title: Correlation between coronary morphology and molecular markers of fibrinolysis in unstable angina pectoris.
abstract: BACKGROUND
  In acute coronary syndromes, marked alterations of coagulation and fibrinolysis have been observed, but no data are available concerning a possible relation to coronary stenosis morphology.
  
  
  METHODS
  Thirty one patients with unstable angina pectoris were included. Culprit stenosis morphology judged from coronary angiography was graded using the modified ACC/AHA classification. Molecular and functional markers of hemostasis and fibrinolysis were determined from venous plasma samples obtained at admission.
  
  
  RESULTS
  Patients with unstable angina pectoris had a moderate procoagulant state, especially a contact phase activation compared with age-matched controls (factor XII 93.9 +/- 5.6 vs 112.8 +/- 5.4%; P < 0.05; high molecular weight kininogen 55.3 +/- 5.4 vs 86.1 +/- 6.5%; P < 0.01). Thrombin-antithrombin (TAT) was not significantly elevated (7.6 +/- 1.9 vs 4.0 +/- 0.5 microg/l). Elevated plasminogen activator mass concentration (16.6 +/- 2.1 vs 5.4 +/- 0.6 ng/ml; P < 0.01) and plasminogen activator inhibitor (PAI) activity (9.9 +/- 3.0 vs 5.6 +/- 3.0 AU/ml; P < 0.05) indicated an alteration of the fibrinolysis. Complexity of coronary stenosis was positively correlated with tissue-type plasminogen activator (TPA) mass concentration (P < 0.01) and PAI activity (P < 0.05). No association was found to markers of a hypercoagulative state.
  
  
  CONCLUSIONS
  These findings indicate a relation between alterations of the fibrinolytic system and coronary morphology, whereas the acute changes of coagulation occur independently of culprit stenosis complexity.
authors.affiliation: Medizinische Universitätsklinik, Abteilung Innere Medizin III, Eberhard-Karls-Universität, Tübingen, Germany.
authors.forename: H M
authors.initials: HM
authors.lastname: Hoffmeister
authors.forename: M
authors.initials: M
authors.lastname: Jur
authors.forename: U
authors.initials: U
authors.lastname: Helber
authors.forename: M
authors.initials: M
authors.lastname: Fischer
authors.forename: W
authors.initials: W
authors.lastname: Heller
authors.forename: L
authors.initials: L
authors.lastname: Seipel
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000000981:diagnostic imaging* / Q000503:physiopathology; D015415:Biomarkers / Q000032:analysis; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood / Q000000981:diagnostic imaging* / Q000503:physiopathology; D005174:Factor XII / Q000032:analysis*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D007704:Kininogens / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D012016:Reference Values; D012680:Sensitivity and Specificity
chemical_list: D015415:Biomarkers; D007704:Kininogens; D017395:Plasminogen Activator Inhibitor 1; D005174:Factor XII