Factors influencing the mechanical behaviour of healthy human descending thoracic aorta

Abstract

In recent times, significant effort has been made to understand the mechanical behaviour of the arterial wall and how it is affected by the different vascular pathologies. However, to be able to interpret the results correctly, it is essential that the influence of other factors, such as aging or anisotropy, be understood. Knowledge of mechanical behaviour of the aorta has been customarily constrained by lack of data on fresh aortic tissue, especially from healthy young individuals. In addition, information regarding the point of rupture is also very limited. In this study, the mechanical behaviour of the descending thoracic aorta of 28 organ donors with no apparent disease, whose ages vary from 17 to 60 years, is evaluated. Tensile tests up to rupture are carried out to evaluate the influence of age and wall anisotropy. Results reveal that the tensile strength and stretch at failure of healthy descending aortas show a significant reduction with age, falling abruptly beyond the age of 30. This fact places age as a key factor when mechanical properties of descending aorta are considered.

Local mechanical properties of human ascending thoracic aneurysms

“…6, Table 3 and 5). This is in agreement with the the existing literature on the effect of aging [10][11][12]29] which found that the healthy thoracic aorta stiffened progressively with age with substantial stiffening occurring between patients aged 30-60 and those over the age of 60. At 55 years old, Patient 6 would be in the younger group while the remainder of the cohort had a mean age of 76.6 yrs.…”

Is There a Role for Biomechanical Engineering in Helping to Elucidate the Risk Profile of the Thoracic Aorta?

“…Opening angle, biaxial, and uniaxial tensile tests 54 aTAA (6 MS, 33 BAV, 15 TAV) Vorp [13] 2003 Uniaxial tensile tests and nonlinear isotropic constitutive model 26 aTAA; 10 nonaneurysmal Fedak [14] 2003 immunohystochemistry, immunofluorescence microscopy, hydroxyproline determination, and gelatinase zymography Cotrufo [17] 2005 Morphometry, immunohistochemistry, Western blot, and PCR 27 BAV (12 with stenosis and 15 with regurgitation); 6 controls Koullias [18] 2005 Epiaortic echocardiography 33 aTAA (caused by atherosclerosis or medial degeneration); 20 normal Tang [19] 2005 Histology, immunohistochemistry, and real-time quantitative RT-PCR 29 aTAA; 28 nonaneurysmal aorta (10 undergoing coronary artery bypass grafting, 3 cardiac transplantation, 15 from cadavers) Sinha [20] 2006 Real-time PCR and immunohistochemistry Growth assessment: 12 dTAA; 12 healthy tissue collections: 8 dTAA Choudhury [21] 2009 Histologic analysis and biaxial tensile tests 10 aTAA (5 TAV, 6 BAV); 5 healthy Iliopoulos [22] 2009 Uniaxial tensile tests 12 aTAA (degenerative but nondissecting) Guinea [23] 2010 Uniaxial tensile tests 28 healthy descending aortas Sokolis [24] 2012 Histologic analysis, uniaxial tensile tests and Fung-type constitutive model 12 degenerative aTAA, associated with TAV; 14 nonaneurysmal ascending aortas Pasta [25] 2012 element and combine it to obtain a solution for the whole structure. Thus, complex geometry is replaced by a set of algebraic equations describing displacements at nodal points for each element and by the applied boundary conditions.…”

“…The process is dynamic, highly heterogeneous, and may fluctuate as a function of local stress and biologic activity. Changes in the tissue microstructure caused by aging [23], disease progression [13], and underlying pathologies [27,28,29,30] significantly affect tissue structural organization and strength. One of the challenges of aneurysm simulation is the integration of dynamic wall weakening in the biomechanical model so that current estimates of local properties and local strength can be used to predict the risk of rupture.…”

Patient-specific finite element analysis of ascending aorta aneurysms

“…In these studies, the peak vessel wall stress was the biomechanical index of interest; however, the accurate AsAA tissue properties and geometries, which can vary greatly among individuals, are necessary for accurate stress prediction. Furthermore, rupture is dependent not only on the vessel wall stress, but also the vessel wall failure strength, which may become compromised in particular patients by underlying microstructural changes brought on by aging (13,26), disease progression (40), or other factors (12,35). Therefore, the patient-specific tissue strength and the aortic wall stress are both critical for assessing AsAA rupture potential.…”