title: Effect of high bolus dose tirofiban on the inflammatory response following percutaneous coronary intervention.
abstract: BACKGROUND
  Tirofiban at the bolus dose of 10 microg/kg does not suppress the inflammatory response following percutaneous coronary intervention (PCI). This may be due to less than optimal inhibition of platelet aggregation. High bolus dose tirofiban (25 microg/kg) allows better inhibition of platelet aggregation but its anti-inflammatory effect remains unknown.
  
  
  OBJECTIVE
  High bolus dose tirofiban exhibits anti-inflammatory activity.
  
  
  METHODS
  A total of 100 patients referred for PCI were randomized to receive high bolus dose tirofiban followed by a 24-h infusion or a bolus and an infusion of saline. Patients with elevated troponin or with thrombus in the culprit lesion were excluded. Inflammatory markers were measured at baseline and at 24 h.
  
  
  RESULTS
  Levels of soluble CD40 ligand (sCD40L) were not affected by PCI while those of interleukin-6 (IL-6) and of high sensitivity C-reactive protein (hs-CRP) significantly increased. Despite inhibiting platelet's aggregation by > 90%, tirofiban did not suppress the rise of IL-6 and hs-CRP. Median (interquartile range) elevation of IL-6 was 0.6 pg/mL (-1.5-3.6) versus 0.4 pg/mL (-0.7-1.8) and that of hs-CRP was 2.1 mg/L (0.7-5.2) versus 2.4 mg/L (1-4.7) in the tirofiban and the control groups, respectively (p = ns). However, in patients with diabetes mellitus, tirofiban significantly suppressed the rise of hs-CRP by 65% (p = 0.01), but did not significantly affect the rise of IL-6.
  
  
  CONCLUSIONS
  In low-risk patients undergoing PCI, tirofiban did not attenuate the rise of inflammatory markers. However, the significant effect in diabetics suggests that tirofiban may have anti-inflammatory activity in higher risk patients.
authors.affiliation: Division of Cardiology, Hotel Dieu de France Hospital Beirut, Lebanon. razar@usj.edu.lb
authors.forename: Rabih R
authors.initials: RR
authors.lastname: Azar
authors.forename: Georges
authors.initials: G
authors.lastname: Badaoui
authors.forename: Antoine
authors.initials: A
authors.lastname: Sarkis
authors.forename: Roland
authors.initials: R
authors.lastname: Kassab
authors.forename: Elie
authors.initials: E
authors.lastname: Salamé
authors.forename: Simon
authors.initials: S
authors.lastname: Aboujaoudé
authors.forename: Righab
authors.initials: R
authors.lastname: Hamdan
authors.forename: Vanda
authors.initials: V
authors.lastname: Barakett
authors.forename: Mirna
authors.initials: M
authors.lastname: Germanos
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D015415:Biomarkers; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism; D019013:CD40 Antigens / Q000187:drug effects; D000077144:Clopidogrel; D052279:Creatine Kinase, MB Form / Q000187:drug effects; D005260:Female; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control*; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D011446:Prospective Studies; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D013997:Time Factors; D000077466:Tirofiban; D014443:Tyrosine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D019013:CD40 Antigens; D015850:Interleukin-6; D010975:Platelet Aggregation Inhibitors; D014443:Tyrosine; D002097:C-Reactive Protein; D000077144:Clopidogrel; D052279:Creatine Kinase, MB Form; D000077466:Tirofiban; D013988:Ticlopidine