Fibrin Degradation Products Are Not Specific Markers for Thrombolysis in Myocardial Infarction

Seifried, Erhard; Tanswell, P.; Rijken, D C; Kluft, C.; Hoegee, E.; Nieuwenhuizen, W.

doi:10.1016/s0140-6736(87)90919-6

Cited by 22 publications

(5 citation statements)

References 4 publications

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“…In healthy volunteers, FgDP did not increase significantly upon infusion of rt-PA. In contrast, FbDP increased significantly with a maximurn value at 30 min, as shown in our previous publications (18,19).…”

Section: Plasma Levels Of Fibrinogensupporting

confidence: 87%

“…There is now good evidence that thrombolytic therapy not only accelerates fibrinolysis but also activates the coagulation system (15,16). The aim of the present study was therefore to extend our earlier investigations on circulating fibrinogen in vivo during thrombolytic therapy with rt-PA in patients with acute myocardial infarction (17) and in healthy volunteers (18)(19)(20). Firstly, we applied a recently developed EIA for "intact fibrinogen" based on two monoclonal antibodies which does not detect fibrinogen degradation products (21).…”

mentioning

confidence: 99%

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Influence of Acute Myocardial Infarction and rt-PA Therapy on Circulating Fibrinogen

Seifried

Oethinger

Tanswell³

et al. 1993

Thromb Haemost

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SummaryIn 12 patients treated with 100 mg rt-PA/3 h for acute myocardial infarction (AMI), serial fibrinogen levels were measured with the Clauss clotting rate assay (“functional fibrinogen”) and with a new enzyme immunoassay for immunologically intact fibrinogen (“intact fibrinogen”). Levels of functional and “intact fibrinogen” were strikingly different: functional levels were higher at baseline; showed a more pronounced breakdown during rt-PA therapy; and a rebound phenomenon which was not seen for “intact fibrinogen”. The ratio of functional to “intact fibrinogen” was calculated for each individual patient and each time point. The mean ratio (n = 12) was 1.6 at baseline, 1.0 at 90 min, and increased markedly between 8 and 24 h to a maximum of 2.1 (p <0.01), indicating that functionality of circulating fibrinogen changes during AMI and subsequent thrombolytic therapy. The increased ratio of functional to “intact fibrinogen” seems to reflect a more functional fibrinogen at baseline and following rt-PA infusion. This is in keeping with data that the relative amount of fast clotting “intact HMW fibrinogen” of total fibrinogen is increased in initial phase of AMI. The data suggest that about 20% of HMW fibrinogen are converted to partly degraded fibrinogen during rt-PA infusion. The rebound phenomenon exhibited by functional fibrinogen may result from newly synthesized fibrinogen with a high proportion of HMW fibrinogen with its known higher degree of phosphorylation. Fibrinogen- and fibrin degradation products were within normal range at baseline. Upon infusion of the thrombolytic agent, maximum median levels of 5.88 μg/ml and 5.28 μg/ml, respectively, were measured at 90 min. Maximum plasma fibrinogen degradation products represented only 4% of lost “intact fibrinogen”, but they correlatedstrongly and linearly with the extent of “intact fibrinogen” degradation (r = 0.82, p <0.01). In contrast, no correlation was seen between breakdown of “intact fibrinogen” and corresponding levels of fibrin degradation products. We conclude from our data that the ratio of functional to immunologically “intact fibrinogen” may serve as an important index for functionality of fibrinogen and select patients at high risk for early reocclusion. Only a small proportion of degraded functional and “intact fibrinogen”, respectively, is recovered as fibrinogen degradation products. There seems to be a strong correlation between the degree of elevation of fibrinogen degradation products and the intensity of the systemic lytic state, i.e. fibrinogen degradation.

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Section: Plasma Levels Of Fibrinogensupporting

confidence: 87%

mentioning

confidence: 99%

Influence of Acute Myocardial Infarction and rt-PA Therapy on Circulating Fibrinogen

Seifried

Oethinger

Tanswell³

et al. 1993

Thromb Haemost

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“…The absence of underlying diseases associated with marked intravascular fibrin deposition (deep vein thrombosis, pulmonary embolism, disseminated intravascular coagulation, malignant disease) as well as the fact that D-dimer maximum was correlated with the length of occlusion make it likely that D-dimer was mainly generated at the site of local thrombolysis. However, other body pools of fibrin may be present and contribute to the increase of D-dimer: in atherosclerotic disease, which was the basis of the thrombotic occlusions in our patients, amounts of lysable systemic fibrin may be higher than in healthy subjects, who were also found to exhibit D-dimer elevation following infusion with rt-PA due to lysis of systemic fibrin (13). In the six patients with successful primary recanalization the increase of D-dimer was at least 5-fold of the initial value.…”

Section: Discussionmentioning

confidence: 61%

D-Dimer in Local Thrombolytic Therapy with Low Doses of Recombinant Human Tissue-Type Plasminogen Activator (rt-PA) in Patients with Peripheral Arterial Occlusive Disease

et al. 1990

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SummaryThe generation of D-dimer was studied in the course of local thrombolytic therapy of peripheral arterial occlusions with low doses of recombinant human tissue-type plasminogen activator (rt-PA) in 7 patients. Intermittent local application of rt-PA resulted in a marked increase in D-dimer exceeding values usually seen after intravenous application of manifold higher doses used in myocardial infarction. The increase in D-dimer was related to the estimated thrombus size (length of the occlusion) and the total dose of rt-PA applied. During local rt-PA infusion 6 of 7 patients maintained plasminogen activator inhibitor capacity (PAI-cap) between 34% and 79% of their corresponding pre-treatment levels; detectable levels of PAI-cap in circulating blood during the procedure did not interfere with the success of therapy.

