Residual strains in human versus animal aortas: a reconciliation of apparent differences

Prior studies report unusual residual stretch behavior in human aortas: radial cutting yields opening angles often exceeding 180° and the release of a non-antisymmetric radial distribution of residual stretches, unlike the smaller angles (<120°) and nearly antisymmetric distributions in animals. Herein, we interpret these differences as consequences of highly nonuniform wall remodeling. Radial-cut opening is governed by the residual strain energy within the media, generating the dominant bending moment, while intima and adventitia provide restraining constraints released upon separation. Supporting this media-dominated mechanism, intact-wall opening angles correlate directly with medial opening angles in both circumferential and axial directions, but not with intimal or adventitial opening. Inverse correlations between intact-wall residual stretches and layer-specific relaxation emerge from compatibility-driven partitioning of growth-induced interlayer mismatch between radial cutting and layer separation. In healthy human aortas, absent correlations between layer thickness and opening angle or residual stretch indicate minimal geometric control once growth-imposed residual stretches dominate. In contrast, aneurysmal aortas exhibit more frequent opening angle-thickness correlations, consistent with enhanced geometric influence following medial degeneration. Variations between healthy and aneurysmal vessels further reflect geometric effects, whereby dilation and curvature redistribute bending and axial stretch, modulating residual stress gradients and interlayer correlations while attenuating medial dominance. Healthy porcine aortas showed few inverse correlations, indicating weaker interlayer mismatch and reduced compatibility-driven stress redistribution; antisymmetric residual stretches of tensile and compressive contributions produced smaller bending moments and opening angles. These findings establish a framework for interpreting human-animal differences in residual stress and motivate growth-remodeling models.