BACKGROUND: We evaluated the clinical utility of TpP in the diagnosis of acute coronary syndrome and changes in the level of TpP and fibrin(ogen) degradation products after low-molecular weight heparin(LMWH) therapy. METHODS: TpP concentration was measured in 12 patients with acute myocardial infarction(AMI), 21 patients with unstable angina(UA), and 9 patients with non-cardiac chest pain and 18 healthy controls. Among them, in 11 patients treated with LMWH(6 patients with deltaparin & 5 patients with enoxaparin), the levels of TpP(American Biogenetic Sciences) and Fibrinostika(R) total degradation product(TDP), fibrinogen degradation product(FgDP) and fibrin degradation product(FbDP, Organon Teknica) was measured from plasma before treatment and at 3, 12, 15 and 24 hours after treatment. RESULTS: TpP was significantly increased in AMI(19.3+/-11.0(microgram/mL) and UA patients(16.8+/-12.4(microgram/mL) compared with the patients with non-cardiac chest pain(7.1+/-5.6(microgram/mL) and healthy controls(2.6+/-1.6(microgram/mL)(P=0.040). The TpP levels was increased in 91.7%(11/12) of AMI patients, 71.4%(15/21) of UA patients and 33.3%(3/9) of the patients with non-cardiac chest pain. TpP was decreased more significantly in enoxaparin treated group than in deltaparin group(P=0.011). No significantly different changes of plasma TDP/FgDP/FbDP levels between enoxaparin and deltaparin treatment. CONCLUSION: TpP, the precursor of thrombus, appears to be a useful index of intravascular thrombotic process. In the treatment with LMWH, enoxaparin reduced TpP more markedly than deltaparin, which may be suggestive of different anti-thrombotic effect of LMWHs on thrombotic process.