Why the study?
Does correcting D-dimer levels for soluble fibrin degradation improve the correlation with angiographically documented clot lysis in patients receiving fibrinolytic therapy?
Does correcting D-dimer levels for soluble fibrin degradation improve the correlation with angiographically documented clot lysis in patients receiving fibrinolytic therapy?
Correcting D-dimer levels for soluble fibrin degradation provides a highly accurate surrogate marker for angiographically documented venous clot lysis during fibrinolytic therapy.
Supports corrected D-dimer as a potential surrogate for clot lysis; hypothesis-generating and requires prospective validation before clinical use.
Plasma cross-linked fibrin-degradation products were analyzed using a D-dimer (DD) immunoassay in patients with deep vein thrombosis (DVT) or acute myocardial infarction (MI) treated with fibrinolytic therapy, and the results were correlated with clot lysis documented angiographically. In 13 patients with DVT, the mean DD concentration increased 10-fold (1,074 +/- 252 to 10,333 +/- 1,004 ng/ml) during therapy, but neither the peak level nor the DD concentration integrated over the course of therapy correlated with clot lysis. Since plasma DD can derive from degradation of soluble plasma fibrin as well as from thrombi, the contribution of the former was estimated by in vitro incubation of the pretreatment plasma with plasminogen activator. Subtraction of this value from the measured posttreatment DD concentration provided a "corrected" level that represented DD originating from lysis of thrombi. This modification resulted in improved correlation of DD levels with clot lysis. The mean corrected peak DD was higher in patients with successful thrombolysis (8,780 +/- 1,352 ng/ml) compared with patients without lysis (3,075 +/- 589 ng/ml, p less than 0.001). There was a moderate correlation between the volume of clot lysed and the corrected peak DD (r = 0.62) and a higher correlation with the corrected DD integrated over the course of treatment (r = 0.97). By contrast, the corrected DD concentrations were near zero in patients treated for MI with or without thrombolytic reperfusion, suggesting that fibrin in small coronary thrombi did not contribute significantly to total plasma DD during therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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Brenner et al. (1990) studied this question.
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