title: Bivalirudin reduces platelet and monocyte activation after elective percutaneous coronary intervention.
abstract: Concomitant antithrombotic therapy is essential for the prevention of ischaemic events in percutaneous coronary intervention (PCI) and stenting. With new anticoagulant medications being developed and applied in PCI, this raises the question of possible interactions with platelet and leukocyte activation. We therefore sought to investigate the influence of bivalirudin and heparin in platelet and leukocyte activation in patients undergoing elective PCI. Forty-six patients were recruited consecutively in the setting of the Intracoronary Stenting and Antithrombotic Regimen-Rapid Early Action for Coronary Treatment (ISAR-REACT)-3 trial and were randomly assigned to receive either unfactionated heparin or bivalirudin during elective PCI. Surface expression of CD62P (P-Selectin), CD42b (GPIbalpha), CD40L, PAC-1 on circulating platelets and CD11b, CD14 and CD15 on circulating leukocytes were evaluated by flow cytometry. Cytokine levels of IL-12p70, tumour necrosis factor (TNF), IL-8, IL-6, IL-1beta and IL-10 were determined by cytometric bead array. Platelet surface expression of PAC-1, P-Selectin and GPIbalpha was significantly reduced after PCI in patients receiving bivalirudin as compared to heparin. Similarly, CD11b expression on CD14+ monocytes was diminished after bivalirudin. However, no differences were observed in cytokine levels between the bivalirudin and the heparin group, before or after PCI. In conclusion, our data suggest that bivalirudin may reduce platelet and monocyte activation in patients undergoing elective PCI. Thereby, bivalirudin might reduce periinterventional thrombotic complications.
authors.affiliation: Deutsches Herzzentrum, Lazarettstrasse 36, 80636 Munich, Germany.
authors.forename: Gabriele
authors.initials: G
authors.lastname: Busch
authors.forename: Birgit
authors.initials: B
authors.lastname: Steppich
authors.forename: Dirk
authors.initials: D
authors.lastname: Sibbing
authors.forename: Siegmund-Lorenz
authors.initials: SL
authors.lastname: Braun
authors.forename: Andreas
authors.initials: A
authors.lastname: Stein
authors.forename: Philipp
authors.initials: P
authors.lastname: Groha
authors.forename: Albert
authors.initials: A
authors.lastname: Schömig
authors.forename: Adnan
authors.initials: A
authors.lastname: Kastrati
authors.forename: Nicolas
authors.initials: N
authors.lastname: von Beckerath
authors.forename: Ilka
authors.initials: I
authors.lastname: Ott
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000925:Anticoagulants / Q000627:therapeutic use; D015703:Antigens, CD / Q000097:blood; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000628:therapy*; D016207:Cytokines / Q000097:blood; D004311:Double-Blind Method; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006493:Heparin / Q000627:therapeutic use*; D006629:Hirudins; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology; D010446:Peptide Fragments / Q000627:therapeutic use*; D015539:Platelet Activation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000627:therapeutic use; D013927:Thrombosis / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000925:Anticoagulants; D015703:Antigens, CD; D016207:Cytokines; D005343:Fibrinolytic Agents; D006629:Hirudins; D010446:Peptide Fragments; D010975:Platelet Aggregation Inhibitors; D010980:Platelet Membrane Glycoproteins; D011994:Recombinant Proteins; D006493:Heparin; C074619:bivalirudin