A constitutive modeling interpretation of the relationship among carotid artery stiffness, blood pressure, and age in hypertensive subjects

• Published in: American Journal of Physiology: Cell Physiology Vol. 308; no. 6; pp. H568 - H582
• Main Authors: Spronck, Bart, Heusinkveld, Maarten H G, Donders, Wouter P, de Lepper, Anouk G W, Op't Roodt, Jos, Kroon, Abraham A, Delhaas, Tammo, Reesink, Koen D
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 15.03.2015
• Subjects: Adult; Age Factors; Aged; Aging; Arterial Pressure; Biomechanical Phenomena; Blood pressure; Carotid Arteries - metabolism; Carotid Arteries - physiopathology; Collagen - metabolism; Computer Simulation; Elastin - metabolism; Female; Humans; Hypertension; Hypertension - metabolism; Hypertension - physiopathology; Load; Male; Middle Aged; Models, Cardiovascular; Residual stress; Stress, Mechanical; Vascular Stiffness; Veins & arteries; collagen; constitutive modeling; aging; pulse wave velocity; elastin
• ISSN: 0363-6135; 0363-6143; 1522-1539
• DOI: 10.1152/ajpheart.00290.2014

Aging has a profound influence on arterial wall structure and function. We have previously reported the relationship among pulse wave velocity, age, and blood pressure in hypertensive subjects. In the present study, we aimed for a quantitative interpretation of the observed changes in wall behavior with age using a constitutive modeling approach. We implemented a model of arterial wall biomechanics and fitted this to the group-averaged pressure-area (P-A) relationship of the "young" subgroup of our study population. Using this model as our take-off point, we assessed which parameters had to be changed to let the model describe the "old" subgroup's P-A relationship. We allowed elastin stiffness and collagen recruitment parameters to vary and adjusted residual stress parameters according to published age-related changes. We required wall stress to be homogeneously distributed over the arterial wall and assumed wall stress normalization with age by keeping average "old" wall stress at the "young" level. Additionally, we required axial force to remain constant over the cardiac cycle. Our simulations showed an age-related shift in pressure-load bearing from elastin to collagen, caused by a decrease in elastin stiffness and a considerable increase in collagen recruitment. Correspondingly, simulated diameter and wall thickness increased by about 20 and 17%, respectively. The latter compared well with a measured thickness increase of 21%. We conclude that the physiologically realistic changes in constitutive properties we found under physiological constraints with respect to wall stress could well explain the influence of aging in the stiffness-pressure-age pattern observed.