Abstract 4574: Impaired Wall Stiffness and Extensibility, but Not Strength of Aneurysmal versus Non-Aneurysmal Ascending Aorta in Age-Matched Subjects
Aim: Biomechanical evidence from previous reports has substantiated mechanical degeneration of aortic aneurysms, including vessel weakening and stiffening, compared to non-aneurysmal aorta. These findings may however be inappropriate, as the subject groups examined have not been aged-matched and aging reportedly deteriorates the mechanical properties of large arteries. This study, therefore, compared the rupture properties of ascending aortic aneurysms (AsAA) and non-aneurysmal aorta (Control) in aged-matched subject groups.
Methods: Whole fresh degenerative, non-dissecting AsAA were resected from 15 patients undergoing elective aneurysm repair and 10 Control aortas during autopsy. Specimens were prepared with circumferential (nAsAA=149, nControl=76) and axial (nAsAA=158, nControl=79) direction, and submitted to biomechanical testing up to rupture. Rupture strain (extensibility), rupture stress (strength), peak elastic modulus (stiffness), and wall thickness were measured.
Results: No difference was noted in patient age (68±2 vs. 67±3 years, P>0.2) among subject groups, while aortic diameter was higher in AsAA than Control (5.6±0.2 vs. 3.3±0.1 cm, P<0.001). AsAA specimens displayed lower wall thickness (circumferential: 1.79±0.03 vs. 2.05±0.04 cm, P<0.001; axial: 1.75±0.03 vs. 2.03±0.04 cm, P<0.001) than Control, but higher peak elastic modulus (circumferential: 930.8±40.0 vs. 778.7±38.7 N/cm2, P=0.02; axial: 558.4±22.5 vs. 344.0±21.9 N/cm2, P<0.001). Rupture strain of AsAA was lower than Control in axial (0.53±0.01 vs. 0.60±0.02, P<0.001), but not in circumferential specimens (0.56±0.01 vs. 0.57±0.02, P>0.2). Rupture stress of AsAA equaled Control in circumferential (172.2±6.2 vs. 161.0±7.5 N/cm2, P>0.2) and was higher in axial specimens (114.8±4.4 vs. 87.6±5.1 N/cm2, P<0.001).
Conclusions: Our findings contradict past studies on aortic aneurysms, suggesting that AsAA development is not associated with biomechanical weakening, but with stiffening and impaired tissue extensibility. The present data facilitate our understanding of the pathogenesis of AsAA rupture, occurring when the stresses exerted on the aortic wall by hemodynamic loads overcome the tissue’s strength.