Impaired Fibrinolytic Capacity and Tissue Plasminogen Activator Release in Patients with Restenosis after Percutaneous Transluminal Coronary Angioplasty (PTCA)

W Kirschstein; S Simianer; C E Dempfle; H Keller; B Stegaru; P Rentrop; D L Heene

doi:10.1055/s-0038-1646900

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1989; 62(02): 772-775
DOI: 10.1055/s-0038-1646900

Original Article

Schattauer GmbH Stuttgart

Impaired Fibrinolytic Capacity and Tissue Plasminogen Activator Release in Patients with Restenosis after Percutaneous Transluminal Coronary Angioplasty (PTCA)

W Kirschstein

The I. Medizinische Klinik, Klinikum Mannheim, Mannheim, FRG

,

S Simianer

The I. Medizinische Klinik, Klinikum Mannheim, Mannheim, FRG

,

C E Dempfle

The I. Medizinische Klinik, Klinikum Mannheim, Mannheim, FRG

,

H Keller

The I. Medizinische Klinik, Klinikum Mannheim, Mannheim, FRG

,

B Stegaru

The I. Medizinische Klinik, Klinikum Mannheim, Mannheim, FRG

,

P Rentrop

^*The St. Vincent Hospital, New York, NY, USA

,

D L Heene

The I. Medizinische Klinik, Klinikum Mannheim, Mannheim, FRG

› Institutsangaben

Abstract

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Summary

To assess the role of the fibrinolytic system in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA), we determined the components of this system in a retrospective study, including 16 patients with restenosis (gr. A) and 19 patients with long-term success (gr. B). In both groups at baseline fibrinolytic activity (FA) is unchanged, whereas tissue plasminogen activator antigen (tPA-Ag) is significantly increased (gr. A: 147.0%; gr. B: 139.8%; p <0.01). Fibrinolytic capacity (FC) and tPA-Ag release are significantly reduced in the restenosis group (FC: 46.5%, p <0.05; tPA-Ag release: 48.3%, p <0.01) compared to normal controls as well as to gr. B (FC: 84.3%, p <0.05; tPA-Ag release: 79.0%, p <0.05).

Relating to the contact activation system, F XII (79.5%, p <0.05) is significantly, and F XI (82.3%) is clearly reduced in gr. A. Protein C (PC) is significantly elevated in gr. B (117.5%, p <0.05). There is a negative correlation between plasminogen activator inhibitor (PAI 1) and HDL-cholesterol (r = 0.37, p <0.05).

It appears, that there is a typical pattern of defective fibrinolysis in patients with restenosis after PTCA and that this might be a pathogenetic factor in the development of restenosis.

Keywords

PTCA - Restenosis - Plasminogen activator inhibitor - Tissue plasminogen activator - Protein C

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Referenzen

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