Biomedical Engineering Reference
In-Depth Information
through extension-inflation tests. Damage to the smooth muscle cells is assumed
to depend on both damage of the passive extracellular matrix and damage of the
active smooth muscle cells themselves. Damage in the passive regime has been ob-
served and characterized experimentally in Famaey et al. ( 2010 ), and calibrated in
this manuscript using these data. It results in a reduced activation capability, which
will only become apparent upon activation. Damage in the active regime is caused
by excessive tension in the direction of the contractile unit, which might cause rup-
tures in the myosin cross-bridges or rupture of the actin and myosin filaments. It is
included here merely theoretically for the sake of completeness, but has not been
calibrated yet. We are currently in the process of further investigating these phe-
nomena to characterize the mechanisms underlying active damage.
Note also that in the finite element model, the artery was modeled as a single
homogeneous layer, even though the wall consists of two solid mechanically rele-
vant layers, i.e. the media and the adventitia. However, in the case of a rat abdominal
artery, the complete wall thickness is only approximately 0.14 mm thick, and in con-
trast to human tissue, it is impossible to separate these two layers from each other.
Therefore, the most accurate approach was to model the wall as a single layer. The
assumption was also made that damage initiates once the energy level exceeds that
of the energy level at systolic blood pressure. This was motivated by the fact that the
morphology and properties of the arterial wall change due to chronic hypertension
(Matsumoto and Hayashi, 1994 ), but whether this actually justifies this assumption
for acute damage scenarios should still be experimentally validated.
Although the three-constituent damage model already captures a number of typ-
ical features of cardiovascular tissue, some characteristic aspects are still not in-
cluded, and a few limitations remain. When qualitatively comparing a simulated
homogeneous cyclic tension test performed on one element with the new material
model to the experimental results of a uniaxial tensile test on a sheep carotid artery,
shown in Fig. 10.7 , it is clear that several features, e.g., tissue nonlinearity and dis-
continuous softening are accurately captured. However, in the tensile test on the
sheep carotid artery, cycling up to a certain strain level was performed five times be-
fore the next strain level was reached, and clearly softening does continue in these
cycles, even though the maximum energy level, the parameter β in our model, is
not increased. This continuous damage behavior was not captured with the damage
model used here. Moreover, the damage variables introduced in this model mainly
capture acute effects, while chronic effects such as repair and/or remodeling have
not been considered for the time being. These effects should be investigated, keep-
ing in mind the trade-off between realism of the model and its usability. The correct
identification of the material parameters obviously becomes more challenging as
more effects are incorporated in the model.
Predictive computational modeling of tolerable damage thresholds is clinically
relevant in two ways: on the one hand, in the short term, the proposed framework
can be used as a simulation tool to optimize surgical tools, for example, to im-
prove clamp design to minimize tissue damage. On the other hand, in the long term,
the proposed framework could enable the prediction of surgically-induced damage
evolution in real-time. This would allow loading thresholds to be imposed on sur-
gical instruments during an operation in a robotic teleoperation setting. The actual
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