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Review article: the metabolic syndrome – a chronic cardiovascular inflammatory condition

The atherosclerotic process is regulated by inflammatory mechanisms, which also appear to be involved in the modulation of insulin‐resistance, a key player in the pathogenesis of the metabolic syndrome (MS). The interaction between components of the clinical phenotype of the MS with its biological phenotype (insulin resistance, dyslipidaemia, etc.) contributes to the development of a pro‐inflammatory state characterized by an increased oxidative stress (i.e. oxidized lipoproteins) and a chronic, subclinical vascular inflammation, as also suggested by the increased C reactive protein (CRP) concentration found in patients with MS. The subclinical inflammatory state peculiar of the MS modulates the atherosclerotic process at different stages, resulting in: (i) endothelial dysfunction and increased expression of endothelial adhesion molecules; (ii) an enhanced recruitment of monocytes within the arterial wall, in the early stages of the atherosclerotic process; leading to (iii) the formation of an unstable atherosclerotic plaque, rich in inflammatory cells, which is the culprit lesion in the vast majority of both coronary and cerebrovascular events observed in with MS.