Effect of glycoprotein IIb-IIIa receptor antagonism on platelet membrane glycoproteins after coronary stent placement

Citation
M. Gawaz et al., Effect of glycoprotein IIb-IIIa receptor antagonism on platelet membrane glycoproteins after coronary stent placement, THROMB HAEM, 80(6), 1998, pp. 994-1001
Citations number
36
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS AND HAEMOSTASIS
ISSN journal
03406245 → ACNP
Volume
80
Issue
6
Year of publication
1998
Pages
994 - 1001
Database
ISI
SICI code
0340-6245(199812)80:6<994:EOGIRA>2.0.ZU;2-Y
Abstract
Platelet membrane glycoproteins play a crucial role in ischemic complicatio ns after coronary stenting. Glycoprotein IIb-IIIa blockade reduces adverse clinical events after angioplasty but is associated with rare bur profound thrombocytopenia that might increase hemorrhagic complications. Changes in platelet membrane glycoproteins of patients with angina who unde rwent coronary stenting and were treated with the GPIIb-IIIa antagonist abc iximab (n = 20) or with heparin (n = 23) were studied. GPIIb-IIIa receptor blockade and membrane glycoproteins were evaluated with immunological marke rs in venous blood samples taken before, 10, 24, 48, 72, and 96 h after ini tial treatment with either abciximab or heparin. Patients receiving abciximab therapy showed a rapid inhibition of binding o f fluorochrome-conjugated mAb CD41 and c7E3 concomitant with a reduction in platelet aggregation which was restored in part in the days after terminat ion of abciximab infusion. Induction of ligand-induced binding sites on GPI Ib-IIIa was increased in patients receiving abciximab. The expression of li gand-induced binding sites correlated inversely with platelet count. No sig nificant change in platelet membrane markers were found in the heparin grou p. In vitro studies showed that abciximab induces ligand-induced binding si tes on isolated platelets and on nuclear cells bearing recombinant GPIIb-II Ia. Abciximab rapidly achieves GPIIb-IIIa receptor blockade after coronary sten t placement that might be beneficial in high-risk settings to bridge the de layed action of ticlopidine. Significant alterations of platelet membrane g lycoproteins during GPIIb-IIIa antagonism might contribute to development o f acute profound thrombocytopenia.