Low-Molecular-Weight Heparin (Fragmin) and Thrombin Active-Site Inhibitor (Argatroban) Compared in Experimental Arterial and Venous Thrombosis and Bleeding Time

1996 ◽  
Vol 28 (1) ◽  
pp. 19-25 ◽  
Author(s):  
William A. Schumacher ◽  
Christopher L. Heran ◽  
Thomas E. Steinbacher
Keyword(s):  
Molecular Weight ◽  
Venous Thrombosis ◽  
Active Site ◽  
Low Molecular Weight Heparin ◽  
Bleeding Time ◽  
Low Molecular Weight

A Comparison Between Low Molecular Weight Heparin (KABI 2165) and Standard Heparin in the Intravenous Treatment of Deep Venous Thrombosis

1985 ◽  
Vol 54 (04) ◽  
pp. 813-817 ◽  
Author(s):  
Göran Bratt ◽  
Eva Törnebohm ◽  
Staffan Granqvist ◽  
Wiveca Åberg ◽  
Dieter Lockner
Keyword(s):  
Molecular Weight ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Low Molecular Weight Heparin ◽  
Bleeding Time ◽  
Low Molecular Weight ◽  
Treatment Groups ◽  
Intravenous Treatment ◽  
Heparin Activity ◽  
The Mean

SummaryIn order to study whether a low molecular weight heparin (LMWH) of mw 4000 D is effective in the treatment of deep venous thrombosis (DVT), patients with DVT verified by phlebography were randomized to treatment by continuous intravenous infusion of either unfractionated heparin (UFH) or LMWH. The initial dose was 240 U (anti F Xa)/kg/12 h. TTiis study (study I) was stopped because of major bleeding in 2 newly operated patients in the LMWH group after 27 patients had been treated. The heparin activity measured as F Xa inhibition assayed in retrospect, was found to be much higher in the LMWH group (mean 1.6-2.0 anti F Xa U/ml) than in the UFH group (mean 0.5-0.8 anti F Xa U/ml).A second study was therefore initiated in which the DVT patients were randomly given UFH (240 U/kg/12 h) or LMWH only 120 U (anti F Xa)/kg/12 h, as initial doses (study II). In this study 27 patients could be evaluated, the mean heparin activity still being higher in the LMWH group (0.9-1.2 anti F Xa U/ml) than in the UFH group (0.5-0.7 anti F Xa U/ml).A second phlebographic investigation showed progression of thrombus size in 3 (11%) of the UFH patients of studies I and II (n = 29) and improvement in 14 (48%). There was no progression in any LMWH patient, 6 (50%) had improved in study I and 10 (77%) in study II. The mean decrease of thrombus size score (according to Marder) during treatment did not differ between the 3 groups.Antithrombin III decreased significantly in the UFH group but not in the LMWH groups. Aminotransferases increased in all 3 groups. There was no difference in mean capillary bleeding time between the 3 treatment groups.Although this material is relatively small, our findings suggest that LMWH seems to be of similar effectivity as UFH.

Markers of Hemostatic System Activation in Acute Deep Venous Thrombosis-Evolution during the First Days of Heparin Treatment

1993 ◽  
Vol 70 (06) ◽  
pp. 0909-0914 ◽  
Author(s):  
Keyword(s):  
Molecular Weight ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Unfractionated Heparin ◽  
Low Molecular Weight Heparin ◽  
Factor Xa ◽  
Low Molecular Weight ◽  
Dose Adaptation ◽  
Heparin Treatment ◽  
Lung Scan

