Thromb Haemost 2001; 85(03): 377-378
DOI: 10.1055/s-0037-1615592
Commentary
Schattauer GmbH

Conventional Fibrinolytic Assays for the Evaluation of Patients with Venous Thrombosis: Don’t Bother

Kenneth A. Bauer
1   Hematology Section, VA Boston Healthcare System and Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
08. Dezember 2017 (online)

Summary

Hypofibrinolysis, as defined by an absent or deficient increase in blood or plasma fibrinolytic activity after an appropriate stimulus, has been known to be present in patients following an episode of deep venous thrombosis for over 30 years. The usual stimulus is 10 min of venous occlusion using a blood pressure cuff inflated to a pressure midway between systolic and diastolic pressures. The early screening fibrinolytic assays were relatively insensitive in detecting fibrinolytic system hypofunction and lacked standardization.

Supported in part by the Medical Research Service of the Department of Veterans Affairs.

 
  • References

  • 1 Nilsson IM, Ljungner H, Tengborn L. Two different mechanisms in patients with venous thrombosis and defective fibrinolysis: low concentration of plasminogen activator or increased concentration of plasminogen activator inhibitor. Br Med J 1985; 290: 1453-56.
  • 2 Wiman B, Ljungberg B, Chmielewska J, Urden G, Blombäck M, Johnsson H. The role of the fibrinolytic system in deep venous thrombosis. J Lab Clin Med 1985; 105: 265-70.
  • 3 Juhan-Vague I, Valadier J, Alessi MC, Aillaud MF, Ansaldi J, Philip-Joet C, Holvoet P, Serradimigni A, Collen D. Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis. Thromb Haemost 1987; 57: 67-72.
  • 4 Nguyen G, Horellou MH, Kruithof EKO, Conard J, Samama MM. Residual plasminogen activator activity after venous stasis as a criterion for hypofibrinolysis: a study in 83 patients with confirmed deep venous thrombosis. Blood 1988; 72: 601-5.
  • 5 Engesser L, Brommer EJP, Kluft C, Briët E. Elevated plasminogen activator inhibitor (PAI), a cause of thrombophilia? – A study in 203 patients with familial or sporadic venous thrombophilia. Thromb Haemost 1989; 62: 673-80.
  • 6 Grimaudo V, Bachmann F, Hauert J, Christe MA, Kruithof EKO. Hypofibrinolysis in patients with a history of idiopathic deep venous thrombosis and/or pulmonary embolism. Thromb Haemost 1992; 67: 397-401.
  • 7 Juhan-Vague I, Alessi MC. Regulation of fibrinolysis in the development of atherthrombosis: Role of adipose tissue. Thromb Haemost 1999; 82: 832-6.
  • 8 Johansson L, Hedner U, Nilsson IM. A family with thromboembolic disease associated with deficient fibrinolytic activity in vessel wall. Acta Med Scand 1978; 203: 477-80.
  • 9 Jorgensen M, Mortensen JZ, Madsen AG, Thorsen S, Jacobsen BA. A family with reduced plasminogen activator activity in blood associated with recurrent venous thrombosis. Scand J Haematol 1982; 29: 217-23.
  • 10 Stead NW, Bauer KA, Kinney TR, Lewis JG, Campbell EE, Shifman MA, Rosenberg RD, Pizzo SV. Venous thrombosis in a family with defective release of vascular plasminogen activator and elevated plasma factor VIII/von Willebrand factor. Am J Med 1983; 74: 33-9.
  • 11 Bolan CD, Krishnamurti C, Tang DB, Carrington LR, Alving BM. Association of protein S deficiency with thrombosis in a kindred with elevated levels of plasminogen activator-1. Ann Intern Med 1993; 119: 779-85.
  • 12 Zöller B, Dahlbäck B, Protein S. deficiency in a large family with thrombophilia previously characterized as having an inherited fibrinolytic defect (abstract). Thromb Haemost 1993; 69: 1256.
  • 13 Korninger C, Lechner K, Niessner H, Gössinger H, Kundi M. Impaired fibrinolytic capacity predisposes for recurrence of venous thrombosis. Thromb Haemost 1984; 52: 127-30.
  • 14 Schulman S, Wiman B. The significance of hypofibrinolysis for the risk of recurrence of venous thromboembolism. Duration of Anticoagulation (DURAC) Trial Study Group. Thromb Haemost 1996; 75: 607-11.
  • 15 Malm J, Laurell M, Nilsson IM, Dählback B. Thromboembolic disease – Critical evaluation of laboratory investigation. Thromb Haemost 1992; 68: 7-13.
  • 16 Crowther MA, Roberts J, Roberts R, Johnston M, Stevens P, Skingley P, Patrassi GM, Sartori MT, Hirsh J, Prandoni P, Weitz JI, Gent M, Ginsberg JS. Fibrinolytic variables in patients with recurrent venous thrombosis: a prospective cohort study. Thromb Haemost 2001; 85: 390-4.
  • 17 Lensing AWA, Prins MH. Recurrent deep vein thrombosis and two coagulation factor gene mutations: Quo vadis?. Thromb Haemost 1999; 82: 1564-6.
  • 18 Koster T, Rosendaal FR, de Ronde H, Briët E, Vandenbroucke JP, Bertina RM. Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden thrombophilia study. Lancet 1993; 342: 1503-6.
  • 19 Bertina RM, Koeleman BPC, Koster T, Rosendaal FR, Dirven RJ, de Ronde H, van der Velden PA, Reitsma PH. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 1994; 369: 64-7.
  • 20 Ridker PM, Hennekens CH, Lindpaintner K, Stampfer MJ, Eisenberg PR, Miletich JP. Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. N Engl J Med 1995; 332: 912-7.
  • 21 Poort SR, Rosendaal FR, Reitsma PH, Bertina RM. A common genetic variation in the 3′-untranslated region of the prothrombin gene is associated with elevated prothrombin levels and an increase in venous thrombosis. Blood 1996; 88: 3698-703.
  • 22 Bouma BN, von dem Borne PAK, Meijers JCM. Factor XI and protection of the fibrin clot against lysis – a role for the intrinsic pathway of coagulation in fibrinolysis. Thromb Haemost 1998; 80: 24-7.
  • 23 von dem Borne PAK, Bajzar L, Meijers JCM, Nesheim ME, Bouma BN. Thrombin-mediated activation of factor XI results in a TAFI (thrombin activatable fibrinolysis inhibitor) dependent inhibition of fibrinolysis. J Clin Invest 1997; 99: 2323-7.
  • 24 Meijers JCM, Tekelenberg W, Bouma BN, Bertina RM, Rosendaal FR. High levels of coagulation factor XI as a risk factor for venous thrombosis. N Engl J Med 1999; 342: 696-701.