Copyright © 1993 by the European Society of Cardiology.
© 1993 The European Society of Cardiology
Platelet function, thrombin and fibrinolytic activity in patients with heart failure


*Heart and Vascular Institute, Henry Ford Hospital Detroit, Michigan, U.S.A.
Wayne State University School of Medicine Detroit, Michigan, U.S.A.
Received 28 January 1992; .
Correspondence: Syed M. Jafri, MD, Heart and Vascular Institute, Division of Cardiovascular Medicine, Henry Ford Hospital, 2799 West Grand Blvd. Detroit, M1 48202, U.S.A.
Abstract
Assays which detect the release of platelet proteins and of pep tides during thrombogenesis and are considered markers of activation of platelets and the coagulation system have recently been developed. This study was designed to utilize these haemostasis-related markers to lest the hypothesis that a prethrombotic state is related to the presence, aetiology and severity of heart failure. Seventy patients with heart failure were evaluated and data were compared with 36 normal volunteers and 41 patients with coronary artery disease without heart failure (CAD). Thrombogenesis was documented using assays which measure platelet function, thrombin activity and fibrinolysis. Platelet function was measured by determining plasma concentrations of platelet factor 4 (PF4) and beta-thromboglobulin (BTG). Thrombin antithrombin III complexes (TAT) and fibrinopeptide A (FPA) were determined to evaluate thrombin activity. Fibrinolyric activity was assessed by measuring D-Dimer levels. Patients with heart failure, when compared to normals, had increased plasma levels of BTG (89±62 IU. ml1 vs 50±59 IU. ml1, P<0.01), TAT (4.6±4.3 µg. l1 vs 2.3±0.64 µg. l1, P<0.005 and D-Dimer levels (506±444 IU. ml1 vs 191±144 IU. ml1, P < 0.0001). Patients with heart failure, when compared to the CAD group, had increased plasma levels of D-Dimer (506±444 ng. ml1 vs 191±144 ng. ml1, P <0.05). Aetiology of heart failure did not affect these measurements. Patients with severe heart failure, as determined by high plasma norepinephrine concentration or low ejection fraction, were more likely to have activation of platelets and the coagulation system. Our study indicates that patients with heart failure have evidence of increased platelet and thrombin activation and fibrinolytic activity. These abnormalities are most pronounced in patients with severe heart failure.
Key Words: Thrombo-embolism Coagulation Platelets thrombogenesis
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
R. C. Becker, T. W. Meade, P. B. Berger, M. Ezekowitz, C. M. O'Connor, D. A. Vorchheimer, G. H. Guyatt, D. B. Mark, and R. A. Harrington The Primary and Secondary Prevention of Coronary Artery Disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) Chest, June 1, 2008; 133(6_suppl): 776S - 814S. [Abstract] [Full Text] [PDF] |
||||
![]() |
C Stumpf, C Lehner, D Raaz, A Yilmaz, T Anger, W G Daniel, and C D Garlichs Platelets contribute to enhanced MCP-1 levels in patients with chronic heart failure Heart, January 1, 2008; 94(1): 65 - 69. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Chung and G. Y.H. Lip Platelets and heart failure Eur. Heart J., November 2, 2006; 27(22): 2623 - 2631. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Nair, B. Sealove, J. L. Halperin, G. Webber, and V. Fuster Anticoagulation in patients with heart failure: who, when, and why? Eur. Heart J. Suppl., September 1, 2006; 8(suppl_E): E32 - E38. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Pulido, A. Aranda, M. A. Zevallos, E. Bautista, M. L. Martinez-Guerra, L. E. Santos, and J. Sandoval Pulmonary Embolism as a Cause of Death in Patients With Heart Disease: An Autopsy Study Chest, May 1, 2006; 129(5): 1282 - 1287. [Abstract] [Full Text] [PDF] |
||||
![]() |
G Y H Lip, L A Pearce, B S P Chin, D S G Conway, and R G Hart Effects of congestive heart failure on plasma von Willebrand factor and soluble P-selectin concentrations in patients with non-valvar atrial fibrillation Heart, June 1, 2005; 91(6): 759 - 763. [Abstract] [Full Text] [PDF] |
||||
![]() |
D Tousoulis, C Antoniades, E Bosinakou, M Kotsopoulou, C Tsioufis, C Tentolouris, A Trikas, C Pitsavos, and C Stefanadis Effects of atorvastatin on reactive hyperaemia and the thrombosis-fibrinolysis system in patients with heart failure Heart, January 1, 2005; 91(1): 27 - 31. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. A. Harrington, R. C. Becker, M. Ezekowitz, T. W. Meade, C. M. O'Connor, D. A. Vorchheimer, and G. H. Guyatt Antithrombotic Therapy for Coronary Artery Disease: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 513S - 548S. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. K. Damas, L. Gullestad, T. Ueland, N. O. Solum, S. Simonsen, S. S Froland, and P. Aukrust CXC-chemokines, a new group of cytokines in congestive heart failure -- possible role of platelets and monocytes Cardiovasc Res, January 14, 2000; 45(2): 428 - 436. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Dikalov, B. Fink, M. Skatchkov, O. Sommer, and E. Bassenge Formation of Reactive Oxygen Species in Various Vascular Cells During Glyceryltrinitrate Metabolism Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1998; 3(1): 51 - 61. [Abstract] [PDF] |
||||





