Biomedical Engineering Reference
In-Depth Information
Fig. 11.3
Delamination
strength in both LONG (
)
and CIRC (
) orientations.
significantly different from
LONG non-aneurysmal aorta
(
p<
0
.
05);
significantly
different from CIRC
non-aneurysmal aorta
(
p<
0
.
05); † significantly
different from CIRC
non-aneurysmal aorta
(
p<
0
.
05). Taken from Pasta
et al. (
2011
)
another and leaves behind the unbroken fibers to bridge the delamination, was ob-
served for both non-diseased and aneurysmal aorta (Fig.
11.6
(B)).
11.4 Discussion
The present investigation was performed to evaluate the delamination properties of
the human ascending aorta to improve our understanding of the mechanics under-
lying aortic dissection in patients with ATAAs, and to compare these properties in
patients with BAV and TAV. The mechanical integrity of the outer versus inner half
of the dissected aorta was also explored to assess the relative probability of exit
through the adventitia (frank disruption) versus propagation of the dissection flap,
respectively, after the onset of AoD. Finally, the failure mechanisms during dissec-
tion were optically investigated. Our findings suggest that the propensity of AoD is
greater in thoracic aneurysms compared to non-aneurysmal aorta, and is intrinsically
greater for BAV ATAAs than those of TAV ATAAs. To our knowledge, these results
have never been reported. Similar dissection properties for the human abdominal
aorta were reported by Sommer et al. (
2008
).
The delamination curves (see Fig.
11.2
) show an oscillation of
T
peel
about a
mean 'plateau' value similar to the results found for tearing tests of the pig de-
scending aorta (Purslow,
1983
) and peeling tests of the human abdominal aorta
(Sommer et al.,
2008
). Therefore, AoDs do not propagate at steady rates but ar-
rest and re-initiate at somewhat regular intervals. The force necessary to drive the
AoD appears to vary widely from a minimum at delamination arrest to a maximum
at delamination initiation. This failure modality is mainly supported by the obser-
vation of a large amount of broken elastin fibers on the dissected tissue surfaces
(see Fig.
11.6
(B)) and is consistent with a fiber bridging failure modality (Gre-
gory and Spearing,
2004
). In this manner, the elastin fibers between halves may
experience high stretch values during delamination testing with a consequent in-
crease in the
T
peel
magnitude. Their subsequent failure induces a rapid decrease
