Pathophysiology and therapeutic modification of thrombin generation in patients with coronary artery disease

Anitha Pothula, Victor L. Serebruany, Paula Gurbel, Marcus E. McKenzie, Dan Atar

Research output: Contribution to journalReview articlepeer-review

Abstract

Thrombin plays a central role in thrombogenesis: it activates platelets, converts fibrinogen to fibrin, and activates factor XIII, which then crosslinks and stabilizes the fibrin clot. In addition, thrombin amplifies coagulation by activating factors VIII and V, key cofactors in the generation of activated factor X and thrombin, respectively. Even platelet function is influenced by thrombin. Hence, thrombin generation is most important both in the chronic progression of coronary atherosclerotic disease and in its conversion to acute events. To date, various therapeutic approaches capitalize on this knowledge by targeting specific thrombin-related pathways. Among the successful and carefully documented pharmacologic strategies in acute or chronic coronary heart disease are the use of unfractioned heparin, low-molecular-weight heparin, thrombolysis, hirudin, and/or inhibition of thrombin generation by glycoprotein IIb/IIIa antagonists, most often utilized on top of antiplatelet therapy (e.g., with acetylsalicylic acid) and/or vitamin K antagonism. The present review provides insights into the pathophysiology of thrombin generation in coronary atherosclerosis and gives an overview over the above mentioned therapeutic thrombin modifications. (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)1-10
Number of pages10
JournalEuropean Journal of Pharmacology
Volume402
Issue number1-2
DOIs
StatePublished - Aug 18 2000

Keywords

  • (Human)
  • Coagulation
  • Coronary artery disease
  • Thrombin

ASJC Scopus subject areas

  • Pharmacology

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