作者: D. A. TREGOUET , R. SCHNABEL , M. C. ALESSI , T. GODEFROY , P. J. DECLERCK
DOI: 10.1111/J.1538-7836.2008.03221.X
关键词: Protein C 、 Cohort 、 Medicine 、 Coronary artery disease 、 Hazard ratio 、 Myocardial infarction 、 Unstable angina 、 Fibrinolysis 、 Proportional hazards model 、 Cardiology 、 Internal medicine
摘要: Summary. Background: Thrombin activatable fibrinolysis inhibitor (TAFI) attenuates fibrinolysis. Results on the association between TAFI levels and risk of coronary artery disease (CAD) are inconsistent. Objectives: We investigated cardiovascular events in CAD. Patients/Methods: 1668 individuals with angiographically proven CAD at baseline were followed for a median 2.3 years, as part prospective AtheroGene cohort. Fifty-six deaths from (CV) causes 35 non-fatal CV observed. Results: At baseline, three measurements available: one evaluating total amount (t-TAFI), measuring TAFIa/TAFIai amount, last released activated peptide (TAFI-AP). associated increased death [hazard ratio (HR) tertile increase, 2.38 (1.56–3.63); P < 10−4]. This remained significant after adjustment conventional factors, CRP levels, white blood count markers thrombin generation [HR = 1.69 (1.07–2.67); P = 0.01]. In addition, CPB2 gene polymorphisms explained 12%, 6%, 3% t-TAFI, TAFI-AP respectively, but none was events. Conclusions: The TAFI, measured by ELISA, not t-TAFI is independently death.