ArticleJournal of neurology2013
Effects of cilostazol against the progression of carotid IMT in symptomatic ischemic stroke patients.
Article in Journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- A Critical Review of the Molecular and Clinical Effects of Cilostazol After Percutaneous Coronary Intervention.Journal of cardiovascular development and disease · 2026Review
- Manifestations of human atherosclerosis across vascular beds.JVS-vascular insights · 2024Article
- Cilostazol: a Review of Basic Mechanisms and Clinical Uses.Cardiovascular drugs and therapy · 2022Review
- Adaptation of the main peripheral artery and vein to long term confinement (Mars 500).PloS one · 2014Article
- The response of carotid intima-media thickness to medical treatment is correlated with that of intracranial atherosclerosis.Journal of clinical neurology (Seoul, Korea) · 2013Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carotid intima-media thickness (IMT) is a surrogate marker for evaluating atherosclerotic vascular diseases. The phosphodiesterase inhibitor cilostazol attenuates the increase in carotid IMT in diabetes patients. We studied whether cilostazol can reduce the progression of carotid IMT in symptomatic ischemic stroke patients. From our prospective registry of acute ischemic stroke patients who were admitted during a 4.5-year period, follow-up carotid ultrasound was performed in a random sample of survivors. Patients were divided into two groups: the cilostazol group, who continued cilostazol treatment during the follow-up period; and the control group, who were prescribed antiplatelets other than cilostazol. Analysis of covariance and propensity score-matched analysis were used to evaluate the difference between groups. Among a total of 1,049 cases in our registry, 208 patients were utilized to construct two comparable sets by propensity score analysis, including 101 who received cilostazol and 107 who took antiplatelet medication without cilostazol. Both maximum and mean carotid IMT values were significantly reduced in the cilostazol group but increased in the control group (maximum left -0.048 ± 0.186 vs. 0.022 ± 0.163 mm, p = 0.001; maximum right -0.037 ± 0.173 vs. 0.050 ± 0.200 mm, p = 0.001; mean left -0.052 ± 0.102 vs. 0.023 ± 0.112 mm, p < 0.001; and mean right -0.038 ± 0.106 vs. 0.042 ± 0.139 mm, p < 0.001). After matching by propensity score, the improvements in both maximum and mean carotid IMT values in the cilostazol group remained significant. This study shows that cilostazol causes a significant regression in carotid IMT in symptomatic stroke patients.
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