Arterial remodeling in response to hypertension using a constituent-based model.
Hypertension-induced arterial remodeling has been previously modeled using stress-driven remodeling rate equations in terms of global geometrical adaptation (Rachev A, Stergiopulos N, Meister JJ. Theoretical study of dynamics of arterial wall remodeling in response to changes in blood pressure. J Biomech 29: 635-642, 1996) and was extended later to include adaptation of material properties (Rachev A, Stergiopulos N, Meister JJ. A model for geometric and mechanical adaptation of arteries to sustained hypertension. J Biomech Eng 120: 9-17, 1998). These models, however, used a phenomenological strain energy function (SEF), the parameters of which do not bear a clear physiological meaning. Here, we extend the work of Rachev et al. (1998) by applying similar remodeling rate equations to a constituent-based SEF. The new SEF includes a statistical description for collagen engagement, and remodeling now affects material properties only through changes in the collagen engagement probability density function. The model predicts asymptotic wall thickening and unchanged deformed inner radius as to conserve hoop stress and intimal shear stress, respectively, at the final adapted hypertensive state. Mechanical adaptation serves to restore arterial compliance to control levels. Average circumferential stress-strain curves show that the material at the final adapted hypertensive state is softer than its normotensive counterpart. These findings as well as the predicted pressure-diameter curves are in good qualitative agreement with experimental data. The novelty in our findings is that biomechanical adaptation leading to maintenance of compliance at the hypertensive state can be perfectly achieved by appropriate readjustment of the collagen engagement profile alone.
Tsamis
Alkiviadis
A
Laboratory of Hemodynamics and Cardiovascular Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland. alkiviadis.tsamis@epfl.ch
Stergiopulos
Nikos
N
D000222:Adaptation, Physiological; D000818:Animals; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003094:Collagen / Q000378:metabolism*; D003198:Computer Simulation; D006801:Humans; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology*; D040542:Mechanotransduction, Cellular; D008955:Models, Cardiovascular