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“…fehlenden prospektiven Aussagewert der Fibrin(ogen)spaltprodukte für den Ausgang der Lyse erklären. Zusätzlich weisen unsere Ergebnisse der FbDP bei gesunden Probanden darauf hin, daß diese spezifisch gemessenen Endprodukte der Fibrinolyse aus einem Fibrinpool zu stammen scheinen, de.r, nicht in der Koronarstrombahn liegt (25,26). Die in den letzten Jahren durchgeführten Studien diskutieren einen löslichen Fibrinpool als Quelle der Fibrinspaltprodukte (10,36,37 …”

Section: Fibrinogen-und Fibrinspaltprodukteunclassified

Verlauf von zirkulierendem Fibrinogen beim akuten Myokardinfarkt unter thrombolytischer Therapie mit rt-PA

Oethinger¹,

Tanswell²,

Nobel³

et al. 1994

LaboratoriumsMedizin

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In 12 patients treated with WO mg rt-PA 3 h for acute myocardial infarction (AMI), serial fibrinogen levels were measured with the Clauss clotting rate assay ("functional 62Lab.med. 18: 62 (1994) Brought to you by | University of Queensland -UQ Library Authenticated Download Date | 6/18/15 8:57 PM Originalie J fibrinogen ") andwith a newenzyme immunoassay for immunologically intact fibrinogen ("intact fibrinogen "). Levels off u national and intact fibrinogen were strikingly different: fuYictional levels were higher at baseline; showed a more pronounced breakdown during rt-PA therapy; and a rebound phenomenon which was not seen for intact fibrinogen. The rat/o offunctionalto intactfibrinogen wascalculatedforeach individual patient and each time point. The mean ratio (n = 12) was 1.6 at baseline, 1.0 at 90 min., and increased markedly between 8 and 24htoa maximum of2.1 (p < 0.01), indicating thatfunctionalityofcirculating fibrinogen changes during AMI and subsequent thrombolytic therapy. The increased ratio offunctional to intact fibrinogen seems to reflect a more functional fibrinogen at baseline and following rt-PA infusion. This is in keeping with data that the relative amount of fast clotting intact HMW fibrinogen of total fibrinogen is increased in initial phase ofAMI. The data suggestthatabout20 % ofHMW fibrinogen are converted to partly degraded fibrinogen during rt-PA infusion. The rebound phenomenon exhibited by functional fibrinogen may result from newly synthesized fibrinogen with a high proportion of HMW fibrinogen with itsknown higher degree of phosphorylation. Fibrinogen-and fibrin degradation products were with i n normal ränge atbaseline. Upon infusion ofthe thrombolytic agent, maximum median levels of 5.88 \ig/ml and 5.28 [ig/ml, respectively, were measured at 90 minutes. Maximum plasma fibrinogen degradation products represented only 4% oflost intact fibrinogen, buttheycorrelatedstrongly and linearly with the extent of intact fibrinogen degradation (r=0.82, p<0.01). In contrast, no correlation was seen between breakdown of intact fibrinogen and corresponding levels of fibrin degradation products. We conclude from our data that the ratio offunctional to immunologically intact fibrinogen may serve äs an important Index for functionality of fibrinogen and select patients at high risk for early reocclusion. Only a small proportion of degraded functional and intactfibrinogen, respectively, is recoveredas fibrinogen degradation products. There seems to be a strong correlation between the degree of elevation of fibrinogen degradation products and the intensity of the Systemic lytic state, i.e. fibrinogen degradation.Keywords: fibrinogen and fibrin degradation products-enzyme immunoassay-intact fibrinogen -functional fibrinogen -acute myocardial infarction -rt-PA therapy

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Fibrin Degradation Products Are Not Specific Markers for Thrombolysis in Myocardial Infarction

Cited by 22 publications

References 4 publications

Influence of Acute Myocardial Infarction and rt-PA Therapy on Circulating Fibrinogen

Influence of Acute Myocardial Infarction and rt-PA Therapy on Circulating Fibrinogen

D-Dimer in Local Thrombolytic Therapy with Low Doses of Recombinant Human Tissue-Type Plasminogen Activator (rt-PA) in Patients with Peripheral Arterial Occlusive Disease

Verlauf von zirkulierendem Fibrinogen beim akuten Myokardinfarkt unter thrombolytischer Therapie mit rt-PA

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