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Volume 51, Issue 1, Pages 51-56 (January 2010)


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Cilostazol reduces restenosis after carotid artery stenting

Tomoji Takigawa, MDaCorresponding Author Informationemail address, Yuji Matsumaru, MDa, Mikito Hayakawa, MDa, Shigeru Nemoto, MDb, Akira Matsumura, MDc

Received 16 April 2009; accepted 7 August 2009. published online 02 November 2009.

Background

Although carotid artery stenting (CAS) has been proposed as an alternative to carotid endarterectomy in cerebral revascularization, restenosis remains an unsolved issue. Cilostazol is a unique antiplatelet drug that has vasodilatory effects and inhibits smooth muscle cell proliferation. We investigated whether cilostazol reduces restenosis after CAS.

Methods

A database of 113 consecutive CAS procedures between April 2002 and December 2007 was assessed retrospectively. All patients received aspirin (100 mg/d) and another antiplatelet drug such as cilostazol (200 mg/d), ticlopidine (200 mg/d), or clopidogrel (75 mg/d) at least 3 days before CAS. Two antiplatelet drugs were continued for 2 to 3 months after CAS and reduced to one thereafter. Patients were evaluated at 3 and 6 months and at 6-month intervals thereafter with duplex ultrasound (DUS) imaging. Angiography was used for confirmation when stenosis was suspected as >50% with DUS imaging.

Results

We were able to monitor 97 patients for a 12-month period. The overall combined rate of stroke, myocardial infarction, and death was 3.1% at 30 days and 4.1% at 1 year. In-stent recurrent stenosis was documented in 11 patients (11%); in 10 patients (9.7%), this occurred ≤12 months of CAS. In-stent restenosis was significantly reduced in the cilostazol (+) group (0% vs 15.7% [11 of 70], P = .03). Patient characteristics were similar between the cilostazol (+) and cilostazol (–) groups.

Conclusions

Although this study was retrospective and nonrandomized, the results suggest that cilostazol administration improves long-term patency after CAS due to its inhibitory effect on smooth muscle cell growth.

a Department of Endovascular Neurosurgery, Toranomon Hospital, Tokyo, Japan

b Department of Endovascular Surgery, Jichi Medical University, Tochigi, Japan

c Department of Neurosurgery, Institute of Clinical Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan

Corresponding Author InformationReprint requests: Tomoji Takigawa, MD, Department of Neurosurgery, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan

 Competition of interest: none.

 The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest.

PII: S0741-5214(09)01681-4

doi:10.1016/j.jvs.2009.08.040


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