Hemocoagulation – New views on the old cascade

Czech version

Authors: Jan F. Vojáček
Authors‘ workplace: I. interní kardioangiologická klinika LF UK a FN Hradec Králové, přednosta doc. MUDr. Josef Šťásek, CSc.
Published in: Vnitř Lék 2015; 61(5): 475-479
Category: Reviews

Overview

The process of hemocoagulation can be generally divided into the following stages: initiation, amplification, propagation and stabilization of thrombus. The most important changes of the hemocoagulation scheme accepted so far concern the position and generally the existence of the coagulation system external and internal branches, the central role of a tissue factor in initiation of hemocoagulation and the newly understood roles of factors XI and XII. Newly an active role of monocytes, leukocytes, erythrocytes and endothelial cells and their receptors in hemocoagulation has been identified, as well as the role of circulating microparticles which transfer some agents and information. The changed scheme of hemocoagulation also reflects the emerging possibilities of anticoagulation with a more favourable proportion of anticoagulation properties to the risk of bleeding and thrombotic events. Over the long term it is increasingly evident that both the internal and external branches of the coagulation system are initially launched through release of an active tissue factor, formation of a complex of a tissue factor with factor VIIa and ensuing activation of factor X on Xa. At the same time the role of factor XII in the intrinsic coagulation system is questioned, its role has now been experimentally proven together with factor XI in propagation and with factor XIII in the final strengthening of thrombus and when seeking new antithrombotic drugs it might be just its blocking which could meet the requirement on high effectiveness with minimum bleeding complications.

Key words:
hemocoagulation – hemocoagulation cascade – microparticles – new antithrombotic drugs – tissue factor – internal branch of coagulation system – external branch of coagulation system

Sources

1. Mackman N. New Targets for Atherothrombosis. Arterioscler Thromb Vasc Biol 2014; 34(8): 1607–1608.

2. Bogdanov VY, Balasubramanian V, Hathcock J et al. Alternatively spliced human tissue factor: a circulating, soluble, thrombogenic protein. Nat Med 2003; 9(4): 458–462.

3. Bode M, Mackman N. Regulation of tissue factor gene expression in monocytes and endothelial cells: Thromboxane A2 as a new player. Vascul Pharmacol 2014; 62(2): 57–62.

4. Vojacek J, Dusek J, Bis J et al. Plasma tissue factor in coronary artery disease: further step to the understanding of the basic mechanisms of coronary artery thrombosis. Physiol Res 2008; 57(1): 1–5.

5. Vojacek J, Sevcikova H, Sevcik R et al. Increased platelet residual activity in patients treated with acetosalicylic acid is associated with increased tissue factor and decreased tissue factor pathway inhibitor plasma levels. Int J Cardiol 2011; 146(3): 479–481.

6. Bis J, Vojacek J, Dusek J et al. Time-course of tissue factor plasma level in patients with acute coronary syndrome. Physiol Res 2009; 58(5): 661–667.

7. Maly M, Vojacek J, Hrabos V et al. Tissue factor, tissue factor pathway inhibitor and cytoadhesive molecules in patients with an acute coronary syndrome. Physiol Res 2003; 52(6): 719–728.

8. Mallat Z, Hugel B, Ohan J et al. Shed membrane microparticles with procoagulant potential in human atherosclerotic plaques: a role for apoptosis in plaque thrombogenicity. Circulation 1999; 99(3): 348–353.

9. Pryzdial EL, Sutherland MR, Ruf W. The Procoagulant Envelope Virus Surface: Contribution to Enhanced Infection. Thromb Res 2014; 133(Suppl 1): S15-S17.

10. Hoffman M, Pawlinski R. Hemostasis: Old System, New Players, New Directions. Thromb Res 2014; 133(Suppl 1): S1-S2.

11. Tilley RE, Holscher T, Belani R et al. Tissue factor activity is increased in a combined platelet and microparticle sample from cancer patients. Thromb Res 2008; 122(5): 604–609.

12. Vatsyayan R, Kothari H, Mackman N et al. Inactivation of Factor VIIa by Antithrombin In Vitro, Ex Vivo and In Vivo: Role of Tissue Factor and Endothelial Cell Protein C Receptor. PLoS ONE 2014; 9(8): e103505. Dostupné z DOI: <http://doi: 10.1371/journal.pone.0103505>.

