title: Incomplete recanalization as an important determinant of Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow after thrombolytic therapy for acute myocardial infarction. TEAM Investigators. Thrombolytic Trial of Eminase in Acute Myocardial Infarction.
abstract: The outcome of patients with Thrombolysis in Myocardial Infarction (TIMI) trial grade 2 flow is worse than that of patients with TIMI grade 3 flow after thrombolytic therapy for acute myocardial infarction. It is unclear whether TIMI grade 2 flow represents incomplete recanalization of the culprit lesion or poor distal runoff. The Thrombolytic Trial of Eminase (anistreplase) in Acute Myocardial Infarction (TEAM)-2 and TEAM-3 were randomized trials comparing anistreplase with streptokinase (TEAM-2, n = 370) or with alteplase (tissue plasminogen activator) (TEAM-3, n = 325). We compared the minimal luminal diameter of the culprit lesion in patients with TIMI grade 2 flow with that in patients with TIMI grade 3 flow both 90 minutes (TEAM-2) and 1 day (TEAM-3) after thrombolysis. Patients with TIMI grade 2 flow had a lower residual luminal diameter in the culprit lesion than patients with TIMI grade 3 flow (TEAM-2, 0.58 +/- 0.03 vs 0.79 +/- 0.02 mm, p = 0.0001; TEAM-3, 0.88 +/- 0.04 vs 1.17 +/- 0.03 mm, p = 0.0001, for patients with TIMI grades 2 and 3 flow). Residual percent stenosis was correspondingly higher in patients with TIMI grade 2 flow. At the early angiogram, 66% of patients with TIMI grade 2 flow, but only 35% of those with TIMI grade 3 flow, had a minimal luminal diameter of 0.6 mm (positive predictive value 87%, negative predictive value 35%). Incomplete recanalization of the culprit lesion may thus be an important determinant of TIMI grade 2 flow after thrombolysis. Whether more complete thrombolysis or rescue angioplasty improves outcome in these patients deserves evaluation.
authors.affiliation: Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California 90048, USA.
authors.forename: D
authors.initials: D
authors.lastname: Zahger
authors.forename: L A
authors.initials: LA
authors.lastname: Karagounis
authors.forename: B
authors.initials: B
authors.lastname: Cercek
authors.forename: J L
authors.initials: JL
authors.lastname: Anderson
authors.forename: S
authors.initials: S
authors.lastname: Sorensen
authors.forename: F
authors.initials: F
authors.lastname: Moreno
authors.forename: P K
authors.initials: PK
authors.lastname: Shah
mesh_terms: D000704:Analysis of Variance; D016255:Anistreplase / Q000627:therapeutic use*; D003251:Constriction, Pathologic; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D004311:Double-Blind Method; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D010960:Plasminogen Activators / Q000627:therapeutic use*; D011379:Prognosis; D013300:Streptokinase / Q000627:therapeutic use*; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*
chemical_list: D005343:Fibrinolytic Agents; D016255:Anistreplase; D013300:Streptokinase; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator