title: High-dose tirofiban with enoxaparin and inflammatory markers in high-risk percutaneous intervention.
abstract: OBJECTIVE
  The study assessed the benefit of high bolus dose tirofiban (HD-tirofiban) with enoxaparin compared with HD-tirofiban with unfractionated heparin (UFH). The study examined markers of platelet activation, thrombin generation and inflammation.
  
  
  METHODS
  The study is a prospective single centre open-label trial of patients with high-risk acute coronary syndrome treated with percutaneous intervention (PCI) who were randomized to anticoagulation with UFH or enoxaparin with HD-tirofiban (25 microg kg(-1) bolus). This study measured a panel of platelet activation markers, inflammatory biomarkers and thrombus generation between the two groups.
  
  
  RESULTS
  Sixty patients undergoing high-risk PCI were enroled in the study. Platelet inhibition as assessed by whole blood aggregometry following HD-tirofiban infusion was similar in both the UFH and enoxaparin groups. CD40 ligand expression on platelets was significantly reduced following PCI with HD-tirofiban and either UFH or enoxaparin. Following PCI, there were significant reductions measured in other markers of platelet activation including PAC-1, P selectin, factor V/Va, platelet-monocyte aggregates and monocyte expression of Mac-1 as determined by analysis of venous blood samples using flow cytometry. Prothrombin fragment 1+2, D-dimer, von Willebrand factor and high sensitive C-reactive protein levels were significantly less post PCI in the enoxaparin group compared with those patients receiving UFH.
  
  
  CONCLUSIONS
  The combination of HD tirofiban with enoxaparin resulted in an attenuated inflammatory response when compared with that of the combination of HD tirofiban with UFH.
authors.affiliation: Cardiology Department, The Prince Charles Hospital Laboratory, Brisbane, Australia. darren_walters@health.qld.gov.au
authors.forename: D L
authors.initials: DL
authors.lastname: Walters
authors.forename: M J
authors.initials: MJ
authors.lastname: Ray
authors.forename: P
authors.initials: P
authors.lastname: Wood
authors.forename: E J
authors.initials: EJ
authors.lastname: Perrin
authors.forename: J H N
authors.initials: JH
authors.lastname: Bett
authors.forename: C N
authors.initials: CN
authors.lastname: Aroney
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000188:drug therapy* / Q000276:immunology / Q000628:therapy; D000368:Aged; D000800:Angioplasty, Balloon; D000925:Anticoagulants / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D001779:Blood Coagulation Factors / Q000032:analysis; D001792:Blood Platelets / Q000276:immunology; D023201:CD40 Ligand / Q000378:metabolism*; D017984:Enoxaparin / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D005434:Flow Cytometry; D006493:Heparin / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D011446:Prospective Studies; D000077466:Tirofiban; D014443:Tyrosine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D000925:Anticoagulants; D015415:Biomarkers; D001779:Blood Coagulation Factors; D017984:Enoxaparin; D010975:Platelet Aggregation Inhibitors; D023201:CD40 Ligand; D014443:Tyrosine; D006493:Heparin; D000077466:Tirofiban