A structure-based model of arterial remodeling in response to sustained hypertension.
A novel structure-based mathematical model of arterial remodeling in response to a sustained increase in pressure is proposed. The model includes two major aspects of remodeling in a healthy matured vessel. First, the deviation of the wall stress and flow-induced shear stress from their normal physiological values drives the changes in the arterial geometry. Second, the new mass that is produced during remodeling results from an increase in the mass of smooth muscle cells and collagen fibers. The model additionally accounts for the effect of the average pulsatile strain on the recruitment of collagen fibers in load bearing. The model was used to simulate remodeling of a human thoracic aorta, and the results are in good agreement with previously published model predictions and experimental data. The model predicts that the total arterial volume rapidly increases during the early stages of remodeling and remains virtually constant thereafter, despite the continuing stress-driven geometrical remodeling. Moreover, the effects of a perfect or incomplete restoration of the arterial compliance on the remodeling outputs were analyzed. For instance, the model predicts that the pattern of the time course of the opening angle depends on the extent to which the average pulsatile strain is restored at the end of the remodeling process. Future experimental studies on the time course of compliance, opening angle, and mass fractions of collagen, elastin, and smooth muscle cells can validate and improve the introduced hypotheses of the model.
Tsamis
Alkiviadis
A
Laboratory of Hemodynamics and Cardiovascular Technology, Ecole Polytechnique Federale de Lausanne, Switzerland. alkiviadis.tsamis@epfl.ch
Stergiopulos
Nikos
N
Rachev
Alexander
A
D000328:Adult; D001013:Aorta, Thoracic / Q000503:physiopathology; D001158:Arteries / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003187:Compliance; D003198:Computer Simulation; D005260:Female; D024022:Fibrillar Collagens / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007700:Kinetics; D040542:Mechanotransduction, Cellular; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D011673:Pulsatile Flow; D013314:Stress, Mechanical; D016474:Weight-Bearing / Q000502:physiology
D024022:Fibrillar Collagens