title: Clinical outcome of percutaneous coronary intervention with antecedent mutant t-PA administration for acute myocardial infarction.
abstract: OBJECTIVE
  We investigated the acute-phrase and chronic-phase outcomes of patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) with or without antecedent mutant tissue-type plasminogen (t-PA) administration.
  
  
  METHODS
  Thirty-nine patients with a first AMI within 6 hours of onset were randomly assigned to the treatment group (1,600,000 IU IV monteplase, n = 19) or the nontreatment group (n = 20), followed by PCI. Clinical outcomes were then evaluated.
  
  
  RESULTS
  Patient characteristics did not differ between the 2 groups. A significantly higher number of patients in the monteplase group achieved Thrombolysis In Myocardial Infarction trial (TIMI) grade 2 flow or more at the first angiography (84.2% vs 40.0%; P <.005), reduced number of devices (1.44 vs 1.80 devices, P <.05), and reduced procedure times (59.7 vs 86.7 minutes; P <.01), with no differences in peak creatine kinase and rates of major complications and no reflow or distal embolization. Observation over an average of 5.5 months revealed a tendency toward lower target lesion revascularization rates in the monteplase group (17.6% vs 31.6%) but no intergroup difference in rates of major complications. Pretreatment quantitative coronary angioplasty only showed a significant difference in minimal lumen diameter and percent diameter stenosis in the acute phase (1.13 mm in the monteplase group vs 0.66 mm in the nontreatment group, 57.0% vs 73.0%; P <.05). (99m)Tc-QGS (quantitative electrocardiographically gated single-photon emission computed tomographic scintigraphy) showed no intergroup differences in left ventricular end-diastolic volume index, end- systolic volume index, and ejection fraction in the acute and chronic phases.
  
  
  CONCLUSIONS
  Our results suggest that PCI with antecedent mutant t-PA for AMI not only accelerates reperfusion, thereby facilitating PCI, but also attenuates restenosis in the chronic phase.
authors.affiliation: Division of Cardiology, Toyonaka Municipal Hospital, Osaka, Japan. cfg63870@syd.odn.ne.jp
authors.forename: Hideaki
authors.initials: H
authors.lastname: Kurihara
authors.forename: Satoru
authors.initials: S
authors.lastname: Matsumoto
authors.forename: Ritsu
authors.initials: R
authors.lastname: Tamura
authors.forename: Kenji
authors.initials: K
authors.lastname: Yachiku
authors.forename: Atsuyuki
authors.initials: A
authors.lastname: Nakata
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Yoshino
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Matsuyama
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001241:Aspirin / Q000627:therapeutic use; D003131:Combined Modality Therapy; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000453:epidemiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000628:therapy*; D020108:Nicorandil / Q000627:therapeutic use; D010960:Plasminogen Activators / Q000627:therapeutic use*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015607:Stents; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; C468277:monteplase; D020108:Nicorandil; D010960:Plasminogen Activators; D001241:Aspirin