Clinical outcome of percutaneous coronary intervention with antecedent mutant t-PA administration for acute myocardial infarction.
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.
Kurihara
Hideaki
H
Division of Cardiology, Toyonaka Municipal Hospital, Osaka, Japan. cfg63870@syd.odn.ne.jp
Matsumoto
Satoru
S
Tamura
Ritsu
R
Yachiku
Kenji
K
Nakata
Atsuyuki
A
Nakagawa
Tsutomu
T
Yoshino
Takashi
T
Matsuyama
Tatsuo
T
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
D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; C468277:monteplase; D020108:Nicorandil; D010960:Plasminogen Activators; D001241:Aspirin