title: Involvement of the hemostatic system in the insulin resistance syndrome. A study of 1500 patients with angina pectoris. The ECAT Angina Pectoris Study Group.
abstract: Hyperinsulinemia, a major indicator of insulin resistance, may exert its influence on the risk of coronary artery disease partially through disturbances of the hemostatic system. The relations of fasting insulin concentrations with the degree of coronary atherosclerosis, other coronary risk factors (including some markers of the insulin resistance syndrome such as body mass index and triglyceride), markers of inflammation, and hemostatic factors were investigated in 1484 patients with angina pectoris. Mean insulin levels were higher in patients with one or more coronary vessel stenoses than in those without (9.9 microU/mL compared with 9.0 microU/mL, P < .0001). However, the association the presence of vessel stenoses was stronger in patients with a previous myocardial infarction than in those without. Insulin increased markedly (P < .0001) and independently of other risk factors with age body mass index, triglyceride concentration, and markers of inflammation, such as white blood cell count and C-reactive protein. The strongest relations between insulin and hemostatic factors were observed with fibrinolytic variables, particularly plasminogen activator inhibitor-1 (PAI-1) levels (r = .44, P < .0001). This relation decreased somewhat (r = .29) after simultaneous adjustment for markers of the insulin resistance syndrome, mainly body mass index and triglycerides, but not after adjustment for markers of inflammation. Therefore, we propose that increased PAI-1 levels, which are essentially related to the classic metabolic aspect of the insulin resistance syndrome, have to be included in this syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Hematology Laboratory, CHU Timone, Marseille, France.
authors.forename: I
authors.initials: I
authors.lastname: Juhan-Vague
authors.forename: S G
authors.initials: SG
authors.lastname: Thompson
authors.forename: J
authors.initials: J
authors.lastname: Jespersen
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000097:blood; D000787:Angina Pectoris / Q000097:blood*; D015992:Body Mass Index; D003327:Coronary Disease / Q000097:blood; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005342:Fibrinolysis; D006487:Hemostasis; D006801:Humans; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D007328:Insulin; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D014841:von Willebrand Factor; D005169:Factor VIII; D005340:Fibrinogen