Correlation between coronary morphology and molecular markers of fibrinolysis in unstable angina pectoris Original Research Article

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 μg/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. Conclusion: 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.