Introduction: Hypofibrinolysis, at least in part due to high levels of plasminogen activator inhibitor-1 (PAI-1), has been reported to occur frequently in patients with coronary artery disease (CAD). A recently described carboxypeptidase, thrombin-activatable fibrinolysis inhibitor (TAFI), is involved in the regulation of the balance between coagulation and fibrinolysis. High TAFI plasma levels may therefore contribute to a hypofibrinolytic state and to an increased risk for thrombotic disorders. There are contradictory results regarding TAFI levels in CAD patients, possibly because the characteristics of patients investigated and the time of blood sampling were different among different studies.
Materials and methods: Fibrinolytic inhibitors (TAFI activity, TAFI antigen and PAI-1 activity plasma levels) were measured in 44 consecutive patients admitted to the Coronary Care Unit of the University of Florence and in a group of 44 healthy controls, matched for age and sex, to detect a possible association of their levels with acute CAD.
Results: No differences were found in TAFI levels, either activity or antigen, between patients and controls. PAI-1 activity was significant different between patients and controls (p=0.0001). The frequencies of TAFI activity and antigen over cut-off levels were similar in patients and controls. Instead, higher PAI-1 levels were more frequent (p=0.04) in patients respect to controls. The univariate analysis confirmed the association of increased PAI-1 levels with acute CAD [OR=3.3; p=0.04]. Among the patients, TAFI and PAI-1 levels were not different according to clinical presentation of symptoms or indication to immediate percutaneous revascularization.
Conclusion: Our study suggests that in acute phase of CAD no increased levels of TAFI are detectable in plasma.