Fibrinolytic function and coronary risk

被引：29

作者：

Juhan-Vague I. ^{[1
]}

Morange P. ^{[1
]}

Alessi M.C. ^{[1
]}

机构：

[1] Laboratoire d'Hématologie, CHU Timone

来源：

Current Cardiology Reports | 1999年 / 1卷 / 2期

关键词：

Arterioscler Thromb Vasc Biol; Human Adipose Tissue; Plasminogen Activator Inhibitor Type; Activator Mass Concentration; Endogenous Fibrinolysis;

D O I：

10.1007/s11886-999-0069-x

中图分类号：

学科分类号：

摘要：

Plasminogen activation potential in the blood is controlled by an equilibrium between plasminogen activators, mainly tissue-type plasminogen activator (t-PA), and inhibitors, mainly plasminogen activator inhibitor (PAI)-1. In cardiovascular practice, imbalance of this fibrinolytic potential is encountered primarily in the insulin-resistance syndrome. This syndrome leads to increased plasma PAI-1 and t-PA antigen levels (reflecting inactive t-PA/PAI-1 complexes) with a consequent decrease in fibrinolytic activity. Increased plasma PAI-1 and t-PA antigen both are predictive of myocardial infarction. The prognostic value of PAI-1 disappears after adjustments for insulin resistance markers, whereas the prognostic value of t-PA antigen disappears after simultaneous adjustments for insulin resistance and inflammation markers, suggesting an additive role of inflammation in inducing plasma fibrinolytic markers. Recently the production of PAI-1 by adipose tissue, in particular by tissue from the omentum, has been shown. PAI-1 produced in this way could be an important contributor to the elevated plasma PAI-1 levels observed in insulin-resistant patients. These results support the notion that PAI-1 may be a link between obesity, insulin resistance, and cardiovascular disease. Genetic control of PAI-1 expression has also been shown, involving a - 675 4G/5G polymorphism, the 4G/4G genotype being associated with higher plasma PAI-1 levels; its proper influence on the development of myocardial infarction is still debated. Copyright © 1999 by Current Science Inc.

引用

页码：119 / 124

页数：5

共 70 条

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