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Intracoronary formation of blood clots on ruptured arteriosclerotic plaques is considered the main cause of acute myocardial infarction (AMI) (1). After such ruptures, exposed tissue factor binds to factor VIIa from plasma, and the resulting tissue factor-factor VIIa complex activates factor X toward factor Xa, the enzyme converting prothrombin to thrombin. By cleavage of fibrinopeptides A and B, thrombin produces desAABBfibrin monomers that polymerize into still-soluble complexes called “thrombus precursor proteins” (TpPs). New antigens formed on these complexes were used for a TpP assay (2).Because the acute thrombotic event precedes coronary occlusion and muscle necrosis, detection of activated coagulation potentially allows early detection of AMI. Until now, attempts in this field have focused on markers for factor Xa and thrombin activity, such as prothrombin fragment 1.2 and thrombin-antithrombin complexes. However, these markers are not necessarily closely related to the actual formation of fibrin clots (3), especially in chronically hypercoagulable patients, and TpP could perform better in this respect. We therefore studied plasma concentrations of TpP and fibrin monomers (FMs) in patients with suspected AMI. The results were compared with two small cytosolic cardiac marker proteins, myoglobin (Mb) and fatty acid-binding protein (FABP), that are early markers for necrosis (4 , 5) and with a highly …

Combined Use of Markers of Muscle Necrosis and Fibrinogen Conversion in the Early Differentiation of Myocardial Infarction and Unstable Angina