title: Randomized comparison of intracoronary tirofiban versus urokinase as an adjunct to primary percutaneous coronary intervention in patients with acute ST-elevation myocardial infarction: results of the ICTUS-AMI trial.
abstract: BACKGROUND
  No randomized trial has been performed to compare the efficacy of an intracoronary bolus of tirofiban versus urokinase during primary percutaneous coronary intervention (PCI). We investigated whether the effects of adjunctive therapy with an intracoronary bolus of urokinase was noninferior to the effects of an intracoronary bolus of tirofiban in patients with ST-elevation myocardial infarction (STEMI) undergoing PCI.
  
  
  METHODS
  A total of 490 patients with acute STEMI undergoing primary PCI were randomized to an intracoronary bolus of tirofiban (10 µg/kg; n = 247) or urokinase (250 kU/20 ml; n = 243). Serum levels of P-selectin, von Willebrand factor (vWF), CD40 ligand (CD40L), and serum amyloid A (SAA) in the coronary sinus were measured before and after intracoronary drug administration. The primary endpoint was the rate of complete ( ≥ 70%) ST-segment resolution (STR) at 90 minutes after intervention, and the noninferiority margin was set to 15%.
  
  
  RESULTS
  In the intention-to-treat analysis, complete STR was achieved in 54.4% of patients treated with an intracoronary bolus of urokinase and in 60.6% of those treated with an intracoronary bolus of tirofiban (adjusted difference: -7.0%; 95% confidence interval: -15.7% to 1.8%). The corrected TIMI frame count of the infarct-related artery was lower, left ventricular ejection fraction was higher, and the 6-month major adverse cardiac event-free survival tended to be better in the intracoronary tirofiban group. An intracoronary bolus of tirofiban resulted in lower levels of P-selectin, vWF, CD40L, and SAA in the coronary sinus compared with an intracoronary bolus of urokinase after primary PCI (P < 0.05).
  
  
  CONCLUSIONS
  An intracoronary bolus of urokinase as an adjunct to primary PCI for acute STEMI is not equally effective to an intracoronary bolus of tirofiban with respect to improvement in myocardial reperfusion assessed by STR. This may be caused by less reduction in coronary circulatory platelet activation and inflammation.
authors: Department of Cardiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
authors: Tian-qi
authors: TQ
authors: Zhu
authors: Qi
authors: Q
authors: Zhang
authors: Feng-hua
authors: FH
authors: Ding
authors: Jian-ping
authors: JP
authors: Qiu
authors: Hui-geng
authors: HG
authors: Jin
authors: Li
authors: L
authors: Jiang
authors: Lin
authors: L
authors: Lu
authors: Rui-yan
authors: RY
authors: Zhang
authors: Jian
authors: J
authors: Hu
authors: Zhen-kun
authors: ZK
authors: Yang
authors: Ying
authors: Y
authors: Shen
authors: Wei-feng
authors: WF
authors: Shen
mesh_terms: D000328:Adult; D000368:Aged; D004562:Electrocardiography; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D062645:Percutaneous Coronary Intervention; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use*; D016277:Ventricular Function, Left
chemical_list: D005343:Fibrinolytic Agents; D014443:Tyrosine; D014568:Urokinase-Type Plasminogen Activator; D000077466:Tirofiban