title: Inflammation, the metabolic syndrome and cardiovascular risk.
abstract: Over the past ten years it has become clear that cardiovascular disease (CVD) and atherosclerosis have a 'microinflammatory' component and are often associated with low levels of inflammatory markers that are in the upper part of the 'normal' range. In particular, diseases that predispose to CVD, such as the metabolic syndrome and type 2 diabetes, appear to have a very strong inflammatory component. While the inflammatory process is very complicated, single measures, such as C-reactive protein (CRP) or fibrinogen, have clear benefits as they summarise many different parts of the inflammatory process and are easy to apply. However, it is important to remember that the process of inflammation includes coagulation, fibrinolysis, complement activation, antioxidation, immune response and hormonal regulation through the hypothalamic-pituitary-adrenal axis. Furthermore, genetic variation, differences in exposure to environmental influences and the mass of inflammation-producing tissue (e.g. adipose tissue) can all influence responses. Thus, the relationship between atherosclerosis, the metabolic syndrome and inflammation is extraordinarily complex. Inflammatory markers such as CRP exhibit strong CVD-risk prediction that is consistent across sexes and a number of different populations. They reflect risk not only for 'vulnerable plaque' and myocardial infarction (MI) but also for other cardiovascular diseases. In fact, inflammation is associated with several, if not all, of the chronic diseases of old age, and it is now clear that there are important links between inflammation and general metabolism. For instance, visceral adiposity exerts a major influence on inflammation status. Medications that affect atherosclerosis appear to do so at least in part by influencing inflammation (for instance, the emerging pleiotropic effects of statins), and this has far-reaching ramifications for chronic diseases of old age and their treatment.
authors.affiliation: University of Vermont College of Medicine, Burlington, Vermont, USA.
authors.forename: Russell P
authors.initials: RP
authors.lastname: Tracy
mesh_terms: D001161:Arteriosclerosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D004967:Estrogens / Q000627:therapeutic use; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications*; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D004967:Estrogens; D000960:Hypolipidemic Agents; D005340:Fibrinogen; D002097:C-Reactive Protein; D001241:Aspirin