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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:114-118.)
© 1997 American Heart Association, Inc.

Articles

Plasma Protein C Inhibitor Is Elevated in Survivors of Myocardial Infarction

Veronica A. Carroll; Margaret R. Griffiths; Margarete Geiger; Christoph Merlo; Miha Furlan; Bernhard Lammle; Bernd R. Binder

the Department of Vascular Biology and Thrombosis Research (V.A.C., M.G., B.R.B.), University of Vienna, Technoclone Inc (V.A.C., M.R.G.), Vienna, Austria, and Central Hematology Laboratory (C.M., M.F., B.L.), Inselspital, University Hospital of Bern, Switzerland.

Correspondence to Prof Dr BR Binder, Department of Vascular Biology and Thrombosis Research, University of Vienna, Schwarzspanierstrasse 17, A-1090 Vienna, Austria. E-mail Bernd.Binder@univie.ac.at.

Many studies have shown alterations of the hemostatic and fibrinolytic systems in patients with atherosclerotic disease, principally in levels of plasminogen activator inhibitor-1. However, in a large prospective study only fibrinogen, von Willebrand factor antigen, and tissue plasminogen activator antigen were found to be independent risk markers for acute coronary events. The present study evaluated the fibrinolytic system in coronary artery disease, paying particular attention to another inhibitor of fibrinolysis, plasminogen activator inhibitor-3, also called protein C inhibitor (PCI). One hundred fifteen nonanticoagulated male survivors of myocardial infarction were investigated for a range of hemostatic and fibrinolytic parameters that were compared with values in 87 age-matched healthy control male subjects. PCI active antigen was significantly (P<.03) elevated in the myocardial infarction group compared with the control group and was associated with the number of acute coronary events suffered (P=.005) but not with the severity of disease as determined by coronary angiography. Elevated PCI plasma levels can be considered as a risk marker for acute coronary events and might be of particular importance in the pathogenesis of this disease due to the interference of PCI in both the anticoagulant and fibrinolytic systems.

Key Words: myocardial infarction • protein C inhibitor • plasminogen activator inhibitor-1 • tissue plasminogen activator

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