Effects of early thrombolytic therapy (anistreplase versus streptokinase) on enzymatic and electrocardiographic infarct size in acute myocardial infarction. TEAM-2 Investigators.
The effects of thrombolytic therapy on enzymatic and electrocardiographic indexes of myocardial infarction were examined in 370 patients who were enrolled within 4 hours of onset of symptoms and were randomized to blinded therapy with intravenous anistreplase (30 U/5 min, n = 188) or streptokinase (1.5 million IU/1 hour, n = 182). Creatine kinase and its MB isoenzyme were initially measured every 4 to 6 hours, and lactic dehydrogenase (LDH) and its cardiac isoenzyme (LDH-1) every 8 to 12 hours. Electrocardiograms were obtained before, and at 90 minutes and 8 hours after starting thrombolysis, and on discharge. Enzymatic and electrocardiographic measures of infarction were compared between drug treatment and patency groups. Early patency was associated with significant reductions in peak values for each of 4 cardiac enzymes (averaging 21 to 25%, p less than 0.01 to 0.001), even though later rescue procedures were often used in the nonpatient group; times to peaks were also reduced for 3 of the enzymes. Treatment with anistreplase was associated with enzymatic peaks that tended to be lower than with streptokinase (6 to 16%), approaching or reaching significance for LDH (p less than or equal to 0.07) and LDH-1 (p less than or equal to 0.04); times to peaks were similar. Early patency favorably affected electrocardiographic indexes. Summed ST-segment elevations resolved more rapidly (p less than or equal to 0.04), summed Q-wave amplitude was reduced by 32% (p less than or equal to 0.01), and total QRS infarct score on discharge was 22% less (p less than or equal to 0.006) in those achieving early patency. Small differences in electrocardiographic indexes between the 2 drug treatment groups were not significant. These results support use of early reperfusion to reduce infarct size in acute myocardial infarction with administration of streptokinase and anistreplase.
Karagounis
L
L
Department of Medicine, University of Utah, Salt Lake City.
Moreno
F
F
Menlove
R L
RL
Ipsen
S
S
Anderson
J L
JL
D016255:Anistreplase / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000097:blood; D004562:Electrocardiography; D006801:Humans; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000201:enzymology / Q000503:physiopathology; D013300:Streptokinase / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D015912:Thrombolytic Therapy; D013997:Time Factors; D014654:Vascular Patency / Q000187:drug effects
D007527:Isoenzymes; D016255:Anistreplase; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D013300:Streptokinase