PMID- 22424853
OWN - NLM
STAT- MEDLINE
DCOM- 20130131
LR  - 20151119
IS  - 1879-2472 (Electronic)
IS  - 0049-3848 (Linking)
VI  - 130
IP  - 3
DP  - 2012 Sep
TI  - Lower tissue factor inhibition in patients with ST segment elevation than in 
      patients with non ST elevation acute myocardial infarction.
PG  - 458-62
LID - 10.1016/j.thromres.2012.02.044 [doi]
AB  - INTRODUCTION: Mechanisms to explain the different course of coronary thrombosis 
      between ST elevation myocardial infarction (STEMI) and non-STEMI patients remain 
      poorly defined. We hypothesize, however, that STEMI patients may present lower 
      tissue factor plasma inhibition to partly account for their more persistent 
      coronary thrombotic occlusion. MATERIALS AND METHODS: Total (t-TFPI ) and free 
      tissue factor plasma inhibitor (f-TFPI), thrombin-antithrombin complex (TAT), 
      plasminogen activator inhibitor 1 (PAI-1), von Willebrand factor (vWF), and 
      fibrinogen were measured on admission and at 3 and 6 months in patients with a 
      first STEMI (n:69) or non-STEMI (n:60). C reactive protein (CRP) was also 
      measured on admission and at 3 months. RESULTS: STEMI patients showed lower 
      admission levels of t-TFPI (p=0.001), f-TFPI (p=0.030) and fibrinogen (p=0.022), 
      and higher vWF levels (p=0.005) than non-STEMI whereas TAT, PAI and CRP levels 
      were comparable. At 3 and 6 months VWF, t-TFPI, f-TFPI, and TAT levels declined 
      significantly in the 2 groups (p=0.002) reaching similar values. CRP levels also 
      declined at 3 months (p=0.002). Moreover, the rate of cardiac mortality, non 
      fatal MI or stroke during a 6 year follow-up were unrelated to admission 
      coagulation parameters. CONCLUSIONS: The lower inhibition of tissue factor and 
      greater endothelial dysfunction in STEMI than in non-STEMI patients may enhance 
      thrombosis at the culprit lesion and adjacent coronary plaques, and hence, 
      account at least in part for their different pathophysiology. This condition, 
      however, is limited to the acute phase.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Figueras, Jaume
AU  - Figueras J
AD  - Unitat Coronaria, Area del Cor, Hospital Universitari Vall d'Hebron, Barcelona, 
      Spain. 5751jfb@comb.es
FAU - Monasterio, Jasone
AU  - Monasterio J
FAU - Lidon, Rosa M
AU  - Lidon RM
FAU - Sambola, Antonia
AU  - Sambola A
FAU - Garcia-Dorado, David
AU  - Garcia-Dorado D
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120316
PL  - United States
TA  - Thromb Res
JT  - Thrombosis research
JID - 0326377
RN  - 0 (Biomarkers)
RN  - 0 (Blood Coagulation Factors)
RN  - 0 (Plasminogen Activator Inhibitor 1)
RN  - 9001-32-5 (Fibrinogen)
RN  - 9035-58-9 (Thromboplastin)
SB  - IM
MH  - Biomarkers/blood
MH  - Blood Coagulation Factors/*analysis
MH  - Comorbidity
MH  - Coronary Thrombosis/*blood/*epidemiology
MH  - Female
MH  - Fibrinogen/*analysis
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*blood/*epidemiology
MH  - Plasminogen Activator Inhibitor 1/blood
MH  - Reproducibility of Results
MH  - Sensitivity and Specificity
MH  - Spain/epidemiology
MH  - Thromboplastin/*analysis/antagonists & inhibitors
EDAT- 2012/03/20 06:00
MHDA- 2013/02/01 06:00
CRDT- 2012/03/20 06:00
PHST- 2011/12/16 00:00 [received]
PHST- 2012/02/20 00:00 [revised]
PHST- 2012/02/22 00:00 [accepted]
PHST- 2012/03/20 06:00 [entrez]
PHST- 2012/03/20 06:00 [pubmed]
PHST- 2013/02/01 06:00 [medline]
AID - S0049-3848(12)00092-8 [pii]
AID - 10.1016/j.thromres.2012.02.044 [doi]
PST - ppublish
SO  - Thromb Res. 2012 Sep;130(3):458-62. doi: 10.1016/j.thromres.2012.02.044. Epub 
      2012 Mar 16.