Effect of Cilostazol, a Phosphodiesterase Inhibitor, on Carotid IMT in Japanese Type 2 Diabetic Patients

Mitsuhashi, Naoki; Tanaka, Yasushi; Kubo, Sachiko; Ogawa, Satoshi; Hayashi, Chisa; Uchino, Hiroshi; Shimizu, Tomoaki; Watada, Hirotaka; Kawasumi, Masahiko; Onuma, Tomio; Kawamori, Ryuzo

doi:10.1507/endocrj.51.545

Cited by 31 publications

(29 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Scanning of the extracranial carotid arteries in the neck was performed bilaterally in three different longitudinal projections. (i.e., anterior-oblique, lateral, and posterior-oblique) and in the transverse projection, as reported previously [15]. This allowed the common carotid artery, carotid bulb, and internal carotid artery to be scanned bilaterally.…”

Section: Assessment Of Common Carotid Artery Imtmentioning

confidence: 90%

Association of C-reactive Protein with Early-stage Carotid Atherosclerosis in Japanese Patients with Early-state Type 2 Diabetes Mellitus

et al. 2006

Self Cite

View full text Add to dashboard Cite

Abstract. The aim of this study was to assess the association between high sensitivity-C-reactive protein (hs-CRP), a sensitive marker of inflammation, and early-stage carotid atherosclerosis, in patients with early-state type 2 diabetes mellitus. The study subjects were 75 patients with type 2 diabetes mellitus without obvious diabetic vascular complications, who were not on any medication, and whose HbA 1c level was less than 6.5%. We evaluated the mean intima-media thickness (IMT) of the common carotid artery (CCA) by ultrasound B-mode imaging. Then, we investigated various factors associated with CCA-IMT including hs-CRP. Serum hs-CRP levels correlated well with factors strongly associated with insulin resistance such as homeostasis model assessment of insulin resistance (HOMA-IR), fasting insulin level, and body mass index. Serum hs-CRP also correlated with mean CCA-IMT and serum levels of soluble intercellular adhesion molecule-1. Multivariate regression analysis using mean CCA-IMT as the dependent variable identified only age, hs-CRP, and diastolic blood pressure as independent determinants of mean CCA-IMT. While hs-CRP associates with insulin resistance and subclinical atherosclerosis in ealy-state type 2 diabetes, our data suggest that hs-CRP is a useful marker of subclinical atherosclerosis in early-state type 2 diabetes mellitus independent of factors that directly reflect insulin resistance.

show abstract

Section: Assessment Of Common Carotid Artery Imtmentioning

confidence: 90%

Association of C-reactive Protein with Early-stage Carotid Atherosclerosis in Japanese Patients with Early-state Type 2 Diabetes Mellitus

et al. 2006

Self Cite

View full text Add to dashboard Cite

show abstract

“…10 On the other hand, 2 studies evaluating the effects of cilostazol therapy on carotid IMT revealed nearly complete prevention of increase in this parameter. 8,20 Furthermore, another study reported a significant decrease in carotid IMT after 1 year of cilostazol treatment. 21 The results of these studies thus indicate that cilostazol prevents an increase in carotid IMT more strongly than aspirin in diabetic subjects.…”

Section: Discussionmentioning

confidence: 99%

The Phosphodiesterase Inhibitor Cilostazol Induces Regression of Carotid Atherosclerosis in Subjects With Type 2 Diabetes Mellitus

et al. 2010

Self Cite

View full text Add to dashboard Cite

Background-Antiplatelet drugs are effective in preventing recurrence of atherosclerosis in type 2 diabetic patients.However, the efficacy and usefulness of 2 different antiplatelet drugs, aspirin and cilostazol, in the progression of carotid intima-media thickening are unknown. 001).In a regression analysis adjusted for possible confounding factors such as lipid levels and hemoglobin A 1c , the improvements in common carotid artery intima-media thickness with cilostazol treatment over aspirin treatment remained significant. Conclusions-Compared with aspirin, cilostazol potently inhibited progression of carotid intima-media thickness, an established surrogate marker of cardiovascular events, in patients with type 2 diabetes mellitus. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: C000000215.

show abstract

“…In addition, cilostazol treatment prevents the overproliferation of aortic SMC in diabetic animals (Fig. 2) and human diabetic patients by decreasing carotid intima media thickness (Ahn et al, 2001;Shinoda-Tagawa et al, 2002;Mitsuhashi et al, 2004). Given that VCAM-1 is also expressed by aortic SMC, one would argue that cilostazol suppresses VCAM-1-mediated overexpression via the NF-B pathway.…”

Section: Discussionmentioning

confidence: 99%

Cilostazol Protects Diabetic Rats from Vascular Inflammation via Nuclear Factor-κB-Dependent Down-Regulation of Vascular Cell Adhesion Molecule-1 Expression

Gao¹,

Wang²,

Wang³

et al. 2006

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Vascular cell adhesion molecule (VCAM)-1 plays a critical role in the initiation and development of vascular inflammation and selective inhibition of adhesion molecules expressed by endothelial cells may present a new therapeutic strategy for the treatment of vascular complications associated with diabetes mellitus. Increasing evidence indicates that cilostazol, a cAMP phosphodiesterase inhibitor, reduces VCAM-1 expression on endothelial cells. In this study, we have tested the effect of cilostazol on the development of vascular inflammation in rats with streptozotocin-induced diabetes and determined the mechanism by which cilostazol prevents diabetes-induced vascular inflammation in the aorta. Diabetic rats were treated with different dose of cilostazol (27 or 9 mg/kg/day) for 8 weeks, and aortae were removed for the evaluation of vascular inflammation. The VCAM-1 protein expression and VCAM-1 mRNA transcripts were analyzed by immunohistochemical staining and in situ hybridization assay, respectively. Our results demonstrated that cilostazol treatment prevents the overexpression of VCAM-1 and protects diabetic rats from vascular inflammation. More importantly, our mechanistic studies suggested that cilostazol controls the VCAM-1 overexpression via inhibiting the activation of nuclear factor-B.

show abstract

Effect of Cilostazol, a Phosphodiesterase Inhibitor, on Carotid IMT in Japanese Type 2 Diabetic Patients

Cited by 31 publications

References 28 publications

Association of C-reactive Protein with Early-stage Carotid Atherosclerosis in Japanese Patients with Early-state Type 2 Diabetes Mellitus

Association of C-reactive Protein with Early-stage Carotid Atherosclerosis in Japanese Patients with Early-state Type 2 Diabetes Mellitus

The Phosphodiesterase Inhibitor Cilostazol Induces Regression of Carotid Atherosclerosis in Subjects With Type 2 Diabetes Mellitus

Cilostazol Protects Diabetic Rats from Vascular Inflammation via Nuclear Factor-κB-Dependent Down-Regulation of Vascular Cell Adhesion Molecule-1 Expression

Contact Info

Product

Resources

About