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Plasmin Activation System in Restenosis: Role in Pathogenesis and Clinical Prediction?

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Abstract

During recent years it has become increasingly recognized that the plasmin activation system is involved in the development of atherosclerosis and restenosis. Responsible pathophysiologic mechanisms, however, remain elusive. This review focuses primarily on the clinicians, point of view, suggesting that increases in plasminogen activator inhibitor type-1 (PAI-1) plasma levels after balloon angioplasty or permanently elevated lipoprotein (a) (Lp(a)) plasma levels might be helpful in the prediction of restenosis after coronary angioplasty. In contrast, tissue-type plasminogen activator (tPA) plasma levels appear unrelated to restenosis, and data regarding a possible role of urokinase-type plasminogen activator (uPA) in circulation are not available at present. Furthermore, a new hypothesis on the pathophysiological role of local PAI-1 overexpression as a beneficial negative feedback mechanism to limit excess cellular proliferation in atherogenesis and restenosis is presented.

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Authors and Affiliations

  1. Department of Cardiology, University of Vienna, Austria

    Gunter Christ, Karam Kostner, Manfred Zehetgruber & Kurt Huber

  2. Department of Thrombosis and Vascular Biology, University of Vienna, Austria

    Bernd R. Binder

  3. Franz-Volhard-Clinic Berlin-Buch, Charite; Humboldt University, Germany

    Dietrich Gulba

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  1. Gunter Christ
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  2. Karam Kostner
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Christ, G., Kostner, K., Zehetgruber, M. et al. Plasmin Activation System in Restenosis: Role in Pathogenesis and Clinical Prediction?. J Thromb Thrombolysis 7, 277–285 (1999). https://doi.org/10.1023/A:1008983110941

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