13. Kuijpers MJE, van der Meijden PEJ, Feijge MAH et al. Factor XII regulates the pathological process of thrombus formation on ruptured plaques. Arterioscler Thromb Vasc Biol 2014; 34(8): 1674–1680.

14. Yarovaya GA, Blokhina TB, Neshkova EA. Contact System. New Concepts on Activation Mechanisms and Bioregulatory Functions. Biochemistry (Mosc) 2002; 67(1): 13–24.

15. Kane WH, Lindhout MJ, Jackson CM et al. Factor Va-dependent binding of factor Xa to human platelets. J Biol Chem 1980; 255(3): 1170–1174.

16. LaBonte ML. Anticoagulant factor V: Factors affecting the integration of novel scientific discoveries into the broader Framework. Stud Hist Philos Biol Biomed Sci 2014; 47(Pt A): 23–34.

17. Rao LVM, Esmon CT, Pendurthi UR. Endothelial cell protein C receptor: a multiliganded and multifunctional receptor. Blood 2014; 124(10): 1553–1562.

18. Navarro S, Bonet E, Estellés A et al. The endothelial cell protein C receptor: Its role in thrombosis. Thromb Res 2011; 128(5): 410–416.

19. López-Sagaseta J, Montes R, Puy C et al. Binding of factor VIIa to the endothelial cell protein C receptor reduces its coagulant activity. J Thromb Haemost 2007; 5(9): 1817–1824.

20. Hopff F. Über die Hämophilie oder die Erbliche Anlage zu Tödlichen Blutungen (Inaugural- Abhandlung). Carl Wilhelm Becker: Würzburg: 1928.

21. Patek AJ, Taylor FH. Hemophilia: Some properties of a substance obtained from normal human plasma effective in accelerating the coagulation of hemophilic blood. J Clin Invest 1937; 16(1): 113–124.

22. Pavlovsky A. Contribution to the pathogenesis of hemophilia. Blood 1947; 2(2): 185–191.

23. Choi Q, Kim JE, Kim SY et al. Influence of ABO type on global coagulation assay results: effect of coagulation factor VIII. Clin Chem Lab Med. 2014; pii: /j/cclm.ahead-of-print/cclm-2014–0909/cclm-2014–0909.xml. Dostupné z DOI: <http://dx.doi.org/10.1515/cclm-2014–0909>.

24. Vacek TP, Yu S, Rehman S et al. Recurrent myocardial infarctions in a young football player secondary to thrombophilia, associated with elevated factor VIII activity. Int Med Case Rep J 2014; 7: 147–154.

25. Hoppe B. Fibrinogen and factor XIII at the intersection of coagulation, fibrinolysis and inflammation. Thromb Haemost 2014; 112(4): 649–658.

26. Aleman MM, Byrnes JR, Wang JG et al. Factor XIII activity mediates red blood cell retention in venous thrombi. J Clin Invest 2014; 124(8): 3590–3600.

27. Mitchell JL, Lionikiene AS, Fraser SR et al. Functional factor XIII-A is exposed on the stimulated platelet surface. Blood 2014; 124(26): 3982–3990.

28. Miszta A, Pelkmans L, Lindhout T et al. Thrombin-dependent Incorporation of von Willebrand Factor into a Fibrin Network. J Biol Chem 2014; 289(52): 35979–3586.

29. Árokszállási A, Kerényi A, Katona É et al. The use of recombinant factor XIII in a major bleeding episode of a patient with congenital factor XIII deficiency – the first experience. Haemophilia 2015; 21(1): e118-e121.

30. Nugent DJ, Ashley C, García-Talavera J et al. Pharmacokinetics and safety of plasma-derived factor XIII concentrate (human) in patients with congenital factor XIII deficiency. Haemophilia 2015; 21(1): 95–101.

31. Ashley C, Chang E, Davis J et al. Efficacy and safety of prophylactic treatment with plasma-derived factor XIII concentrate (human) in patients with congenital factor XIII deficiency. Haemophilia 2015; 21(1): 102–108.

32. van Montfoort ML, Kuijpers MJE, Knaup VL et al. Factor XI Regulates Pathological Thrombus Formation on Acutely Ruptured Atherosclerotic Plaques. Arterioscler Thromb Vasc Biol 2014; 34(8): 1668–1673.