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

Citation
Pa. Sakkinen et al., Clustering of procoagulation, inflammation, and fibrinolysis variables with metabolic factors in insulin resistance syndrome, AM J EPIDEM, 152(10), 2000, pp. 897-907
Citations number
84
Categorie Soggetti
Envirnomentale Medicine & Public Health","Medical Research General Topics
Journal title
AMERICAN JOURNAL OF EPIDEMIOLOGY
ISSN journal
00029262 → ACNP
Volume
152
Issue
10
Year of publication
2000
Pages
897 - 907
Database
ISI
SICI code
0002-9262(20001115)152:10<897:COPIAF>2.0.ZU;2-5
Abstract
The known metabolic cardiovascular disease risk factors associated with ins ulin resistance syndrome (IRS) do not adequately explain the excess cardiov ascular disease risk attributed to this syndrome, and abnormalities in hemo static variables may contribute to this excess risk. Using data from 322 no ndiabetic elderly men and women (aged 65-100 years) participating in the Ca rdiovascular Health Study during 1989-1990, the authors performed factor an alysis on 10 metabolic risk factors associated with IRS and 11 procoagulati on, inflammation, and fibrinolysis variables to examine the clustering of t he 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 n ew factors interpreted as inflammation, Vitamin K-dependent proteins, and p rocoagulant activity. Plasminogen activator inhibitor-1 clustered with the body mass factor, supporting the hypothesis that obesity is related to impa ired fibrinolysis. Fibrinogen clustered with the inflammation summary facto r rather than procoagulant activity, supporting the position that fibrinoge n principally reflects underlying inflammation rather than procoagulant pot ential. The authors conclude that should hemostatic variables be shown to c ontribute to IRS-related cardiovascular disease, apart from plasminogen act ivator inhibitor-1, they may do so independently of the established metabol ic abnormalities.