scholarly journals Turnover of fibrillar collagen in soft biological tissue with application to the expansion of abdominal aortic aneurysms

2012 ◽  
Vol 9 (77) ◽  
pp. 3366-3377 ◽  
Author(s):  
Giampaolo Martufi ◽  
T. Christian Gasser

A better understanding of the inherent properties of vascular tissue to adapt to its mechanical environment is crucial to improve the predictability of biomechanical simulations. Fibrillar collagen in the vascular wall plays a central role in tissue adaptation owing to its relatively short lifetime. Pathological alterations of collagen turnover may fail to result in homeostasis and could be responsible for abdominal aortic aneurysm (AAA) growth at later stages of the disease. For this reason our previously reported multiscale constitutive framework (Martufi, G. & Gasser, T. C. 2011 J. Biomech . 44 , 2544–2550 ( doi:10.1016/j.jbiomech.2011.07.015 )) has been enriched by a collagen turnover model. Specifically, the framework's collagen fibril level allowed a sound integration of vascular wall biology, and the impact of collagen turnover on the macroscopic properties of AAAs was studied. To this end, model parameters were taken from the literature and/or estimated from clinical follow-up data of AAAs (on average 50.7 mm-large). Likewise, the in vivo stretch of the AAA wall was set, such that 10 per cent of collagen fibres were engaged. Results showed that the stretch spectrum, at which collagen fibrils are deposed, is the most influential parameter, i.e. it determines whether the vascular geometry grows, shrinks or remains stable over time. Most importantly, collagen turnover also had a remarkable impact on the macroscopic stress field. It avoided high stress gradients across the vessel wall, thus predicted a physiologically reasonable stress field. Although the constitutive model could be successfully calibrated to match the growth of small AAAs, a rigorous validation against experimental data is crucial to further explore the model's descriptive and predictive capabilities.

2013 ◽  
Vol 135 (2) ◽  
Author(s):  
Giampaolo Martufi ◽  
T. Christian Gasser

AAA disease is a serious condition and a multidisciplinary approach including biomechanics is needed to better understand and more effectively treat this disease. A rupture risk assessment is central to the management of AAA patients, and biomechanical simulation is a powerful tool to assist clinical decisions. Central to such a simulation approach is a need for robust and physiologically relevant models. Vascular tissue senses and responds actively to changes in its mechanical environment, a crucial tissue property that might also improve the biomechanical AAA rupture risk assessment. Specifically, constitutive modeling should not only focus on the (passive) interaction of structural components within the vascular wall, but also how cells dynamically maintain such a structure. In this article, after specifying the objectives of an AAA rupture risk assessment, the histology and mechanical properties of AAA tissue, with emphasis on the wall, are reviewed. Then a histomechanical constitutive description of the AAA wall is introduced that specifically accounts for collagen turnover. A test case simulation clearly emphasizes the need for constitutive descriptions that remodels with respect to the mechanical loading state. Finally, remarks regarding modeling of realistic clinical problems and possible future trends conclude the article.


2021 ◽  
Vol 74 (3) ◽  
pp. e158-e159
Author(s):  
Nadin Elsayed ◽  
Maryam A. Khan ◽  
Isaac Naazie ◽  
Jaideep Das Gupta ◽  
Randall De Martino ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Miao Wang ◽  
Jane Stubbe ◽  
Eric Lee ◽  
Wenliang Song ◽  
Emanuela Ricciotti ◽  
...  

Microsomal (m) prostaglandin (PG) E 2 synthase(S)-1, an enzyme that catalyzes the isomerization of the cyclooxygenase (COX) product, PGH 2 , into PGE 2 , is a major source of PGE 2 in vivo . mPGES-1 deletion in mice was found to modulate experimentally evoked pain and inflammation and atherogenesis is retarded in mPGES-1 knockout (KO) mice. The impact of mPGES-1 deletion on formation of angiotensin II (Ang II)-induced abdominal aortic aneurysms (AAA) was studied in mice lacking the low density lipoprotein receptor (LDLR −/− ). AngII infusion increased aortic macrophage recruitment and nitrotyrosine staining while upregulating both mPGES-1 and COX-2 and urinary excretion of the major metabolite of PGE 2 (PGE-M). Deletion of mPGES-1 decreased both the incidence and severity of AAA and depressed excretion of both PGE-M and 8, 12-iso-iPF 2a -VI, which reflects lipid peroxidation in vivo . While Ang II infusion augmented prostaglandin biosynthesis, deletion of mPGES-1 resulted in rediversion to PGD 2 , reflected by its major urinary metabolite. However, deletion of the PGD 2 receptor, DP1, did not affect AAA in Ang II infused LDLR −/− mice. These observations indicate that deletion of mPGES-1 protects against AAA formation by AngII in hyperlipidemic mice, perhaps by decreasing oxidative stress. Inhibition of mPGES-1 may represent an effective treatment to limit aneurysm occurrence and expansion.


Author(s):  
Abigail Swillens ◽  
Lieve Lanoye ◽  
Julie De Backer ◽  
Nikos Stergiopulos ◽  
Frank Vermassen ◽  
...  

The economical growth and increased welfare in the Western world have a reverse side, with an increased death toll due to cardiovascular diseases. Among these, aortic aneurysms (a local dilation) are particularly lethal as they may grow unnoticed until rupture occurs. In this study, we assessed the impact of the presence of an abdominal aortic aneurysm on arterial hemodynamics and wave reflection in particular. Experimental and numerical methods were applied. Linear wave separation was used to quantify the reflections; wave intensity analysis was applied to assess the nature of the reflected waves. In both the experimental and numerical models, negative reflections were found in the upper aorta corresponding to a backward expansion wave caused by the sudden expansion of the aorta. A numerical parameter study demonstrated that larger diameters and more compliant aneurysms generate stronger negative reflections.


Sign in / Sign up

Export Citation Format

Share Document