Effect of cilostazol on arterial stiffness and vascular adhesion molecules in type 2 diabetic patients with metabolic syndrome

A randomised, double-blind, placebo-controlled, crossover trial

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5 Citations (Scopus)

Abstract

Background: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. Methods. In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Results: Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95% CI -55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 ± 285.6 to 1168.2 ± 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95% CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Conclusion: Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers. Trial registration. (Clinical trial reg. no. NCT00573950, clinicaltrials.gov.).

Original languageEnglish
Article number41
JournalDiabetology and Metabolic Syndrome
Volume5
Issue number1
DOIs
Publication statusPublished - 2013 Aug 14

Fingerprint

Vascular Stiffness
Cross-Over Studies
Blood Vessels
Placebos
Pulse Wave Analysis
Ankle
Arm
Therapeutics
Biomarkers
Phosphodiesterase Inhibitors
Chemokine CCL2
Adiponectin
Intercellular Adhesion Molecule-1
cilostazol
Serum
C-Reactive Protein
Interleukin-6
Atherosclerosis
Tumor Necrosis Factor-alpha
Clinical Trials

Keywords

  • Arterial stiffness
  • Cilostazol
  • Metabolic syndrome
  • Phosphodiesterase inhibitor
  • Type 2 diabetes
  • Vascular adhesion molecules

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

@article{05a277f6623747908178cadf6cfa02b4,
title = "Effect of cilostazol on arterial stiffness and vascular adhesion molecules in type 2 diabetic patients with metabolic syndrome: A randomised, double-blind, placebo-controlled, crossover trial",
abstract = "Background: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. Methods. In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Results: Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95{\%} CI -55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 ± 285.6 to 1168.2 ± 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95{\%} CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Conclusion: Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers. Trial registration. (Clinical trial reg. no. NCT00573950, clinicaltrials.gov.).",
keywords = "Arterial stiffness, Cilostazol, Metabolic syndrome, Phosphodiesterase inhibitor, Type 2 diabetes, Vascular adhesion molecules",
author = "Kim, {Nam Hoon} and Kim, {Hee Young} and Hyonggin An and Seo, {Ji A} and Kim, {Nan Hee} and Choi, {Kyung Mook} and Sei-Hyun Baik and Choi, {Dong Seop} and Kim, {Sin Gon}",
year = "2013",
month = "8",
day = "14",
doi = "10.1186/1758-5996-5-41",
language = "English",
volume = "5",
journal = "Diabetology and Metabolic Syndrome",
issn = "1758-5996",
publisher = "BioMed Central",
number = "1",

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TY - JOUR

T1 - Effect of cilostazol on arterial stiffness and vascular adhesion molecules in type 2 diabetic patients with metabolic syndrome

T2 - A randomised, double-blind, placebo-controlled, crossover trial

AU - Kim, Nam Hoon

AU - Kim, Hee Young

AU - An, Hyonggin

AU - Seo, Ji A

AU - Kim, Nan Hee

AU - Choi, Kyung Mook

AU - Baik, Sei-Hyun

AU - Choi, Dong Seop

AU - Kim, Sin Gon

PY - 2013/8/14

Y1 - 2013/8/14

N2 - Background: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. Methods. In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Results: Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95% CI -55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 ± 285.6 to 1168.2 ± 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95% CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Conclusion: Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers. Trial registration. (Clinical trial reg. no. NCT00573950, clinicaltrials.gov.).

AB - Background: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. Methods. In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Results: Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95% CI -55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 ± 285.6 to 1168.2 ± 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95% CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Conclusion: Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers. Trial registration. (Clinical trial reg. no. NCT00573950, clinicaltrials.gov.).

KW - Arterial stiffness

KW - Cilostazol

KW - Metabolic syndrome

KW - Phosphodiesterase inhibitor

KW - Type 2 diabetes

KW - Vascular adhesion molecules

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