Articles |
From the Washington University School of Medicine, Cardiovascular Division, St. Louis, Mo.
Correspondence to Paul R. Eisenberg, MD, MPH, Washington University School of Medicine, Cardiovascular Division, Box 8086, 660 S Euclid Ave, St. Louis, MO 63110. E-mail eisenber{at}visar.wustl.edu
Abstract Recently, increases in the plasma concentration of soluble fibrin (SF) have been suggested to be sensitive and specific for myocardial infarction (MI). However, the relationship between elevations in the SF concentration and the onset of symptoms and clinical course of MI is unknown. In addition, there are no data regarding the relationship between SF concentrations and concentrations of other markers of procoagulant (fibrinopeptide A [FPA]) and fibrinolytic (cross-linked fibrin degradation products [XL-FDPs]) activity in patients with MI. In this study, concentrations of SF were measured with a novel antigen-based assay for 93 MI patients and 29 control subjects, and the relationship between SF concentrations and those of XL-FDPs and FPA was determined. Increases in SF, FPA, and XL-FDP concentrations were documented in 55.9%, 45.2%, and 73.9%, respectively, of patients with MI, but there was no relationship between the concentrations of these markers. Increases in the concentration of SF or XL-FDPs did not show a relationship to increases in the concentration of FPA. Concentrations of XL-FDPs but not of SF were elevated to a greater extent in patients with MI complications (defined as death, ventricular arrhythmia, severe congestive heart failure, or mural thrombus). Increases in SF and XL-FDPs were not sensitive enough for the diagnosis of MI, but increased concentrations of XL-FDPs appear to predict those patients who are at higher risk for MI-related complications.
Key Words: myocardial infarction soluble fibrin fibrinopeptide A cross-linked fibrin degradation products
This article has been cited by other articles:
![]() |
J. L. Mega, D. A. Morrow, J. A. de Lemos, S. Mohanavelu, C. P. Cannon, and M. S. Sabatine Thrombus precursor protein and clinical outcomes in patients with acute coronary syndromes. J. Am. Coll. Cardiol., June 24, 2008; 51(25): 2422 - 2429. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Derhaschnig, A. N. Laggner, M. Roggla, M. M. Hirschl, S. Kapiotis, C. Marsik, and B. Jilma Evaluation of Coagulation Markers for Early Diagnosis of Acute Coronary Syndromes in the Emergency Room Clin. Chem., November 1, 2002; 48(11): 1924 - 1930. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Oldgren, R. Linder, L. Grip, A. Siegbahn, and L. Wallentin Coagulation Activity and Clinical Outcome in Unstable Coronary Artery Disease Arterioscler Thromb Vasc Biol, June 1, 2001; 21(6): 1059 - 1064. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. J. Teede, B. P. McGrath, J. J. Smolich, E. Malan, D. Kotsopoulos, Y.-L. Liang, and R. E. Peverill Postmenopausal Hormone Replacement Therapy Increases Coagulation Activity and Fibrinolysis Arterioscler Thromb Vasc Biol, May 1, 2000; 20(5): 1404 - 1409. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Linder, J. Oldgren, N. Egberg, L. Grip, G. Larson, A. Siegbahn, and L. Wallentin The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease Eur. Heart J., April 1, 1999; 20(7): 506 - 518. [Abstract] [PDF] |
||||
![]() |
R. H. Christenson and H. M. E. Azzazy Biochemical markers of the acute coronary syndromes Clin. Chem., August 1, 1998; 44(8): 1855 - 1864. [Abstract] [Full Text] [PDF] |
||||
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1997 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |