Association between plasma levels of D-dimer and fibrinogen/fibrin degradation products (FDP) for exclusion of thromboembolic disorders.

BACKGROUND: D-dimer and fibrinogen/fibrin degradation products (FDP) levels are elevated in subjects with thromboembolic disorders, and the assays for detection of D-dimer and FDP are used in many laboratories for the investigation of these disorders. The aim of this study was to evaluate the association between the plasma levels of D-dimer and FDP in the investigation of thromboembolic disorders. METHODS: D-dimer and FDP immunoassays were performed in 217 consecutive blood samples from subjects with suspected of thromboembolic disorders by use of Liatest D-dimer and Plasma FDP. RESULTS: FDP results were classified in: <5, 5-20, >20 microg/mL, and D-dimer levels obtained in these groups ranged to 350-1,210 ng/mL, 420-1,960 ng/mL, and 1,190-51,170 ng/mL, respectively. A significant association between D-dimer levels and the reaction times necessary to occur agglutination in latex agglutination test for FDP was observed. CONCLUSIONS: There was an association between plasma levels of D-dimer and FDP. The preliminary determination of FDP levels could be useful because it allows estimating the D-dimer levels before of the automated systems analysis, reducing costs associated to dilutions of plasma samples.

Lack of association between cardiac troponin T and D-dimer in the evaluation of myocardial damage.

Acute myocardial infarction (AMI) disrupts cardiac cell membranes, releasing intracellular cardiac proteins into the vascular system. Some of these proteins, including the cardiac troponin subunits T and I, have proven useful for diagnosing myocardial damage. Intracoronary thrombosis plays a key role in the pathogenesis of AMI, and the formation of an occlusive thrombus usually precedes the development of myocardial damage. To evaluate whether there is an association between the size of intracoronary thrombosis and myocardial damage, we analyzed D-dimer and cTnT levels in blood samples from patients suspected to have myocardial damage. We investigated 102 patients who were admitted to emergency service for suspected myocardial damage. D-dimer was assessed with the use of the immunoassay Liatest D-dimer, and cTnT levels were measured with an electrochemiluminescence immunoassay (Troponin T STAT). D-dimer levels were lower in patients with cTnT < 0.01 than in patients presenting cTnT > 0.01 ng/mL. We investigated the relationship between D-dimer and cTnT levels in the patients with cTnT > 0.01 ng/mL (0.40 +/- 0.10 ng/mL), and no significant agreement (r = 0.20, P > 0.05) was observed. The levels of D-dimer were not associated with the levels of cTnT in patients with cTnT > 0.01 ng/mL.