Coarctation-induced Abdominal Aortic Aneurysm in a Porcine Model

Hemodynamic stress participates in the initiation and progression of aneurysmal degeneration. Coarctation increases flow-mediated stress on the aortic wall. We tested the hypothesis that prolonged coarctation of an infrarenal abdominal aorta (AA) segment leads to abdominal aortic aneurysm (AAA) formation in mini pigs. An infrarenal AA segment of Taiwanese Lanyu mini pigs was wrapped with an 8 mm-wide ePTFE Teflon strip to create a funnel-shaped flow-path with constrictive outlet for 4 weeks (4 w), 8 weeks (8 w), and 12 weeks (12 w). This treatment resulted in moderate coarctation, manifested by pulsatility index reduced to one third the inherent levels, increased downstream flow-mediated stress and induced significant flow disturbance. Sham control pigs received Teflon wrapping without coarctation. Aneurysm characterized by progressive medial degeneration occurred at the terminal AA after 12 w coarctation. The outer dimension of the distal AA increased 50% compared to that of the proximal AA at 4 w, 8 w, and 12 w post-coarctation. Lumen ratio of the distal-to-suprarenal AA increased time-dependently with 12 w post-coarctation exhibiting significant increase. In the distal AA, elastic lamellae exhibited fragmentation at 4w and more pronounced fragmentation with decreased density at 8 w and 12 w post-coarctation. Smooth muscle exhibited disarray and nuclear density decrease at 8 w and 12 w post-coarctation. Gelatin zymography results showed that matrix metalloproteinase-9 activity markedly increased at 4 w post-coarctation. These results indicate that prolonged moderate coarctation caused regional hemodynamic stress and thereby induced degenerative AAA in the terminal