Abstract 105: Increased Dynamic Mechanical Energy Dissipation in Human Abdominal Aortic Aneurysm

Abstract

Objectives: Individualized patient rupture risk for abdominal aortic aneurysms (AAA) remains elusive due to a limited understanding of the biomechanical events that trigger aneurysm growth and aortic wall failure. To date there has been a paucity of data describing how physiologic pulsatile energy is stored (E') and lost (E'') from AAA tissue. Our hypothesis is that AAA tissue dissipates more cyclic energy at a physiologic frequency, as determined by (E''/ E'), when compared to healthy aortic tissue. Methods: Human healthy aortic and AAA samples were obtained from cadaveric and surgical specimens. Specimens were stored at 4 o C in 0.9%NS and mechanically tested within 36 hrs of explant. Uniaxial mechanical testing (ADMET BioTense) was performed in the circumferential orientation with the tissue pre-loaded to an equivalent physiologic stress of a 5 cm at a 110 mmHg mean pressure. A sinusoidal ±5% strain was applied at 1 Hz for 40 cycles with simultaneous force measurements. After mechanical testing, immunohistochemical staining was performed to confirm tissue viability. Results: AAA tissue was significantly stiffer when compared to healthy aorta, as demonstrated by a greater average static modulus (E) 1555.4 ± 384 vs. 970 ± 128 kPa (n=5, p=0.03). Dynamic testing of the AAA tissue noted a significantly greater energy loss (E'') 137.8±36.7 vs. 43.1±21.7 (p<0.01) and loss ratio (E''/ E') 0.090 ± 0.023 vs. 0.044 ± 0.023 (p=0.02), when compared to normal specimens. Figure #1 compares the static modulus (E) to the loss ratio (E''/ E') for the aortic tissue specimens. Histologic analysis confirmed tissue viability during of all specimens. Conclusions: Our data demonstrates that AAA tissue dissipates more energy (E'') and has a greater energy loss ratio (E''/ E'), suggesting that more pulsatile energy is dissipated in diseased tissue. Future work is needed to determine how this energy dissipation influences the biologic pathogenesis of AAA growth and rupture.