PMID- 15201252
OWN - NLM
STAT- MEDLINE
DCOM- 20040720
LR  - 20240413
IS  - 1468-201X (Electronic)
IS  - 1355-6037 (Print)
IS  - 1355-6037 (Linking)
VI  - 90
IP  - 7
DP  - 2004 Jul
TI  - Distinct yet complementary mechanisms of heparin and glycoprotein IIb/IIIa 
      inhibitors on platelet activation and aggregation: implications for restenosis 
      during percutaneous coronary intervention.
PG  - 794-9
AB  - OBJECTIVE: To study the effect of unfractionated heparin (UFH) versus low 
      molecular weight heparin (LMWH) in combination with glycoprotein (Gp) IIb/IIIa 
      blockers on platelet activation and aggregation. METHODS: Washed platelets were 
      stimulated with thrombin in the presence or absence of UFH (monoparin), LMWH 
      (enoxaparin), and a Gp IIb/IIIa blocker (abciximab, eptifibatide, or tirofiban). 
      RESULTS: Although Gp IIb/IIIa antagonists blocked the final common pathway of 
      thrombin induced platelet aggregation, UFH and LMWH were better at blocking 
      upstream platelet activation. UFH was significantly more effective than LMWH at 
      inhibiting P selectin expression (p = 0.001) and platelet derived growth factor 
      release from thrombin activated platelets (p = 0.012). CONCLUSIONS: UFH and LMWH 
      exert complementary effects to Gp IIb/IIIa blockers by inhibiting afferent 
      pathways of platelet activation. Coadministration of heparin with Gp IIb/IIIa 
      blockers provides improved protection against persistent platelet activation, 
      thereby improving outcome after percutaneous coronary intervention. Judging from 
      these data, UFH may be more effective in this regard than LMWH, at least in 
      vitro. The use of LMWH in preference to UFH during percutaneous coronary 
      intervention, although initially attractive, may inadequately protect against 
      platelet activation despite the presence of Gp IIb/IIIa blockers.
FAU - Day, J R S
AU  - Day JR
AD  - British Heart Foundation Cardiovascular Medicine and Cardiac Surgery Unit, 
      National Heart and Lung Institute, Imperial College School of Medicine, 
      Hammersmith Hospital, Du Cane road, London W12 0NN, UK. j.day@imperial.ac.uk
FAU - Malik, I S
AU  - Malik IS
FAU - Weerasinghe, A
AU  - Weerasinghe A
FAU - Poullis, M
AU  - Poullis M
FAU - Nadra, I
AU  - Nadra I
FAU - Haskard, D O
AU  - Haskard DO
FAU - Taylor, K M
AU  - Taylor KM
FAU - Landis, R C
AU  - Landis RC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Heart
JT  - Heart (British Cardiac Society)
JID - 9602087
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Anticoagulants)
RN  - 0 (Enoxaparin)
RN  - 0 (Hemostatics)
RN  - 0 (Immunoglobulin Fab Fragments)
RN  - 0 (Peptides)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 0 (Platelet Glycoprotein GPIIb-IIIa Complex)
RN  - 0 (Platelet Membrane Glycoproteins)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (platelet activating factor receptor)
RN  - 42HK56048U (Tyrosine)
RN  - 9005-49-6 (Heparin)
RN  - EC 3.4.21.5 (Thrombin)
RN  - GGX234SI5H (Tirofiban)
RN  - NA8320J834 (Eptifibatide)
RN  - X85G7936GV (Abciximab)
SB  - IM
MH  - Abciximab
MH  - Angioplasty, Balloon, Coronary
MH  - Antibodies, Monoclonal/pharmacology
MH  - Anticoagulants/*pharmacology
MH  - Coronary Restenosis/blood
MH  - Enoxaparin/administration & dosage/pharmacology
MH  - Eptifibatide
MH  - Flow Cytometry
MH  - Hemostatics/*pharmacology
MH  - Heparin/administration & dosage/*pharmacology
MH  - Humans
MH  - Immunoglobulin Fab Fragments/pharmacology
MH  - Peptides/pharmacology
MH  - Platelet Activation/*drug effects
MH  - Platelet Aggregation/drug effects
MH  - Platelet Aggregation Inhibitors/*pharmacology
MH  - Platelet Glycoprotein GPIIb-IIIa Complex/administration & dosage/*antagonists & 
      inhibitors
MH  - Platelet Membrane Glycoproteins/antagonists & inhibitors
MH  - Receptors, G-Protein-Coupled/antagonists & inhibitors
MH  - Thrombin/*pharmacology
MH  - Tirofiban
MH  - Tyrosine/*analogs & derivatives/pharmacology
PMC - PMC1768310
EDAT- 2004/06/18 05:00
MHDA- 2004/07/21 05:00
PMCR- 2007/07/01
CRDT- 2004/06/18 05:00
PHST- 2004/06/18 05:00 [pubmed]
PHST- 2004/07/21 05:00 [medline]
PHST- 2004/06/18 05:00 [entrez]
PHST- 2007/07/01 00:00 [pmc-release]
AID - 90/7/794 [pii]
AID - 0900794 [pii]
AID - 10.1136/hrt.2003.017749 [doi]
PST - ppublish
SO  - Heart. 2004 Jul;90(7):794-9. doi: 10.1136/hrt.2003.017749.