Carotid artery stenting is an alternative treatment
method to CEA for carotid artery stenosis. However,
it has a serious disadvantage due to the high incidence
of SBI after the procedure.[
13,
14] Silent brain infarction has adverse effects on the patients’ cognitive functions
in the long-term; therefore, it is important to
identify patients with a high risk of SBI during CAS
planning.[
15] In this study, the patients were evaluated
with MDCT during CAS planning. A significant
difference was found in the aortic arch structure and
plaque characteristics of the carotid artery between the
patients with and without SBI after CAS.
In a study, Kastrup et al.[16] reported ipsilateral
SBI after CAS with and without EPD as 49% and
67%, respectively. In this study, EPD was used for
all procedures, and the ratio of ipsilateral SBI after
CAS was similar to Kastrup et al.[16] Acute SBI was
determined in 13 (54.1%) patients and, according to
treated carotid artery distribution, ipsilateral SBI was
observed in 10 (41.6%) patients and contralateral SBI
was observed in three (12.5%) patients.
In another study, Wyers et al.[17] detected that
anatomical variation or elongation of the aortic arch
negatively affected the technical success and increased
the risk of SBI. In this study, the presence of plaque
in the aortic arch was significantly more frequent in
the patients who developed SBI after CAS (p=0.047).
However, there was no significant difference between
the groups in terms of anatomical variation and
elongation of the aortic arch. This may be due to
the limited sample size of our study. Anatomical
variations and degenerative changes (elongation and
atherosclerosis) in the aortic arch lead to prolonged
catheter manipulation time and predisposition to SBI
during the procedure.[18] Wyers et al.[17] suggested that
evaluation of aortic arch structure using MDCT for
CAS planning and that patients having anatomical
variation or significant elongation in the structure of
aortic arch should be referred to other treatments.
Furthermore, Krapf et al.[19] investigated the effects
of carotid artery plaque length and the degree of
stenosis on the development of SBI after CAS. A
significantly high correlation was found between the
plaque length and development of acute SBI; however,
no significant correlation was observed between the
degree of stenosis and the development of SBI. In
the present study, carotid artery plaque length was
significantly higher in the group in which ipsilateral
SBI developed after CAS (p=0.045). The contact
between the long plaque and the catheter used in
the procedure is greater than the short plaque, which
increases the risk of ruptured plaque capsule and distal
embolism of its components.[19]
In their study, Rosenkranz et al.[20] evaluating the
effect of surface morphology of carotid artery plaque
on the development of SBI after CAS measured
the number of microembolism during CAS by
dual-frequency Doppler ultrasound. The number
of microembolism was higher in plaques with an
irregular surface than other plaques (p=0.030). Our
study revealed that the surface morphology of carotid
artery plaque in Group 1 was significantly more
frequently irregular, compared to Group 2 (p=0.047).
The irregular surface morphology is a sign of the defect
in the plaque capsule. The plaques are more vulnerable
due to high blood levels of pro-inflammatory markers.
Therefore, catheter contact more often causes distal
embolism of plaque components.[21]
Moreover, Matsumoto et al.[22] found that the
amount of development SBI during CAS was
positively correlated with the total volume of plaque
and proportion of lipid component in total volume
(r=0.480, p=0.015 and r=0.561, p=0.001, respectively).
Uchiyama et al.[23] found that lipid componentweighted
plaques, with a mean HU value of <0, were
found to be more prone to the development of SBI
after CAS. In the present study, the total volume
of plaque and percentage of lipid component was
significantly higher in patients who developed SBI
than the others (p=0.015 and p=0.026, respectively).
For differentiation of the patients with and without
SBI after CAS, the percentage of lipid component in
total volume of >17.8% was found to be a selectivity
cut-off value. As the total volume of plaque and
proportion of lipid component in total volume increase,
plaque resistance to mechanical stress decreases and a
predisposition to microembolism occurs due to the
catheter contact.[24]
In the current study, we found no significant
differences in the percentages of calcific components
between the groups (p=0.519). Rather than the
percentage of the calcific components, the localization
of the calcific components appears to be the factor
affecting the development of SBI. The calcific
component can be located in the blood vessel wall
in two different locations: tunica intima and tunica
media/adventitia. Peripheral calcific plaques located
on tunica media/adventitia are larger and less elastic
and, therefore, the risk of development SBI is higher
in such plaques.[25]
Nonetheless, there are several limitations to this
study. First, this study has a retrospective design with a small sample size which may have affected the
statistical results. Unfortunately, most of the patients
who underwent CAS in our hospital were advanced
age and prone to contrast nephropathy and, therefore,
the number of patients evaluated using MDCT was
limited. Second, we did not include intraplaque
hemorrhage in plaque component classification.
Intraplaque hemorrhage cause plaque instability and
predisposition to SBI. Third, the study included only
a single observer, inter-observer agreement was unable
to be measured.
In conclusion, in CAS planning, it is of utmost
importance to identify patients at high risk of
developing SBI after CAS. Structures of the aortic
arch and characteristics of carotid artery plaque may
be useful markers to predict the risk of development of
SBI. Post-processing analysis of high-spatial resolution
images obtained using MDCT may be helpful to
determine these properties successfully.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the research
and/or authorship of this article.