Carotid artery mechanical properties and stresses quantified using in vivo data from normotensive and hypertensive humans

• DOI: 10.1007/s10237-010-0279-6
• Publication Date: 2011-01-04T07:35:26Z
• Authors: Ingrid Masson; Hélène Beaussier; Pierre Boutouyrie; Stéphane Laurent; Jay D. Humphrey; Mustapha Zidi
• Keywords: Adult; Male; Aging; Fibrillar Collagens; 0206 medical engineering; Models, Cardiovascular; Blood Pressure; 02 engineering and technology; Middle Aged; Biomechanical Phenomena; Young Adult; Carotid Arteries; Hypertension; Humans; Female; Stress, Mechanical; Aged

The goal of this study was to model the in vivo non-linear mechanical behavior of human common carotid arteries (CCAs) and then to compare wall stresses and associated contributions of micro-constituents in normotensive (NT) and treated hypertensive (HT) subjects. We used an established theoretical model of 3D arterial mechanics that assumes a hyperelastic, anisotropic, active-passive, and residually stressed wall. In vivo data were obtained non-invasively from CCAs in 16 NT (21-64 years old) and 25 treated HT (44-69 years old) subjects. The associated quasi-static boundary value problem was solved semi-analytically over a cardiac cycle while accounting for surrounding perivascular tissue. Best-fit values of model parameters, including those describing contributions by intramural elastin, fibrillar collagen, and vascular smooth muscle, were estimated by a non-linear least-squares method. The model (1) captured temporal changes in intraluminal pressure, (2) estimated wall stress fields that appeared to reflect the presence or absence of age and disease, and (3) suggested changes in mechanical characteristics of wall micro-constituents despite medical treatment of hypertension. For example, age was positively correlated with residual stresses and altered fibrillar collagen in NT subjects, which indirectly validated the modeling, and HT subjects had higher levels of stresses, increased smooth muscle tone, and a stiffer elastin-dominated matrix despite treatment. These results are consistent with prior reports on effects of age and hypertension, but provide increased insight into evolving contributions of cell and matrix mechanics to arterial behavior in vivo.