The development of coronary artery disease, and specificallymyocardial infarction, involves hyperplasia of arterial smoothmuscle, the development of fatty streaks, atheroma formation,plaque rupture, and ultimately thrombus formation and vesselocclusion.1 These changes are in part genetically determined,as demonstrated by the fact that the risk of myocardial infarctionin persons who have a first-degree relative with myocardialinfarction is seven times the risk in persons who do not.2,3This finding is often used to argue that coronary artery diseasehas a genetic basis, but the extent to which a shared environmentcontributes to the risk must also be . . . [Full Text of this Article]
Mechanisms in the Formation and Degradation of Fibrin
Formation and Stabilization
Inhibition of Fibrinolysis
Activation of Fibrinolysis
Interaction of PAI-1 and t-PA with Fibrin
Effect of Fibrin Formation on Enzyme-Inhibitor Reactions
PAI-1 in Coronary Artery Disease
PAI-1 and the Progression of Vascular Disease
PAI-1 in Vessel Walls and Plaques
PAI-1 and Cellular Migration
Relation between PAI-1 and Cardiovascular Risk Factors
Regulation of PAI-1
Influence of Glucose and Insulin on the Production of PAI-1
Influence of Estrogen on the Production of PAI-1
The ReninAngiotensin System
Regulation of PAI-1 Gene Expression
PAI-1 Gene Polymorphisms
PAI-1 Genotype and Coronary Artery Disease
PAI-1, Factor XIII wGenotype, and Insulin Resistance
Conclusions
Source Information
From the Department of Trauma and Emergency Medicine and the Laboratory for Thrombosis Research, Department of Clinical Research, University Hospital of Bern, Inselspital, Bern, Switzerland (H.P.K.); and the Unit of Molecular Vascular Medicine, Leeds General Infirmary, University of Leeds, Leeds, United Kingdom (P.J.G.).
Address reprint requests to Dr. Kohler at the Department of Trauma and Emergency Medicine, University Hospital of Bern, Inselspital, 3010 Bern, Switzerland, or at hanspeter.kohler@insel.ch.
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