The results of this study would show that cilostazol is effective for the prevention of restenosis and intimal hyperplasia after placement of a self-expandable stent in the carotid artery.
Cilostazol has been reported to be effective for the prevention of restenosis after stent placement in the coronary [9,10],
superficial femoral [11],
and carotid [6,7] arteries.
There are several possible mechanisms to explain the reduction of restenosis after CAS.
Cilostazol has a comparable inhibiting platelet aggregation effect [12,13] and it has a more rapid effect after administration [14] to prevent early occlusion by thrombus.
The TASC II guidelines for peripheral artery disease [15] recommend it as first-line pharmacotherapy for claudication.
Cilostazol may suppress neointimal hyperplasia.
The major mechanism of restenosis is migration and proliferation of vascular smooth muscle cells caused by local vascular injury after intervention [16,17] In addition,
cilostazol elevates cyclic adenosine monophosphate (cAMP) levels in vascular smooth muscle cells,
leading to an increase in p53 protein,
which in turn stops cell cycle progression and leads cells to apoptosis; i.e.,
it directly suppresses proliferation of vascular smooth muscle cells [18].
Other effects of cilostazol include improvement and protection of endothelial function and growth acceleration [19,20].
Another effect of cilostazol is vasodilation induced by continuous relaxation of vascular smooth muscle,
which may contribute to the reduction of restenosis assessed by duplex.
In this study,
a significant reduction of intimal hyperplasia at 6-month follow-up was found in patients who received cilostazol (0.43mm vs.
0.99mm,
p=0.007 by unpaired t-test); however,
there was no difference in 12- and 24- month follow-up.
These results suggest that cilostazol administration should be continued for at least 1 year.
However,
we do not know whether the incidence of restenosis would increase if cilostazol administration were suspended after 1 year of treatment; therefore,
a further investigation of this issue is required.
There are several limitations to this study.
There were several chances for bias before registration.
Patients who were worried about the possibility of one antiplatelet follow-up suffering from diabetes,
peripheral artery disease and cardiovascular disease,
tended not to be registered.
Resistance to aspirin and clopidogrel,
which could occur in a certain percentage of patients,
would also be one reason for refusing registration.
A large,
prospective,
randomized multicenter study is needed to verify these findings.
In conclusion,
within the limitations of the study,
cilostazol would be effective for reducing restenosis and intimal hyperplasia following CAS.