title: Platelet-monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab.
abstract: BACKGROUND
  Platelet-monocyte aggregates and other markers of platelet activation were investigated before and after percutaneous coronary intervention (PCI) with abciximab therapy. The study sought to assess the relationship between the level of platelet-monocyte aggregation and increases in cardiac troponin I post coronary intervention.
  
  
  METHODS
  Blood samples were collected from 40 patients before PCI and 10 min after abciximab administration. These were tested for platelet activation markers by flow cytometry. Cardiac troponin I levels were assayed at baseline and at 24 h post PCI.
  
  
  RESULTS
  Compared to healthy controls, patients with coronary artery disease had elevated markers of platelet activation including platelet-monocyte aggregates, P-selectin and PAC-1 (a marker specific for activated glycoprotein IIb/IIIa) prior to PCI. Increased levels of platelet-monocyte aggregates before PCI were associated with increased expression of P-selectin on the platelet surface. Abciximab therapy reduced platelet-monocyte aggregate levels but had no effect on P-selectin expression. The high levels of expression of activated glycoprotein IIb/IIIa (PAC-1) on platelets prior to PCI was reduced with abciximab therapy. Patients with higher levels of platelet-monocyte aggregates prior to PCI were more likely to develop an elevation of cardiac troponin I during the 24 h after PCI.
  
  
  CONCLUSIONS
  Increased levels of platelet-monocyte aggregates may predict patients at risk for troponin elevation following PCI and identify those most likely to benefit from abciximab.
authors.affiliation: Department of Haematology, The Prince Charles Hospital, Brisbane, Australia.
authors.forename: M J
authors.initials: MJ
authors.lastname: Ray
authors.forename: D L
authors.initials: DL
authors.lastname: Walters
authors.forename: J N H
authors.initials: JN
authors.lastname: Bett
authors.forename: J
authors.initials: J
authors.lastname: Cameron
authors.forename: P
authors.initials: P
authors.lastname: Wood
authors.forename: C N
authors.initials: CN
authors.lastname: Aroney
mesh_terms: D000077284:Abciximab; D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D016022:Case-Control Studies; D002449:Cell Aggregation / Q000187:drug effects; D003324:Coronary Artery Disease / Q000097:blood* / Q000628:therapy; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology*; D019007:P-Selectin / Q000097:blood* / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000187:drug effects / Q000378:metabolism*; D019210:Troponin I / Q000097:blood* / Q000187:drug effects
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019210:Troponin I; D000077284:Abciximab