title: Glycoprotein IIB/IIIA inhibitor to reduce postpercutaneous coronary intervention myonecrosis and improve coronary flow in diabetics: the 'OPTIMIZE-IT' pilot randomized study.
abstract: BACKGROUND
  Subgroup analyses of trials enrolling acute coronary syndrome patients suggest that inhibition of glycoprotein IIb/IIIa can improve the outcome of diabetic patients undergoing percutaneous coronary interventions (PCIs), possibly by improving microvascular perfusion. However, the efficacy of small-molecule IIb/IIIa receptor inhibitors to improve microvascular perfusion in stable diabetic patients undergoing elective PCI has not been specifically investigated.
  
  
  METHODS
  We randomized consecutive stable diabetic patients, undergoing elective PCI, to tirofiban or placebo groups along with double antiplatelet therapy. High-dose bolus (25 microg/kg per 3 min) of tirofiban was administered immediately before PCI followed by 8 h continuous infusion (0.15 microg/kg per min). Postprocedural myonecrosis was assessed prospectively by measurement of cardiac troponin T (cTnT) at 6 and 24 h after PCI. The primary end-points were post-PCI coronary flow estimated by corrected thrombolysis in myocardial infarction frame count and post-PCI myocardial infarction. Platelet aggregation was measured by platelet function analyser-100 values.
  
  
  RESULTS
  Forty-six patients entered the study (22 randomized to placebo and 24 randomized to tirofiban). The study drug was associated with a significant increase of platelet function analyser-100 values that peaked immediately after PCI and was maintained at 6 h (pre-PCI: 131 +/- 65 s; post-PCI: 222 +/- 49 s; after 6 h: 219 +/- 55 s).Post-PCI corrected thrombolysis in myocardial infarction frame count was similar in tirofiban and in placebo groups (10.2 +/- 3.6 vs. 12.0 +/- 7.6, P = 0.30, respectively). The prevalence of raised cTnT levels was similar in the two groups (25 vs. 30%, P = 0.56, respectively). At multivariate analysis, direct stenting (associated with reduced myonecrosis) and postdilatation (associated with increased myonecrosis) predicted cTnT elevation.
  
  
  CONCLUSIONS
  A high-dose bolus of tirofiban in stable diabetic patients undergoing elective PCI, along with double antiplatelet therapy, was associated with a significant further inhibition of platelet aggregation which, however, did not translate in a lower incidence of post-PCI distal embolization.
authors.affiliation: Institute of Cardiology, Catholic University, Rome, Italy.
authors.forename: Giovanni Paolo
authors.initials: GP
authors.lastname: Talarico
authors.forename: Marta
authors.initials: M
authors.lastname: Brancati
authors.forename: Francesco
authors.initials: F
authors.lastname: Burzotta
authors.forename: Italo
authors.initials: I
authors.lastname: Porto
authors.forename: Carlo
authors.initials: C
authors.lastname: Trani
authors.forename: Maria
authors.initials: M
authors.lastname: De Vita
authors.forename: Daniel
authors.initials: D
authors.lastname: Todaro
authors.forename: Maura
authors.initials: M
authors.lastname: Giammarinaro
authors.forename: Antonio Maria
authors.initials: AM
authors.lastname: Leone
authors.forename: Giampaolo
authors.initials: G
authors.lastname: Niccoli
authors.forename: Felicita
authors.initials: F
authors.lastname: Andreotti
authors.forename: Mario Attilio
authors.initials: MA
authors.lastname: Mazzari
authors.forename: Giovanni
authors.initials: G
authors.lastname: Schiavoni
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects* / Q000295:instrumentation; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000628:therapy*; D003326:Coronary Circulation / Q000187:drug effects*; D048909:Diabetes Complications / Q000000981:diagnostic imaging / Q000628:therapy*; D004359:Drug Therapy, Combination; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D010865:Pilot Projects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011446:Prospective Studies; D015607:Stents; D013997:Time Factors; D000077466:Tirofiban; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood; D014443:Tyrosine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D020107:Troponin T; D014443:Tyrosine; D000077466:Tirofiban