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(Circulation. 1996;94:2052-2054.)
© 1996 American Heart Association, Inc.

Articles

Impaired Fibrinolysis and the Risk for Coronary Heart Disease

H. Roger Lijnen, PhD; Desire Collen, MD, PhD

the Center for Molecular and Vascular Biology, University of Leuven, Belgium.

Correspondence to D. Collen, Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, O & N, Herestraat 49, B-3000 Leuven, Belgium. E-mail desire.collen@med.kuleuven.ac.be.

Key Words: fibrinolysis • coronary disease • plasminogen activators • Editorials

	Introduction

 
Ischemic heart disease is most frequently caused by coronary atherosclerosis. The main triggering event of unstable coronary heart disease is rupture of an atherosclerotic plaque with superimposed thrombosis.¹ Reduced fibrinolytic capacity is presumed to be involved in the development and/or progression of atherosclerotic plaque, but its pathogenetic role is not fully established. This may be due in part to complex interrelations of fibrinolysis with lipoproteins, with insulin or insulinlike peptides, and with different cell types in the normal and atherosclerotic vessel wall. Specific assays for antigen and activity levels of the main components of the fibrinolytic system have recently made it possible to establish an association between low fibrinolytic activity and atherothrombosis.² Prospective studies have revealed correlations between changes in fibrinolytic parameters and coronary disease, but it appeared to be difficult to identify independent risk factors. The article by Juhan-Vague et al³ (on behalf of ECAT) sheds a new light on the confounding variables governing the correlation between PAI-1 and TPA antigen on the one hand and coronary disease on the other.

The fibrinolytic system, which is responsible for the removal of fibrin from the circulation, contains an inactive proenzyme, plasminogen, which is activated to the serine proteinase plasmin by plasminogen activators, which comprise TPA and UPA. Plasmin degrades fibrin as well as extracellular matrix proteins. Inhibition of the fibrinolytic system may occur at the level of the plasminogen activator (by specific plasminogen activator inhibitors, mainly PAI-1) or at the level of plasmin, mainly by ₂-antiplasmin. TPA-mediated plasminogen activation is . . . [Full Text of this Article]

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