (normal infrarenal aorta diameter is 1.5-2.5 cm) or >50% increase over normal diameter. The pathogenesis involves degradation of the aortic media through an imbalance of matrix metalloproteinases (MMP-2, MMP-9) and their tissue inhibitors (TIMPs). Elastin fragmentation and collagen degradation weaken the structural integrity of the aortic wall, leading to progressive dilation under systolic pressure.
Chronic transmural inflammation drives aneurysm progression: infiltrating macrophages and lymphocytes release proteolytic enzymes and inflammatory cytokines (TNF-alpha, IL-1beta, IL-6) that perpetuate extracellular matrix destruction. Oxidative stress and smooth muscle cell apoptosis further thin the media. The infrarenal aorta is preferentially affected due to lower elastin content, absence of vasa vasorum (relying on luminal diffusion for nutrition), and reflected wave hemodynamics that increase wall stress.
The Law of Laplace governs rupture risk: wall tension = (pressure × radius) / (2 × wall thickness). As the aneurysm enlarges, wall tension increases exponentially, explaining the dramatically higher rupture risk at larger diameters. Annual rupture risk by size: <4.0 cm = 0%, 4.0-4.9 cm = 0.5-5%, 5.0-5.9 cm = 3-15%, 6.0-6.9 cm = 10-20%, ≥7.0 cm = 20-40%. Ruptured AAA carries 80-90% mortality, with 50% dying before reaching the hospital.