A 68-year-old male smoker is found to have a maximum infrarenal aortic diameter of 3.2 cm on screening ultrasound. The structure marked **A** in the diagram represents the fusiform infrarenal aortic dilatation. Which of the following pathophysiologic mechanisms is MOST directly responsible for the progressive enlargement of the structure marked **A** in abdominal aortic aneurysm?
A. Impaired fibrinolysis resulting in accumulation of fibrin within the media
B. Overactivity of matrix metalloproteinases (MMP-2, MMP-9) degrading elastin and collagen in the aortic wall
C. Chronic elevation of angiotensin II leading to smooth muscle cell hypertrophy
D. Increased intimal proliferation secondary to endothelial dysfunction and lipid deposition
Explanation
Why "Overactivity of matrix metalloproteinases (MMP-2, MMP-9) degrading elastin and collagen in the aortic wall" is right
The SVS 2022 Practice Guidelines and contemporary pathophysiology literature establish that the overwhelming majority (>90%) of infrarenal AAAs are atherosclerotic/degenerative in origin, driven by chronic inflammation and matrix metalloproteinase (MMP-2, MMP-9) overactivity. These enzymes degrade the structural proteins (elastin and collagen) of the aortic wall, leading to loss of mechanical integrity and progressive dilatation. This is the primary mechanism underlying the fusiform infrarenal aortic dilatation marked A. The question directly tests understanding of the biochemical basis of AAA pathogenesis as stated in the clinical anchor.
Why each distractor is wrong
Increased intimal proliferation secondary to endothelial dysfunction and lipid deposition: While atherosclerotic changes (intimal ulceration marked C) are present in AAA, intimal proliferation is the hallmark of atherosclerotic plaque formation and stenosis, not aneurysmal dilatation. The pathology of AAA is medial degeneration, not intimal hyperplasia.
Chronic elevation of angiotensin II leading to smooth muscle cell hypertrophy: Angiotensin II elevation causes hypertensive remodeling and smooth muscle hypertrophy, which leads to wall thickening and stenosis (as in hypertensive arterial disease), not aneurysmal dilatation. AAA involves loss of structural proteins, not hypertrophic remodeling.
Impaired fibrinolysis resulting in accumulation of fibrin within the media: While laminated mural thrombus (marked B) is a consequence of AAA, impaired fibrinolysis is not the primary driver of aneurysmal dilatation. Thrombus formation is secondary to the altered hemodynamics within the dilated aorta.
High-YieldNEET PG
AAA pathogenesis = MMP-mediated degradation of elastin/collagen in the setting of chronic inflammation and oxidative stress; this is the rate-limiting mechanism, not intimal disease or smooth muscle hypertrophy.
SVS 2022 Practice Guidelines for Abdominal Aortic Aneurysm; USPSTF 2019 Screening Recommendations
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