title: Morphological characteristics of culprit atheromatic plaque are associated with coronary flow after thrombolytic therapy: new implications of optical coherence tomography from a multicenter study.
abstract: OBJECTIVE
  This study investigated the association between morphological characteristics of culprit atheromatic lesions as assessed by optical coherence tomography and Thrombolysis In Myocardial Infarction (TIMI) flow grade after thrombolysis in patients with ST-segment elevation myocardial infarction (STEMI).
  
  
  BACKGROUND
  Although several variables have been found to predict coronary flow after thrombolysis in patients with STEMI, the impact of culprit lesion morphology has not been studied.
  
  
  METHODS
  Fifty-five patients with STEMI from 3 tertiary centers that were treated with thrombolysis and underwent optical coherence tomography examination in the culprit lesion between 24 and 48 h after thrombolysis were included in the study. Patients were categorized on the basis of TIMI flow grade into patients with TIMI flow grade 3 versus TIMI flow grade < or =2.
  
  
  RESULTS
  Patients with TIMI flow grade < or =2 had plaques with more lipid quadrants than patients with TIMI flow grade 3 (p < 0.001), and presented with greater incidence of plaque rupture (p = 0.001). Mean minimal cap thickness was greater in patients with patent arteries than in patients with impaired flow (87 +/- 26 microm vs. 48 +/- 18 microm, p < 0.0001). Minimal cap thickness was independently associated with TIMI flow grade.
  
  
  CONCLUSIONS
  The morphological characteristics of the culprit atheromatic lesion in patients with STEMI are associated with coronary flow after thrombolysis. The lipid content, the existence of rupture, and mainly the thickness of the fibrous cap are associated with the outcome of thrombolysis.
authors.affiliation: First Department of Cardiology, Athens Medical School, Hippokration Hospital, Athens, Greece. ktoutouz@otenet.gr
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Toutouzas
authors.forename: Elefterios
authors.initials: E
authors.lastname: Tsiamis
authors.forename: Antonios
authors.initials: A
authors.lastname: Karanasos
authors.forename: Maria
authors.initials: M
authors.lastname: Drakopoulou
authors.forename: Andreas
authors.initials: A
authors.lastname: Synetos
authors.forename: Costas
authors.initials: C
authors.lastname: Tsioufis
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Periklis
authors.initials: P
authors.lastname: Davlouros
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Alexopoulos
authors.forename: Konstantina
authors.initials: K
authors.lastname: Bouki
authors.forename: Thomas
authors.initials: T
authors.lastname: Apostolou
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000368:Aged; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects*; D003328:Coronary Thrombosis / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D005355:Fibrosis; D006115:Greece; D006801:Humans; D008055:Lipids / Q000032:analysis; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012421:Rupture; D000077785:Tenecteplase; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D041623:Tomography, Optical Coherence; D016896:Treatment Outcome
chemical_list: D005343:Fibrinolytic Agents; D008055:Lipids; D010959:Tissue Plasminogen Activator; D000077785:Tenecteplase