New interpretation of arterial stiffening due to cigarette smoking using a structurally motivated constitutive model

• Published in: Journal of biomechanics 2011-04, Vol.44 (6), p.1209-1211
• Main Authors: Enevoldsen, M.S, Henneberg, K.-A, Jensen, J.A, Lönn, L, Humphrey, J.D
• Format: Article
• Language: English
• Subjects: Animals; Anisotropy; Aortic Aneurysm, Abdominal - etiology; Aortic Aneurysm, Abdominal - metabolism; Aortic Aneurysm, Abdominal - pathology; Aortic Aneurysm, Abdominal - physiopathology; Arteries; Arteries - metabolism; Arteries - pathology; Arteries - physiopathology; Atherosclerosis; Atherosclerosis - etiology; Atherosclerosis - metabolism; Atherosclerosis - pathology; Atherosclerosis - physiopathology; Biological and medical sciences; Biomechanics; Blood vessels and receptors; Cigarettes; Collagen; Collagen - metabolism; Constitutive relationships; Elastin; Fundamental and applied biological sciences. Psychology; Humans; Mathematical models; Medical sciences; Models, Cardiovascular; Physical Medicine and Rehabilitation; Rats; Rats, Sprague-Dawley; Regression; Smoking; Smoking - adverse effects; Smoking - metabolism; Smoking - pathology; Smoking - physiopathology; Stiffening; Stress; Tobacco, tobacco smoking; Toxicology; Vertebrates: cardiovascular system
• ISSN: 0021-9290; 1873-2380
• DOI: 10.1016/j.jbiomech.2011.01.032

Abstract Cigarette smoking is the leading self-inflicted risk factor for cardiovascular diseases; it causes arterial stiffening with serious sequelea including atherosclerosis and abdominal aortic aneurysms. This work presents a new interpretation of arterial stiffening caused by smoking based on data published for rat pulmonary arteries. A structurally motivated “four fiber family” constitutive relation was used to fit the available biaxial data and associated best-fit values of material parameters were estimated using multivariate nonlinear regression. Results suggested that arterial stiffening caused by smoking was reflected by consistent increase in an elastin-associated parameter and moreover by marked increase in the collagen-associated parameters. That is, we suggest that arterial stiffening due to cigarette smoking appears to be isotropic, which may allow simpler phenomenological models to capture these effects using a single stiffening parameter similar to the approach in isotropic continuum damage mechanics. There is a pressing need, however, for more detailed histological information coupled with more complete biaxial mechanical data for a broader range of systemic arteries.