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Influence of acute myocardial infarction and rt-PA therapy on circulating fibrinogen
E Seifried1, M Oethinger, P Tanswell
1Medizinische Klinik und Poliklinik, Universität Ulm, Germany.
Insights
This study shows functional fibrinogen levels change significantly during acute myocardial infarction (AMI) and thrombolytic therapy, with a rebound phenomenon not seen in intact fibrinogen levels.
Area of Science:
- Biochemistry
- Cardiology
- Hematology
Background:
- Acute myocardial infarction (AMI) requires prompt treatment, often involving thrombolytic therapy.
- Fibrinogen is a key protein in clot formation and is affected by thrombolytic agents.
- Assessing fibrinogen functionality alongside its intact levels provides deeper insights into its behavior during treatment.
Purpose of the Study:
- To compare functional and intact fibrinogen levels in patients with AMI undergoing thrombolytic therapy.
- To investigate changes in the ratio of functional to intact fibrinogen over time.
- To explore the implications of these changes for fibrinogen functionality during AMI and treatment.
Main Methods:
- Serial measurement of fibrinogen levels using Clauss clotting assay (functional) and enzyme immunoassay (intact).
- Calculation of the ratio between functional and intact fibrinogen at various time points.
- Analysis of fibrinogen and fibrin degradation products.
Main Results:
- Functional fibrinogen levels were higher at baseline, showed more breakdown during rt-PA therapy, and exhibited a rebound phenomenon absent in intact fibrinogen.
- The ratio of functional to intact fibrinogen increased significantly between 8 and 24 hours post-treatment (p < 0.01).
- Data suggest approximately 20% of high molecular weight (HMW) fibrinogen converts to degraded forms during rt-PA infusion.
Conclusions:
- Circulating fibrinogen functionality changes during AMI and thrombolytic therapy.
- An increased functional to intact fibrinogen ratio indicates altered fibrinogen behavior, potentially due to HMW fibrinogen changes.
- Functional fibrinogen rebound may involve newly synthesized, highly phosphorylated HMW fibrinogen.
Abstract:
In 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 micrograms/ml and 5.28 micrograms/ml, respectively, were measured at 90 min.(ABSTRACT TRUNCATED AT 250 WORDS)