PMID- 16113834
OWN - NLM
STAT- MEDLINE
DCOM- 20051221
LR  - 20181201
IS  - 0340-6245 (Print)
IS  - 0340-6245 (Linking)
VI  - 94
IP  - 2
DP  - 2005 Aug
TI  - Abciximab therapy is associated with increased platelet activation and decreased 
      heparin dosage in patients with acute myocardial infarction.
PG  - 422-6
AB  - The inhibition of the glycoprotein (GP) IIb/IIIa receptor for reducing 
      periprocedural ischemic events in patients undergoing coronary intervention is 
      known to influence platelet reactivity. Suboptimal doses of GP IIb/IIIa 
      antagonists have been suggested to be prothrombotic and proinflammatory. This 
      study was performed to observe platelet activation markers, whole blood 
      aggregation and the dosage of unfractionated heparin (UFH) in the presence or 
      absence of the GP IIb/IIIa inhibitor abciximab. Patients with acute myocardial 
      infarction undergoing percutaneous coronary intervention were treated with (n = 
      15) or without (n = 15) abciximab. Platelet activation markers were flow 
      cytometrically measured before and after PCI. Whole blood platelet aggregation 
      was tested by a platelet function assay. The patients with abciximab showed a 
      significant increase in platelet activation markers (P-selectin: 7.12 +/- 0.36 AU 
      vs 11.05 +/- 0.79 AU) and a lower requirement of UFH to prolong aPTT > 60 sec 
      during the infusion. 12 hours after infusion P-selectin level decreased (7.20 +/- 
      0.58 AU), whereas whole blood aggregation was increasing again. After stopping 
      abciximab, requirement of UFH to prolong aPTT increased in the treated group to a 
      greater extent to a level similar to the untreated group even when most of the 
      platelets were still inhibited. The increased platelet activation found at the 
      end of abciximab treatment points to a procoaguable condition that should be 
      carefully monitored and treated by adapting anticoagulation and antiplatelet 
      drugs.
FAU - Piorkowski, Michael
AU  - Piorkowski M
AD  - Department of Internal Medicine/Cardiology, Charite - Universitatsmedizin Berlin, 
      Campus, Germany.
FAU - Priess, Jana
AU  - Priess J
FAU - Weikert, Ulf
AU  - Weikert U
FAU - Jaster, Markus
AU  - Jaster M
FAU - Schwimmbeck, Peter-Lothar
AU  - Schwimmbeck PL
FAU - Schultheiss, Heinz-Peter
AU  - Schultheiss HP
FAU - Rauch, Ursula
AU  - Rauch U
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Thromb Haemost
JT  - Thrombosis and haemostasis
JID - 7608063
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Immunoglobulin Fab Fragments)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 0 (Platelet Glycoprotein GPIIb-IIIa Complex)
RN  - 9005-49-6 (Heparin)
RN  - X85G7936GV (Abciximab)
SB  - IM
MH  - Abciximab
MH  - Aged
MH  - Antibodies, Monoclonal/*therapeutic use
MH  - Blood Platelets/*drug effects/metabolism
MH  - Body Mass Index
MH  - Female
MH  - Flow Cytometry
MH  - Heparin/pharmacology/*therapeutic use
MH  - Humans
MH  - Immunoglobulin Fab Fragments/*therapeutic use
MH  - Inflammation
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*blood/*drug therapy
MH  - Partial Thromboplastin Time
MH  - Platelet Activation/*drug effects
MH  - Platelet Aggregation Inhibitors/pharmacology/therapeutic use
MH  - Platelet Glycoprotein GPIIb-IIIa Complex/metabolism
MH  - Risk
MH  - Risk Factors
MH  - Time Factors
EDAT- 2005/08/23 09:00
MHDA- 2005/12/22 09:00
CRDT- 2005/08/23 09:00
PHST- 2005/08/23 09:00 [pubmed]
PHST- 2005/12/22 09:00 [medline]
PHST- 2005/08/23 09:00 [entrez]
AID - 05080422 [pii]
AID - 10.1160/TH04-12-0835 [doi]
PST - ppublish
SO  - Thromb Haemost. 2005 Aug;94(2):422-6. doi: 10.1160/TH04-12-0835.