PMID- 22538774
OWN - NLM
STAT- MEDLINE
DCOM- 20121112
LR  - 20171116
IS  - 2567-689X (Electronic)
IS  - 0340-6245 (Linking)
VI  - 108
IP  - 1
DP  - 2012 Jul
TI  - Fibrinolytic status in acute coronary syndromes: evidence of differences in 
      relation to clinical features and pathophysiological pathways.
PG  - 32-40
LID - 10.1160/TH12-01-0011 [doi]
AB  - Limited data are available on the role of innate fibrinolysis in acute coronary 
      syndromes (ACS). In the present study we evaluated the dynamic alterations of 
      fibrinolytic markers in patients presenting with ACS. Tissue-type-(tPA) and 
      urokinase type-(uPA) plasminogen activators, plasminogen activator inhibitor 
      (PAI-1) antigen and activity and thrombin activatable fibrinolysis inhibitor 
      (TAFI) were analysed in 50 patients with ST elevation myocardial infarction 
      (STEMI), 47 non-STEMI patients (NSTEMI), 40 patients with stable coronary artery 
      disease (CAD) and 39 controls. The parameters were measured on day 1 and days 3, 
      7 and 30. Counts of monocyte subsets, monocyte-platelet aggregates and plasma 
      inflammatory cytokines were assessed on admission. On day 1, TAFI was higher in 
      NSTEMI vs. STEMI (p<0.001) while PAI-1 activity was higher in STEMI (p<0.001). In 
      STEMI, uPA activity levels was low on day 1 but significantly increased on day 30 
      (p<0.001). TAFI levels were increased in NSTEMI on day 1 and gradually reduced by 
      day 30 (p<0.05). In STEMI, TAFI levels peaked at day 7 (p<0.05) and dropped 
      significantly by day 30 (p<0.05). CD14++CD16+ monocytes were independently 
      associated with PAI-1 activity in ACS (p=0.03). Monocyte-platelet aggregates 
      rather than platelet-free monocytes were an independent determinant of tPA, PAI-1 
      antigen and TAFI on a multivariate analysis (p<0.05). There are significant 
      differences in fibrinolytic activity between patients with STEMI and NSTEMI. 
      These changes could reflect the role of these factors in post-MI myocardial 
      healing. Monocyte-platelet interactions are independently associated with the 
      regulation of the fibrinolytic status in ACS.
FAU - Shantsila, Eduard
AU  - Shantsila E
AD  - University of Birmingham Centre for Cardiovascular Sciences, City Hospital, 
      Birmingham, UK.
FAU - Montoro-Garcia, Silvia
AU  - Montoro-Garcia S
FAU - Tapp, Luke D
AU  - Tapp LD
FAU - Apostolakis, Stavros
AU  - Apostolakis S
FAU - Wrigley, Benjamin J
AU  - Wrigley BJ
FAU - Lip, Gregory Y H
AU  - Lip GY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120427
PL  - Germany
TA  - Thromb Haemost
JT  - Thrombosis and haemostasis
JID - 7608063
RN  - 0 (Biomarkers)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (Plasminogen Activator Inhibitor 1)
RN  - 0 (Receptors, IgG)
RN  - EC 3.4.17.20 (Carboxypeptidase B2)
RN  - EC 3.4.21.- (Serine Endopeptidases)
RN  - EC 3.4.21.- (urokinase-converting protease)
RN  - EC 3.4.21.68 (Tissue Plasminogen Activator)
SB  - IM
MH  - Acute Coronary Syndrome/*blood/*physiopathology
MH  - Aged
MH  - Biomarkers/blood
MH  - Blood Platelets/*physiology
MH  - Carboxypeptidase B2/blood
MH  - Cell Adhesion
MH  - Female
MH  - Fibrinolysis/*physiology
MH  - Humans
MH  - Lipopolysaccharide Receptors/biosynthesis
MH  - Male
MH  - Middle Aged
MH  - Monocytes/*physiology
MH  - Myocardial Infarction/diagnosis/*physiopathology
MH  - Plasminogen Activator Inhibitor 1/blood
MH  - Receptors, IgG/biosynthesis
MH  - Serine Endopeptidases/blood
MH  - Tissue Plasminogen Activator/blood
EDAT- 2012/04/28 06:00
MHDA- 2012/11/13 06:00
CRDT- 2012/04/28 06:00
PHST- 2012/01/10 00:00 [received]
PHST- 2012/03/24 00:00 [accepted]
PHST- 2012/04/28 06:00 [entrez]
PHST- 2012/04/28 06:00 [pubmed]
PHST- 2012/11/13 06:00 [medline]
AID - 12-01-0011 [pii]
AID - 10.1160/TH12-01-0011 [doi]
PST - ppublish
SO  - Thromb Haemost. 2012 Jul;108(1):32-40. doi: 10.1160/TH12-01-0011. Epub 2012 Apr 
      27.