title: Intracoronary morphology of culprit lesions after reperfusion in acute myocardial infarction: serial angioscopic observations.
abstract: OBJECTIVE
  This study sought to elucidate the morphologic and pathologic characteristics of culprit lesions in patients with acute myocardial infarction.
  
  
  BACKGROUND
  The pathogenic mechanisms of acute myocardial infarction have been discussed on the basis of postmortem histologic examinations. Disruption of lipid-rich plaques is thought to render them thrombogenic. However, the details of coronary morphology have not been elucidated in survivors of myocardial infarction. The quality of angioscopic images has been greatly improved, and clear visualization of the intracoronary milieu can now be obtained.
  
  
  METHODS
  Eleven patients with acute myocardial infarction and angiographic demonstration of the culprit lesion were entered into the study. Angioscopic observations were made immediately after reperfusion and at 1-month follow-up.
  
  
  RESULTS
  Angioscopic observations were successfully performed in 10 patients immediately after reperfusion and in 10 at 33 +/- 26 (mean +/- SD) days of follow-up. Immediately after reperfusion, red thrombus, white thrombus, yellow plaques and intimal flaps were recognized in 30% (95% confidence interval [CI] 25.7 to 35.7), 100%, 100% and 50% (95% CI 45.0 to 55.0) of patients, respectively. At follow-up, these were recognized in 10% (95% CI 6.6 to 16.4), 60% (95% CI 54.6 to 64.7), 100% and 40% (95% CI 35.3 to 45.4) of patients, respectively.
  
  
  CONCLUSIONS
  The thrombus in acute myocardial infarction was always recognized over the yellow plaques. The thrombus formed directly over the plaque was mainly white. Red thrombus might be formed after the blood flow was obstructed by the white thrombus. At approximately 1 month, yellow plaques remained in all patients, and > 50% still had adherent white thrombus.
authors.affiliation: Cardiovascular Division, Osaka Police Hospital, Osaka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ueda
authors.forename: M
authors.initials: M
authors.lastname: Asakura
authors.forename: A
authors.initials: A
authors.lastname: Hirayama
authors.forename: K
authors.initials: K
authors.lastname: Komamura
authors.forename: M
authors.initials: M
authors.lastname: Hori
authors.forename: K
authors.initials: K
authors.lastname: Komada
mesh_terms: D000368:Aged; D017546:Angioscopy; D003131:Combined Modality Therapy; D003324:Coronary Artery Disease / Q000150:complications / Q000473:pathology; D003328:Coronary Thrombosis / Q000150:complications / Q000473:pathology; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology* / Q000628:therapy; D009204:Myocardial Revascularization
chemical_list: D005343:Fibrinolytic Agents