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The impact of metabolic syndrome and CRP on vascular phenotype in type 2 diabetes mellitus

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Author: Alizadeh Dehnavi, R. · Beishuizen, E.D. · Ree, M.A. van de · Le Cessie, S. · Huisman, M.V. · Kluft, C. · Princen, H.M.G. · Tamsma, J.T.
Type:article
Date:2008
Institution: TNO Kwaliteit van Leven
Source:European Journal of Internal Medicine, 2, 19, 115-121
Identifier: 240693
doi: doi:10.1016/j.ejim.2007.06.011
Keywords: Health · C-reactive protein · Diabetes mellitus type 2 · Endothelial function · Intima media thickness · Metabolic syndrome · PAI-1 · C reactive protein · endothelial leukocyte adhesion molecule 1 · fibrinogen · high density lipoprotein · plasminogen activator inhibitor 1 · thrombomodulin · tissue plasminogen activator · vascular cell adhesion molecule 1 · von Willebrand factor · adult · aged · arterial wall thickness · article · atherosclerosis · cholesterol blood level · diastolic blood pressure · dyslipidemia · female · human · kidney function · major clinical study · male · metabolic syndrome X · non insulin dependent diabetes mellitus · phenotype · risk factor · sex difference · systolic blood pressure · Aged · Biological Markers · C-Reactive Protein · Diabetes Mellitus, Type 2 · E-Selectin · Female · Fibrinogen · Humans · Inflammation · Male · Metabolic Syndrome X · Middle Aged · Phenotype · Plasminogen Activator Inhibitor 1 · Thrombomodulin · Tissue Plasminogen Activator · Tunica Intima · Tunica Media · Vascular Cell Adhesion Molecule-1 · von Willebrand Factor

Abstract

Background: The burden of cardiovascular disease in diabetes mellitus type 2 (DM2) patients is variable. We hypothesize that metabolic syndrome (MS) and low-grade systemic inflammation modify the extent of atherosclerosis in DM2. Methods: Vascular phenotype was determined using the following endothelium-related, hemostatic, and sonographic endpoints in 62 DM2 patients with mild dyslipidemia: sVCAM, sE-selectin, von Willebrand factor (VWF), fibrinogen, s-thrombomodulin (sTM), tPA, PAI-1, flow-mediated dilation (FMD), and intima media thickness (IMT). The impact of MS load (number of criteria present), MS components, and CRP on these parameters was assessed. Results: Serum sVCAM, sTM, and tPA levels significantly increased with increasing MS load. IMT also significantly increased from 0.602 ± 0.034 (one MS criterion) to 0.843 ± 0.145 (four MS criteria, p = 0.007). LogCRP significantly correlated with fibrinogen, PAI-1, and IMT. In a multiple regression (MR) model with age and gender as covariates, MS load predicted sVCAM and sTM; CRP predicted PAI-1 and fibrinogen; MS load and CRP simultaneously predicted tPA and IMT. For each MS criterion present, IMT significantly increased by 0.04 mm. An increase in CRP from 1 to 3 mg/L resulted in a significant increase of 0.04 mm. Patients with four MS criteria and inflammation (CRP ≥ 3 mg/L) are predicted to have a 0.21 mm thicker IMT than those without. A second stepwise MR analysis based on gender, traditional risk factors, diabetes-related parameters, renal function, individual MS criteria, and LogCRP as explanatory variables showed a significant effect of systolic and diastolic blood pressure, HDL, and LogCRP on IMT(r2 = 0.36, p < 0.001). Conclusion: MS and low-grade chronic inflammation have an independent impact on vascular phenotype including IMT in DM2. © 2007 European Federation of Internal Medicine. Chemicals / CAS: C reactive protein, 9007-41-4; endothelial leukocyte adhesion molecule 1, 128875-25-2; fibrinogen, 9001-32-5; plasminogen activator inhibitor 1, 140208-23-7; thrombomodulin, 112049-68-0; tissue plasminogen activator, 105913-11-9; von Willebrand factor, 109319-16-6; Biological Markers; C-Reactive Protein, 9007-41-4; E-Selectin; Fibrinogen, 9001-32-5; Plasminogen Activator Inhibitor 1; Thrombomodulin; Tissue Plasminogen Activator, EC 3.4.21.68; Vascular Cell Adhesion Molecule-1; von Willebrand Factor