Elevated serum D dimer: A degradation product of cross-linked fibrin (XDP) after intravenous streptokinase during acute myocardial infarction

Lew, Allan S.; Berberian, Linda; Cercek, Bojan; Lee, Stephen; Shah, Prediman K.; Ganz, William

doi:10.1016/s0735-1097(86)80153-x

Cited by 44 publications

(16 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…39 Some observed elevations of Ddimer in patients with myocardial infarction 40 , although others observed elevations of D-dimer infrequently among conventionally treated patients. 41 Congestive heart failure also causes elevations of D-dimer. 42 …”

Section: D-dimermentioning

confidence: 99%

Diagnosis of pulmonary embolism in the coronary care unit

2016

Pulmonary Embolism

View full text Add to dashboard Cite

Section: D-dimermentioning

confidence: 99%

Diagnosis of pulmonary embolism in the coronary care unit

2016

Pulmonary Embolism

View full text Add to dashboard Cite

“…[16][17][18]34 Because high-molecular-weight cross-linked polymers may occur in such patients, Francis et a122 have suggested lysis of these polymers may be a major source of increased concentrations of XL-FDP after thrombolysis. Increased XL-FDP immunoreactivity after incubation of plasma in vitro with t-PA was thought by these investigators to be due to release of D-dimer fragments from fibrin polymers.…”

Section: Sources Of Xl-fdp In Vivomentioning

confidence: 99%

Validity of enzyme-linked immunosorbent assays of cross-linked fibrin degradation products as a measure of clot lysis.

et al. 1990

View full text Add to dashboard Cite

Concentrations of cross-linked fibrin degradation products (XL-FDPs) in plasma, measured by enzyme-linked immunosorbent assays (ELISAs) based on monoclonal antibodies (MAbs) raised against fragment D-dimer of cross-linked fibrin, increase when patients are given fibrinolytic agents. Whether XL-FDPs derive from circulating cross-linked fibrin polymers in plasma, compared with clot-associated fibrin, has been questioned because increases in XL-FDP are measured by some assays after fibrinolysis in vitro in the absence of clot. We characterized the source of XL-FDP immunoreactivity in plasma of patients with acute myocardial infarction and ischemic heart disease and the response to plasminogen activation in vitro induced by pharmacological concentrations of tissue-type plasminogen activator (t-PA) and streptokinase. XL-FDPs were measured with two different ELISA. One, "pan-specific tag ELISA," was based on a capture MAb specific for XL-FDP and a tag MAb that recognizes an epitope exposed in the fragment D region of both fibrin and fibrinogen, whereas the other, "fibrin-specific tag ELISA," was based on a capture and tag MAbs both specific for fibrin. After plasminogen activation was induced in vitro in plasma from patients with myocardial infarction, increased concentrations of XL-FDP were measured by the pan-specific tag ELISA; however, concentrations measured with the fibrin-specific tag ELISA were not increased. To determine the mechanism for this discrepancy, plasma was subjected to immunoadsorption with a MAb specific for fragment D-dimer before and after in vitro activation of the fibrinolytic system and immunoblotting with a fragment D-dimer-specific MAb and with the pan-specific MAb. Increased concentrations of fragment D-dimer, as well as fibrinogen fragment D at high concentrations, were recognized by the specific MAb. Non-cross-linked fragments were also shown by immunoblotting with the pan-specific MAb to coprecipitate with cross-linked fibrin fragments. This suggested the increased concentrations of XL-FDP measured by the panspecific tag ELISA after in vitro activation of the fibrinolytic system were due to detection of non-cross-linked fibrinogen fragments. However, fibrin fragment D-dimer concentrations were found to increase in plasma of 15 patients given t-PA for acute myocardial infarction. We conclude fragment D-dimer in plasma of patients during thrombolysis does not originate from circulating soluble cross-linked fibrin but rather is a marker of solid-phase fibrin dissolution, which may be quantitated with assays based on capture and tag antibodies that do not detect fibrinogen or its degradation products. (Circulation 1990;82:1159-1168

show abstract

“…3,4 Reduced HRV is also associated with the processes linked to AMI, such as atherosclerosis 5 and inflammation. 6 Abnormal plasma markers of endothelial damage (von Willebrand factor (vWF)), 7 platelet activation (soluble P-selectin (s-Psel), 8 CD 40 -ligand (CD 40 L)) 9 and thrombogenesis (D-dimer) 10 are recognized in AMI, but their linkage to autonomic tone is untested. Autonomic tone and platelet-induced thrombosis in vitro is linked by α 2 receptor mediation 11,12 and seen in vivo 13 in studies examining mental stress and dynamic exercise.…”

Section: Introductionmentioning

confidence: 99%

Markers of Thrombosis and Hemostasis in Acute Coronary Syndromes: Relationship to Increased Heart Rate and Reduced Heart‐Rate Variability

Hamaad

Sosin

Blann

et al. 2009

Clinical Cardiology

View full text Add to dashboard Cite

Background: Acute coronary syndromes (ACS) are characterized by abnormal heart-rate variability (HRV) and biomarkers of endothelial damage and thrombosis. Hypothesis: We hypothesized an association between these factors in patients with ACS. Methods: We studied 99 patients with ACS measuring HRV and plasma markers of endothelial damage/dysfunction (von Willebrand factor, vWF) and thrombosis/hemostasis (soluble P-selectin (s-Psel); CD 40 -ligand (CD 40 -L); D-dimer). HRV and plasma indices were compared to age-and gender-matched controls. Measures were repeated at 4 months in a subset. vWF, s-Psel and D-Dimer levels were raised compared to control. Results: HRV indices were reduced (mean RR, SDNN, SDNNi, RMSSD, Triangular index, LF and HF). There were weak correlations between mean RR and s-Psel (R = −0.234, p = 0.023) and D-dimer (R = −0.219, p = 0.041). At 4-month follow-up, significant correlations were between mean RR and CD 40 L (R = −0.414, p = 0.008) and D-dimer (R = −0.363, p = 0.012). On multivariate logistic regression analysis statin use (p = 0.046) was the only independent predictor of acute s-Psel levels. Age (p = 0.004) and mean RR interval (p = 0.01) were independent predictors of D-dimer levels at follow-up. Conclusions: Abnormal HRV is associated with markers of hemostasis and thrombosis in ACS, and present both in the acute and rehabilitation phases.

show abstract

Elevated serum D dimer: A degradation product of cross-linked fibrin (XDP) after intravenous streptokinase during acute myocardial infarction

Cited by 44 publications

References 16 publications

Diagnosis of pulmonary embolism in the coronary care unit

Diagnosis of pulmonary embolism in the coronary care unit

Validity of enzyme-linked immunosorbent assays of cross-linked fibrin degradation products as a measure of clot lysis.

Markers of Thrombosis and Hemostasis in Acute Coronary Syndromes: Relationship to Increased Heart Rate and Reduced Heart‐Rate Variability

Contact Info

Product

Resources

About