Biomedical Engineering Reference
In-Depth Information
Fig. 11.5
(
A
) Tensile strength in LONG and (
B
) CIRC directions for INT-DEL halves (
)and
ADV-DEL halves (
).
significantly different from INT-DEL LONG BAV ATAA (
p<
0
.
001);
significantly different from INT-DEL LONG BAV ATAA (
p
=
0
.
016); † significantly different
from INT-DEL CIRC TAV ATAA (
p
=
0
.
024). Taken from Pasta et al. (
2011
)
be caused by predisposing structural disorders. A deficit in the smooth muscle cell
response to the oxidative stress could be responsible for example of the inherent
lower
S
d
in BAV tissues (Phillippi et al.,
2009
,
2010
).
Our results demonstrate a weaker
S
T
of the intimal half of the aortic wall (i.e.
the INT-DEL half; see Figs.
11.5
(A) and (B)), imparting an apparent risk of the
propagation of AoD. Exit through the outer residual layer (i.e. the ADV-DEL half)
causing frank aortic disruption is less common than dissection propagation, and this
may be explained by the relatively stronger
S
T
of the adventitial half of the aortic
wall in this study. These results are consistent to the disparate strengths of healthy
arterial layers found in the literature (Holzapfel et al.,
2007
).
Anisotropic dissection properties of the non-aneurysmal ascending aorta are con-
sistent with SEM imaging results. Indeed, the elastin and collagen fibers are ori-
ented mainly in the circumferential direction in the non-aneurysmal aortic wall
and, as a result, may provide a greater strength to AoD in LONG direction. For
the non-aneurysmal aorta, the creation of a rougher dissection surface may explain
both higher mean and variance in
S
d
of LONG strips compared to those oriented
in CIRC direction, see Fig.
11.2
. The dissection in LONG direction frequently
crosses the elastic layers while that in CIRC strips propagate mainly between ad-
jacent elastic laminae (Fig.
11.6
(A)) resulting in a 'flat' broken surface as found by
Sommer et al. (
2008
) for the non-aneurysmal human abdominal aorta. Moreover,
the fracture surfaces of both BAV and TAV ATAAs appear rougher than those for
normal aorta (see Fig.
11.6
(A)), likely due to the more disorganized microstruc-
ture caused by the disease. Disorganization of elastin and collagen fibers due to
aneurysm appears to impact the mechanical properties of ATAAs. For the healthy
aorta, the formation of a rougher surface may clarify the non-significant difference
in
S
d
between the LONG and CIRC directions, suggesting isotropic dissection prop-
erties.
These results are limited by the fact that delamination testing does not accu-
rately model the spontaneous initiation of AoD that occurs in vivo. Other models
