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Clustering of procoagulation, inflammation, and fibrinolysis variables with metabolic factors in insulin resistance syndrome.

TitleClustering of procoagulation, inflammation, and fibrinolysis variables with metabolic factors in insulin resistance syndrome.
Publication TypeJournal Article
Year of Publication2000
AuthorsSakkinen, PA, Wahl, P, Cushman, M, Lewis, MR, Tracy, RP
JournalAm J Epidemiol
Volume152
Issue10
Pagination897-907
Date Published2000 Nov 15
ISSN0002-9262
KeywordsAged, Aged, 80 and over, Antigens, Blood Coagulation, Cardiovascular Diseases, Cluster Analysis, Factor Analysis, Statistical, Factor VII, Female, Fibrinogen, Fibrinolysis, Humans, Inflammation, Insulin Resistance, Male, Middle Aged, Plasminogen Activator Inhibitor 1, Risk Factors
Abstract<p>The known metabolic cardiovascular disease risk factors associated with insulin resistance syndrome (IRS) do not adequately explain the excess cardiovascular disease risk attributed to this syndrome, and abnormalities in hemostatic variables may contribute to this excess risk. Using data from 322 nondiabetic elderly men and women (aged 65-100 years) participating in the Cardiovascular Health Study during 1989-1990, the authors performed factor analysis on 10 metabolic risk factors associated with IRS and 11 procoagulation, inflammation, and fibrinolysis variables to examine the clustering of the metabolic and hemostatic risk markers. Factor analysis of the metabolic variables confirmed four uncorrelated factors: body mass, insulin/glucose, lipids, and blood pressure. Adding the hemostatic variables yielded three new factors interpreted as inflammation, vitamin K-dependent proteins, and procoagulant activity. Plasminogen activator inhibitor-1 clustered with the body mass factor, supporting the hypothesis that obesity is related to impaired fibrinolysis. Fibrinogen clustered with the inflammation summary factor rather than procoagulant activity, supporting the position that fibrinogen principally reflects underlying inflammation rather than procoagulant potential. The authors conclude that should hemostatic variables be shown to contribute to IRS-related cardiovascular disease, apart from plasminogen activator inhibitor-1, they may do so independently of the established metabolic abnormalities.</p>
DOI10.1093/aje/152.10.897
Alternate JournalAm J Epidemiol
PubMed ID11092431
Grant ListN01-HC-85079 / HC / NHLBI NIH HHS / United States
N01-HC-85086 / HC / NHLBI NIH HHS / United States
T32-HL-07594 / HL / NHLBI NIH HHS / United States