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

被引:296
作者
Sakkinen, PA
Wahl, P
Cushman, M
Lewis, MR
Tracy, RP
机构
[1] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT USA
[2] Univ Washington, Sch Publ Hlth & Community Med, Dept Biostat, Seattle, WA 98195 USA
[3] Univ Vermont, Coll Med, Dept Med, Burlington, VT 05405 USA
[4] Univ Vermont, Coll Med, Dept Biochem, Burlington, VT 05405 USA
关键词
aged; 80 and over; factor analysis; statistical; hemostasis; inflammation; insulin resistance; metabolism; multivariate analysis;
D O I
10.1093/aje/152.10.897
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
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.
引用
收藏
页码:897 / 907
页数:11
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