Mechanical characterization of dissected and dilated human ascending aorta using Fung-type hyperelastic models with pre-identified initial tangent moduli for low-stress distensibility

Ascending aortic dissection (AD) is a potentially fatal vascular disease associated with degradation and fragmentation of the elastic fibers in the aortic media, increasing low-stress distensibility, and a dilated aorta may lead to dissection. In this study, a Fung-type hyperelastic model was formulated incorporating the initial tangent moduli (ITM) of stress–strain curves as an index of low-stress distensibility. ITM were correlated with the material constants by linearizing incompressible stress–strain relationships at zero strain. For uniaxial loading tests, the robustness of the material constants was examined in the stress ranges of 0–200, 0–180, and 0–160 kPa and to the ITM values of 100%, 95%, and 90%. Examination revealed stable changes in the material constants of 80% of the specimens. For equibiaxial stretch tests, the material constants were determined for each curve of the isotropic and anisotropic deformation groups by pre-identifying the ITM and minimizing fitting errors using isotropic or anisotropic models. The errors for all groups were <6% using a transversely isotropic model, and <10% for an orthotropic model. Comparisons with experimental curves showed that Fung-type models described both the ITM and significant stiffening at high stress levels. The mechanical characteristics of the aorta in the stage prior/posterior to dissection is such that while hardening occurs under both low- and high-stress levels with an increase in collagen content as an aging response, softening occurs under low-stress conditions due to histological abnormalities such as elastin deficiency and fragmentation. Numerical simulations using Fung-type models implied that elastic fiber degeneration and fragmentation in AD tissues reduced not only the low-stress stiffness but also the elastic stiffness with superimposed shear. The latter stiffness was modulated by the stiffening at high stress levels in tensile deformation behavior and normal-strain state under physiological loading conditions, and therefore provides further insight into wall rupture.