Abstract

Thrombin activatable fibrinolysis inhibitor (TAFI) is involved in the regulation of the balance between coagulation and fibrinolysis. After activation by the thrombin‐thrombomodulin complex, TAFI downregulates plasmin formation, and thereby inhibits degradation of the fibrin clot [1]. High TAFI plasma levels may therefore contribute to an increased risk of thrombotic disorders. Elevated TAFI levels were found in patients with coronary artery disease [2,3]. In patients with venous thrombosis, TAFI levels above the 90th percentile were associated with an increased risk of thrombosis [4]. There are no data available on the role of TAFI levels in patients with pulmonary embolism (PE). The aim of the present case-control study was to examine TAFI antigen levels in relation to markers of coagulation and fibrinolysis in patients with and without acute PE. We investigated 120 patients with suspected PE and D-dimer levels � 500 ng mL � 1 . PE was diagnosed in 71 patients and excluded in 49 patients with a diagnostic strategy including pretest probability and spiral computed tomography (CT) [5]. In patients with proven PE, pulmonary occlusion rate was assessed by spiral CT using the modified Miller index described by Remy-Jardin et al. [6]. Deep vein thrombosis (DVT) was confirmed by compression sonography in 16 and excluded in 50 patients with confirmed PE and clinically suspected DVT. All patients gave written informed consent according to a protocol approved by the local ethics committee. Blood samples were drawn from an antecubital vein within 1 h after admission of the patients. Coagulation assays were performed in citrated plasma, C-reactive protein (CRP) was measured in heparinized blood samples. Total TAFI antigen levels were determined by an enyzme-linked immunosorbent assay (ELISA) (Milan Analytica, La Roche, Switzerland). TAFI levels were expressed as percentage of normal pooled plasma. Fibrinogen levels were measured according to Clauss, and D-dimer levels using an automated ELISA techni

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