The metabolic syndrome (MS) has been represented as a `clustering` of strongly interrelated risk factors for cardiovascular disease (CVD). These include dyslipidemia, hypertension, obesity and insulin resistance. The components of metabolic syndrome can act directly and indirectly on endothelial function. A common mechanism underlying endothelial dysfunction is related with increase of oxidative stress. Free radicals cause the initial disturbances of endothelial function, enhance the release of Endothelin-1 (ET-1), the main endothelial constrictor peptide, im pair of NO metabolism and decrease of endothelium-dependent vasodilatation, stimulate release of proinflamatory mediators- adhesion molecule 1 (ICAM-1) and vascular adhesion molecule-1(VCAM-1), enhance the release of plasmingen activator inhibitor-1 (PAI-1) and von Willebrand factor (vWF), modulate the PI2/TxA2 ration, leading to a prothrombogenic state, formatting represent a key early step in atherogenesis. Plasma ET-1, adhesion molecules VCAM-1 and ICAM-1, PAI-1 and vWF may serve as biomarkers pointing to endothelial disfunction (ED) and increased cardiovascular risk. Significant in creased plasma levels of these biomarkers along other biochemical parameters can be seen in condition like obesity, diabetes of type 2 and others component of metabolic syndrome. Thus measurement of endothelial function might indetify atherogenic risk individuals at the early stage long before clinical diagnosis of CVD.This may prove to be a useful means of assessing response to treatment aimed at reducing long-term morbility and mortality from CVD.
Scripta Scientifica Medica 2007;39(2):133-135
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