scholarly journals The insulin resistance syndrome: implications for thrombosis and cardiovascular disease

2002 ◽  
Vol 32 (5-6) ◽  
pp. 269-273 ◽  
Author(s):  
Irène Juhan-Vague ◽  
Pierre E. Morange ◽  
Marie-Christine Alessi
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Insulin Resistance Syndrome

Insulin resistance and cardiovascular disease

2002 ◽  
Vol 2 (1_suppl) ◽  
pp. S9-S11 ◽  
Author(s):  
Markku Laakso
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Insulin Resistance Syndrome ◽  
Plasminogen Activator Inhibitor 1 ◽  
Factors Associated

Insulin resistance is characterised by a decreased rate of insulin-mediated glucose uptake and is associated with adverse changes in cardiovascular risk factors, such as high triglyceride levels, low levels of high-density lipoprotein cholesterol, raised blood pressure, obesity and increased levels of plasminogen activator inhibitor 1. The term `insulin resistance syndrome' (IRS) is used to describe the complex of factors associated with insulin resistance that is found in patients both with and without type 2 diabetes. Although the presence of insulin resistance syndrome is generally considered to be a risk factor for cardiovascular disease, there is a lack of definitive evidence for a causal link. Recently, however, a statistical method known as factor analysis has been applied to the cluster of cardiovascular risk factors associated with IRS. This has been able to show that the `insulin resistance factor' (high plasma insulin and glucose levels, body mass index, waist-to-hip ratio and triglyceride levels) predicted coronary heart disease events in elderly non-diabetic men as well as in patients with type 2 diabetes. Therefore, treatment of insulin resistance whether by pharmacological (eg. thiazolidinediones) or nonpharmacological means has the potential to offer both improvements in glycaemic control and in cardiovascular events.

scholarly journals Clustering of Procoagulation, Inflammation, and Fibrinolysis Variables with Metabolic Factors in Insulin Resistance Syndrome

2000 ◽  
Vol 152 (10) ◽  
pp. 897-907 ◽  
Author(s):  
Pamela A. Sakkinen ◽  
Patricia Wahl ◽  
Mary Cushman ◽  
Michael R. Lewis ◽  
Russell P. Tracy
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Plasminogen Activator Inhibitor ◽  
Insulin Resistance Syndrome ◽  
Plasminogen Activator Inhibitor 1 ◽  
Factors Associated ◽  
Activator Inhibitor

Abstract 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. Am J Epidemiol 2000;152:897–907.

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