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Metabolic syndrome is associated with markers of subclinical atherosclerosis in a French population-based sample

Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). The relation of MetS with early stages of atherosclerosis, more important from a prevention perspective, has not been evaluated extensively. We examined the association of MetS, using WHO and NCEP definition...

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Published in:Atherosclerosis 2006-06, Vol.186 (2), p.345-353
Main Authors: Ahluwalia, N., Drouet, L., Ruidavets, J.-B., Perret, B., Amar, J., Boccalon, H., Hanaire-Broutin, H., Ferrières, J.
Format: Article
Language:English
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Summary:Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). The relation of MetS with early stages of atherosclerosis, more important from a prevention perspective, has not been evaluated extensively. We examined the association of MetS, using WHO and NCEP definitions, with number of carotid and femoral plaques; carotid intima-media thickness (IMT); pulse wave velocity (PWV) in a random population-based sample of 1153 French adults (35–65 year). Impact of inflammatory factors (C-reactive protein and soluble intercellular adhesion molecule-1) on these parameters was also evaluated. Prevalence of MetS was 14.5 (CI: 12.3–16.0) and 17.5 (CI: 15.1–20.2)%, using NCEP and WHO definitions, respectively. MetS significantly predicted number of plaques, IMT, and PWV after adjustment for traditional risk factors ( P < 0.05). Inflammatory factors predicted peripheral plaques only. The risk of subclinical atherosclerosis was considerably increased with MetS ( P < 0.05); odds ratios ranged 1.80–2.15 with NCEP definition, and 1.48–1.97 with WHO definition. Individuals meeting both NCEP and WHO definitions had slightly greater risk of increased plaques, IMT, and PWV. MetS was strongly associated with subclinical atherosclerosis and aortic stiffness, and can be used as a surrogate marker for high CVD risk, deserving aggressive treatment.
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2005.07.021