This paper demonstrates the feasibility of material identification and wall stress computation for human common carotid arteries based on non-invasive in vivo clinical data: dynamical intraluminal pressure measured by applanation tonometry, and medial diameter and intimal-medial thickness measured by a high-resolution ultrasound echotracking. The mechanical behavior was quantified assuming an axially pre-stretched, thick-walled, cylindrical artery subjected to dynamical blood pressure and perivascular constraints. The wall was further assumed to be three-dimensional and to consist of a nonlinear, hyperelastic, anisotropic, incompressible material with smooth muscle activity and residual stresses. Mechanical contributions by individual constituents an elastin-dominated matrix, collagen fibers, and vascular smooth muscle were accounted for using a previously proposed microstructurally-motivated constitutive relation. The in vivo boundary value problem was solved semi-analytically to compute the inner pressure during a mean cardiac cycle. Using a nonlinear leastsquares method, optimal model parameters were determined by minimizing differences between computed and measured inner pressures over a mean cardiac cycle. The fit-to-data from two healthy patients was very good and the predicted radial, circumferential, and axial stretch and stress fields were sensible. Hence, the proposed approach was able to identify complex geometric and material parameters directly from non-invasive in vivo human data.

Aortic diseases are diverse, and involve a multiplicity of biological systems in the vascular wall and at the interface with blood. Future research needs to unravel distinct cellular and molecular mechanisms causing the clinical events, in particular, dissection, expansion of already formed aneurysms and rupture.

Abstract-The analysis of plaque mechanics along the longitudinal axis (bending strain) may provide useful information because repetitive bending strain of an atherosclerotic plaque can fatigue the wall material and result in plaque rupture. Whether essential hypertension is associated with a specific pattern of bending strain has not yet been determined. The study included 92 patients with an atherosclerotic plaque on the common carotid artery: 66 patients with essential hypertension, either treated or not, and 26 normotensive patients. A novel noninvasive echotracking system (ArtLab; Esaote, The Netherlands) was used to measure intima-media thickness, diameter, and distensibility at 128 sites on a 4-cm-long carotid segment. Carotid plaque was either less elastic than adjacent carotid artery (inward strain) or more elastic (outward strain). Inward strain was more frequently associated with an inward plaque remodeling, whereas an outward strain was more frequently associated with an outer remodeling. In multivariate logistic regression analysis, patients with essential hypertension were more likely to exhibit an inward strain of carotid plaque (odds ratioϭ6. Key Words: carotid artery Ⅲ atherosclerotic plaque Ⅲ hypertension Ⅲ stiffness Ⅲ arterial remodeling H ypertension is a major risk factor for coronary, cerebrovascular, and renal diseases and is the greatest cause of stroke. 1 Half of stroke events are the result of cerebrovascular atherosclerosis, including carotid plaques. Hypertension increases the tensile stress applied on the carotid artery, thus carotid intima-media thickness (IMT) and stiffness, and favors atherosclerotic plaque progression. 2-8 Hemodynamic disturbances caused by hypertension result in atherosclerotic plaque complications like fissuring, rupture, and hemorrhage, which are critical steps for plaque evolution and for ischemic stroke.Plaque rupture has become identified as a critical step in the evolution of atherosclerotic plaque. It is of major importance to detect which plaques are vulnerable, 9 even though not yet ruptured, and, specifically, to identify which patients will have a stroke. Rupture mechanisms are complex processes that are dependent on plaque morphology and composition and mechanical characteristics. 9 -11 Mildly stenotic carotid plaques with thin fibrous cap and lipid-rich core are more susceptible to rupture than plaques with a high degree of fibrosis and calcifications. 9