Fibrinolysis and thrombosis

Research output: Contribution to journalArticle

Abstract

The fibrinolytic system generates plasmin, which dissolves fibrin in haemostatic plugs and in thrombi. It is often regarded simply as a secondary phenomenon responsive to the generation of thrombi but it is, rather, in dynamic balance with fibrin formation, such that abnormalities in either can lead to thrombosis. This chapter summarizes the fibrinolytic system and its regulation. It considers the components of the system in blood, both in plasma and in circulating cells, with emphasis on protease-inhibitor balance. It goes on to discuss local fibrinolytic potential in thrombi, both venous and arterial, and in the diseased vessel wail, presenting evidence that increased local inhibition of fibrinolysis by PAI-1, PAI-2 and alpha(2)-antiplasmin is intimately involved in thrombus stability and in the generation of fibrin-rich vessel wall lesions. Finally, it reviews the evidence that defective plasma fibrinolysis has a causal role in venous and arterial thrombosis.

Original languageEnglish
Pages (from-to)423-433
Number of pages11
JournalBest Practice & Research Clinical Obstetrics & Gynaecology
Volume12
Publication statusPublished - 1999

Keywords

  • fibrinolysis
  • thrombosis
  • tissue plasminogen activator
  • plasminogen activator inhibitor
  • risk factors
  • prospective studies
  • haemostasis
  • myocardial ischaemia
  • atherosclerosis
  • PLASMINOGEN-ACTIVATOR INHIBITOR
  • ISCHEMIC-HEART-DISEASE
  • DEEP-VEIN THROMBOSIS
  • ACUTE MYOCARDIAL-INFARCTION
  • PLATELET ALPHA-GRANULES
  • FAST-ACTING INHIBITOR
  • VENOUS THROMBOSIS
  • T-PA
  • ENDOTHELIAL-CELLS
  • ANGINA-PECTORIS

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