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Soft Tissue Biomechanics

It is well known that arteries stiffen as we get older and this changes arterial pressure, haemodynamics and ultimately how your heart performs. Therefore, vascular disease can have a profound impact on the mechanical integrity of the tissue.

At VascLab we are very interested in the affect disease has on the mechanical behaviour of soft tissues and we have designed and built custom equipment to mechanically characterise this behaviour.

Aortic Wall Tissue

We use aortic tissue from both healthy and diseased humans (excised during surgery like the sample shown below), as well as animal tissue that we can artificially create disease in. We use techniques to understand how the tissue behaves when in vivo (pressure-diameter tests) or when we want to determine failure properties (tensile tests) like in the image shown on the right, using samples cut in different orientations from larger tissue specimens. 

Besides the impact of disease on the tissue itself, an important research area is the influence of medical devices on diseased tissue. In the case of most vascular problems, such as aneurysms, plaques, blockages, dissections, etc, the typical treatment will be the insertion of a stent or stent-graft to treat the issue. In most cases a stent is made of a metal and if this metal object is inserted into a region where the diseased wall is extremely weak and sensitive, it creates an obvious problem. Not only can the device penetrate the wall more than planned, but it can also trigger further mechanobiological responses.

We have recently published our data on AAA wall tissue in the Annals of Biomedical Engineering and on porcine aortic tissue in the Journal of the Mechanical Behavior of Biomedical Materials.



Intraluminal Thrombus (ILT)

Disease brings many physical changes to the vasculature; one of which is thrombus. Intraluminal thrombus (ILT) is found in the vast majority of AAAs and often forms into a somewhat well-developed laminated structure (like in the image below), with the older abluminal layer adjacent to the aortic wall and the younger, fresher luminal layer in contact with the flowing blood. The role of ILT in AAA is unclear. Current computer models represent ILT as a ‘mechanical buffer’ that reduce AAA wall stress in regions of thick ILT, while computational rupture indices account for ILT thickness by reducing the wall strength in ILT-thick areas. A reduction in tensile stregnth is appropriate as it is well known that ILT starves the wall of oxygen. However, it has also been shown that the ILT does not really reduce the pressure transmitted to the wall and may be more akin to a ‘series of ropes’ anchored to the wall that can withstand some loading, yet allowing pressure transmission.


One of the many problems with ILT is that it is perhaps even more patient-specific than the aortic wall itself. It develops due to specific haemodynamics (which we are also attempting to model and understand), but trying to create a population-averaged model of ILT is tricky. You can see in the images above that ILT can be a ‘structured mass’ or an ‘unstructured mess’!
How do we characterise such materials and how do we account for them in computer simulations?

We have recently published this work in the Journal of Biomechanics.



Mechanobiology and Soft Tissue Biomechanics

We also investigate the impact biological process have on the tissue behaviour. In particular, inflammation and calcification, both of which are recognised markers of CVD. Together with samples of human tissue, we are exploring the use of animal models of vascular inflammation and calcification. There is limited work on the biomechanical influence of inflammation on vascular tissue, whereas some studies have investigated calcification - with varied results. By coupling experimental data with our Functional Bioengineering work, we can help advance the clinical-relevance of our computer simulations.

The image on the right shows an entire piece of calcified aortic tissue, harvested from the AAA wall specimen shown in the image earlier on. Using samples of calcified tissue this big (which are not uncommon) allows mechanical testing to determine both behaviour and tensile strength. Such calcified tissue is much stiffer than the surrounding vascular wall as calcifications somewhat resemble bone. For example, in the work of Maier et al. they determined the Young's modulus to be 50 MPa, whereas the aorta is often assumed to be about 3 MPa.

However, the role of the calcified tissue (and the calcification process itself) is of major interest. The mismatch of materials where the soft vascular tissue meets the hard calcified tissue is undesirable. Not only will this create a stress gradient when under loading but also the connection of these two materials may be a susceptible failure spot, particularly in the case of AAA.

The impact of the calcification process can also be examined after mechanical testing with scanning electron microscopy (SEM). This allows us to visualise the failure site at very high magnification and see if the tissue failed where the wall tissue bonds with the calcified tissue. Fig-A shows the separation of the fibrous tissue (f) from the calcium deposit (c) prior to the failure of fibres. Fig-B shows the streching of fibres away from the calcium deposit. Fig-C and D shows the differing calcification microstructures - smooth, plate-like structures (Fig-C) and conglomeraions of smooth-surfaced spheres (Fig-D).   

In all samples we have tested, calcification deposits typically greater than 1mm were found in close proximity to the failure site. This work has recently been published in the Journal of the Mechanical Behavior of Biomedical Materials.