title: Calculation of the outcomes of remodeling of arteries subjected to sustained hypertension using a 3D two-layered model.
abstract: Arteries manifest a remodeling response to long-term alterations in arterial pressure and blood flow by changing geometry, structure, and composition through processes driven by perturbations of the local stresses in the vascular wall from their baseline values. The objective of this study is twofold--to develop a general method for calculating the remodeling responses of an artery considered as a two-layered tube; and to provide results for adaptive and maladaptive remodeling of a coronary artery. By formulating an inverse problem of vascular mechanics, the geometrical dimensions and mechanical properties of an artery are calculated from a prescribed deformed configuration, stress field, structural stiffness, and applied load. As an illustrative example we consider a human LAD coronary artery in both a perfect and incomplete adaptive response to a sustained step-wise change in pressure and a maladaptive response due to impaired remodeling of adventitia. The results obtained show that adventitia plays an important role in vascular mechanics when an artery is subjected to high arterial pressure. In addition to its well-known short term function of preventing over-inflation of an artery, it seems reasonable to accept that the manner by which adventitia remodels in response to a chronic increase in pressure is essential for preserving normal arterial function or may lead to an increased risk of developing vascular disorders.
authors.affiliation: College of Engineering and Computing, University of South Carolina, 300 Main, Columbia, SC, USA. a.i.rachev@gmail.com
authors.forename: Alexander
authors.initials: A
authors.lastname: Rachev
authors.forename: W Robert
authors.initials: WR
authors.lastname: Taylor
authors.forename: Raymond P
authors.initials: RP
authors.lastname: Vito
mesh_terms: D003331:Coronary Vessels / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008955:Models, Cardiovascular; D013314:Stress, Mechanical