Document Detail

Usefulness of fibrinogenolytic and procoagulant markers during thrombolytic therapy in predicting clinical outcomes in acute myocardial infarction. TIMI-5 Investigators. Thrombolysis in Myocardial Infarction.
MedLine Citation:
PMID:  8806332     Owner:  NLM     Status:  MEDLINE    
Thrombin activity is increased in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic therapy for acute infarction. This increase in thrombin activity may play an important role in the 15% to 25% rate of failure to achieve initial reperfusion and in the 5% to 15% rate of early reocclusion after initially successful thrombolysis. To investigate potential mechanisms of thrombin formation in vivo, to understand better the balance of coagulation and fibrinolysis during treatment with recombinant tissue-type plasminogen activator (rt-PA), and to investigate the role of hemostatic markers as predictors of clinical events, we measured 3 markers of procoagulant activity: fibrinopeptide A (FPA), thrombin-antithrombin III complexes (TAT), and prothrombin fragment 1.2 (F1.2), and a marker of fibrinogenolytic activity (B beta 1-42) in patients enrolled in the Thrombolysis in Myocardial Infarction (TIMI)-5 study. This trial was a randomized, dose-ranging, pilot trial of hirudin versus heparin as adjunctive antithrombotic therapy with rt-PA administered to patients with AMI. Correlation of markers at 1 hour with clinical outcomes revealed that increased FPA and TAT levels were associated with increased mortality and TIMI grades 0, 1, or 2 flow at 90 minutes; increased F1.2 levels were associated with TIMI grade 0 or 1 flow at 90 minutes; and increased levels of all 3 procoagulant markers were associated with hemorrhagic events. Late (12 to 24 hours) increases in F1.2, TAT, and B beta 1-42 may be predictive of recurrent ischemia. These results suggest that selected markers of procoagulant and fibrinogenolytic activity may be useful in predicting clinical outcomes in patients treated with thrombolytic therapy for AMI.
J S Scharfstein; D R Abendschein; P R Eisenberg; D George; C P Cannon; R C Becker; B Sobel; L A Cupples; E Braunwald; J Loscalzo
Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial    
Journal Detail:
Title:  The American journal of cardiology     Volume:  78     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  1996 Sep 
Date Detail:
Created Date:  1996-10-22     Completed Date:  1996-10-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  503-10     Citation Subset:  AIM; IM    
Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts, USA.
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MeSH Terms
Antithrombin III / analysis*
Biological Markers
Fibrin Fibrinogen Degradation Products / analysis*
Fibrinolytic Agents / therapeutic use
Fibrinopeptide A / analysis*
Heparin / therapeutic use*
Hirudin Therapy
Myocardial Infarction / drug therapy*
Peptide Fragments / analysis*
Peptide Hydrolases / analysis*
Pilot Projects
Prothrombin / analysis*
Recombinant Proteins
Thrombolytic Therapy*
Treatment Outcome
Reg. No./Substance:
0/Biological Markers; 0/Fibrin Fibrinogen Degradation Products; 0/Fibrinolytic Agents; 0/Peptide Fragments; 0/Recombinant Proteins; 0/antithrombin III-protease complex; 0/fibrinogen Bbeta (15-42); 0/prothrombin fragment 1.2; 25422-31-5/Fibrinopeptide A; 9000-94-6/Antithrombin III; 9001-26-7/Prothrombin; 9005-49-6/Heparin; EC 3.4.-/Peptide Hydrolases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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