P2980 Proteolysis of tissue factor pathway inhibitor-1 on circulating tissue factor bearing microparticles by thrombolysis in acute myocardial infarction is associated to an increased thrombin generation

2003 ◽  
Vol 24 (5) ◽  
pp. 579 ◽  
Author(s):  
B STEPPICH
2000 ◽  
Vol 75 (2-3) ◽  
pp. 267-274 ◽  
Author(s):  
Nobuyasu Yamamoto ◽  
Hisao Ogawa ◽  
Shuichi Oshima ◽  
Hirofumi Soejima ◽  
Hiromi Fujii ◽  
...  

2001 ◽  
Vol 78 (2) ◽  
pp. 115-119 ◽  
Author(s):  
Vanessa Roldán ◽  
Francisco Marín ◽  
Pascual Fernández ◽  
Juan Luján ◽  
Juan G. Martínez ◽  
...  

Blood ◽  
2001 ◽  
Vol 97 (12) ◽  
pp. 3721-3726 ◽  
Author(s):  
Ilka Ott ◽  
Martin Andrassy ◽  
Dominik Zieglgänsberger ◽  
Stefanie Geith ◽  
Albert Schömig ◽  
...  

In acute myocardial infarction (AMI), monocyte procoagulant activity is increased and may contribute to the risk for recurrence and other thrombotic events. This study sought to investigate the role tissue factor (TF) and tissue factor pathway inhibitor-1 (TFPI-1) in the regulation of monocyte procoagulant activity in AMI. Serial venous blood samples were obtained from 40 patients with AMI undergoing revascularization by stent placement. Twenty patients with elective stenting for stable angina served as control subjects. TF proteolytic activity was measured with spectrozyme factor Xa (FXa), TF and TFPI-1 surface expression on monocytes by flow cytometry, RNA expression in whole blood by reverse transcription–polymerase chain reaction, and concentrations of plasma prothrombin fragments F1 + 2 by immunoassay. Forty-eight hours after AMI, an increase was found in TF RNA, followed by an increase in TF surface expression by 24% ± 4% and in plasma concentration of F1 + 2 by 103% ± 17% (P < .05). These changes could not be attributed to the intervention because they did not occur in the control group. TFPI-1 RNA and binding to the monocyte surface remained unchanged. FXa generation by monocytes of patients with AMI increased 53.6% ± 9% in the presence of polyclonal antibodies to TFPI-1, indicating that cell-associated TFPI-1 inhibits monocyte TF activity. The increased monocyte procoagulant activity in AMI was caused by an up-regulation of TF that was partially inhibited by surface-bound TFPI-1. Anticoagulant therapy by direct inhibition of TF activity may, thus, be particularly effective in AMI.


Circulation ◽  
2002 ◽  
Vol 105 (3) ◽  
pp. 279-281 ◽  
Author(s):  
Ilka Ott ◽  
Valerie Malcouvier ◽  
Albert Schömig ◽  
Franz-Josef Neumann

Author(s):  
Yuko Kamikura ◽  
Hideo Wada ◽  
Atsushi Yamada ◽  
Minori Shimura ◽  
Katsuyo Hiyoyama ◽  
...  

2017 ◽  
Vol 14 (2) ◽  
pp. 144-151 ◽  
Author(s):  
Vibeke Bratseth ◽  
Rune Byrkjeland ◽  
Ida U Njerve ◽  
Svein Solheim ◽  
Harald Arnesen ◽  
...  

We investigated the effects of 12-month exercise training on hypercoagulability in patients with combined type 2 diabetes mellitus and coronary artery disease. Associations with severity of disease were further explored. Patients ( n = 131) were randomized to exercise training or a control group. Blood was collected at inclusion and after 12 months. Tissue factor, free and total tissue factor pathway inhibitor, prothrombin fragment 1 + 2 (F1 + 2) and D-dimer were determined by enzyme-linked immunosorbent assay and ex vivo thrombin generation by the calibrated automated thrombogram assay. Tissue factor and ex vivo thrombin generation increased from baseline to 12 months ( p < 0.01, all), with no significant differences in changes between groups. At baseline, free and total tissue factor pathway inhibitor significantly correlated to fasting glucose ( p < 0.01, both) and HbA1c ( p < 0.05, both). In patients with albuminuria ( n = 34), these correlations were strengthened, and elevated levels of D-dimer, free and total tissue factor pathway inhibitor ( p < 0.01, all) and decreased ex vivo thrombin generation ( p < 0.05, all) were observed. These results show no effects of exercise training on markers of hypercoagulability in our population with combined type 2 diabetes mellitus and coronary artery disease. The association between poor glycaemic control and tissue factor pathway inhibitor might indicate increased endothelial activation. More pronounced hypercoagulability and increased tissue factor pathway inhibitor were demonstrated in patients with albuminuria.


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