SummaryFibrin D-Dimer (D-Di), prothrombin activation fragment (F 1+2) and thrombin-antithrombin III complexes (TAT) were measured using ELISA procedures in the plasma of patients with an acute deep venous thrombosis (DVT), at presentation and on days 2, 6 and 10 after initiation of heparin treatment. Patients were randomly allocated into two treatment groups: 44 patients received adapted doses of continuous intravenous unfractionated heparin (UH) whereas 47 received 1 mg/kg every twelve hours of a low molecular weight heparin (enoxaparin) subcutaneously. A phlebography and a perfusion lung scan were performed before inclusion and on day 10. Failure of therapy (n = 9) was defined by venogram worsening or confirmed pulmonary embolism. Improvement (n = 44) or stationary state (n = 38) were defined by venogram evolution in the absence of new leg scan defects.At presentation, D-Di, F 1 + 2 and TAT were above cut-off values in 97, 66 and 89% of patients respectively. D-Di levels correlated with the extent of venous thrombosis whereas TAT and F 1 + 2 did not. Mean levels of D-Di decreased sharply during the first days of treatment but were still abnormal on day 10. A secondary increase of D-Di on days 6 or 10 by more than 3 μg/ml occurred in 4 of the 9 patients who developed a thromboembolic recurrence but in none of the 72 patients who had a more favorable outcome. F 1 + 2 and TAT time-courses were not related to clinical evolution. In the Enoxaparin group, there was no relationship between antifactor Xa activities and any biological markers. TAT and F 1 + 2 levels fell on day 2 and remained stable until day 10. In contrast, in the UH group, TAT and F 1 + 2 did not significantly decrease on day 2, probably due to a delay in dose adaptation, but they declined slowly until day 10.In conclusion, D-Di displays a higher sensitivity than F 1 + 2 or TAT for the diagnosis of D\T. D-Di, but not TAT or F 1 + 2, follow-up seems to be of potential value for early detection of recurrency. Hemostatic activation is controlled earlier by fixed doses of a low molecular weight heparin, irrespective of the plasma anti-factor Xa activities, than by unfractionated heparin at adapted doses.

scholarly journals Unfractionated or Low–Molecular Weight Heparin for the Treatment of Cerebral Venous Thrombosis

Stroke ◽  
2010 ◽  
Vol 41 (11) ◽  
pp. 2575-2580 ◽  
Author(s):  
Jonathan M. Coutinho ◽  
José M. Ferro ◽  
Patrícia Canhão ◽  
Fernando Barinagarrementeria ◽  
Marie-Germaine Bousser ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Venous Thrombosis ◽  
Cerebral Venous Thrombosis ◽  
Low Molecular Weight Heparin ◽  
Low Molecular Weight

scholarly journals Low-dose low–molecular-weight heparin is anti-inflammatory during venous thrombosis

1998 ◽  
Vol 28 (5) ◽  
pp. 848-854 ◽  
Author(s):  
L.Joseph Downing ◽  
Robert M. Strieter ◽  
Amy M. Kadell ◽  
Carol A. Wilke ◽  
Lazar J. Greenfield ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Venous Thrombosis ◽  
Low Molecular Weight Heparin ◽  
Low Dose ◽  
Low Molecular Weight ◽  
Anti Inflammatory

PLATELET ADHESION AND THROMBIN DEPENDENT AGGREGATION OF PATIENTS WITH AN UREMIC BLEEDING TENDENCY

1987 ◽  
Author(s):  
Jaap J Zwaginga ◽  
Philip G de Groot ◽  
Jan J Sixma
Keyword(s):  
Molecular Weight ◽  
Whole Blood ◽  
Low Molecular Weight Heparin ◽  
Platelet Adhesion ◽  
Umbilical Artery ◽  
Bleeding Time ◽  
Low Molecular Weight ◽  
Bleeding Tendency ◽  
Perfusion Chamber ◽  
Normal Plasma

Five patients with chronic renal insufficiency (CRI) presented a Simplate bleeding time of > 30’, two patients had normal bleeding times (< 9’)- Blood was collected before standard hemodialysis into 19 mM citrate (plasma concentration). It was circulated fojr 5’ through an annular perfusion chamber at a shear of 1300 s™1 over inverted umbilical artery segments. CRI blood’s hematocrit was raised to .3 by adding their own RBC’s. Control whole blood perfusates with Ht .3 were made by addition of their own plasma. After perfusion platelet adhesion on the artery was evaluated by microscope, corrected for platelet count of the perfusate and given as percentage surface covered. Control donors showed a 37.4 ± 5.2% coverage not different from ‘bleeding’ patients 38.0 ± 4.5% ’non bleeding’ CRI patients: 32.3 ± 3.9. We also perfused blood of three ’bleeding’ CRI patients in a new thrombus forming system. In a rectangular perfusion chamber (J Lab Clin Med 1983, 522-532) blood anticoagulated with low molecular weight heparin (Fragmin1, Kabi Vitrum) was circulated over tissue factor containing matrix of 43-phorbol 12-myristate 13-acetate perturbed endothelial cells. Locally formed thrombin stimulated platelet aggregation on this matrix. Aggregation was expressed as percentage of spread platelets covered with aggregates. Perfusions with the following perfusates were performed: whole blood of controls (WBc) and patients (WBp), CRI platelets with normal plasma and RBC’s (A), CRI plasma with normal platelets and RBC’s (B) and normal platelets with normal plasma and RBC’s (C).Platelet adhesion of CRI whole blood is not defective, aggregation, however, is. Uremic platelets in normal plasma may have an adhesion defect (A). The defective aggregation caused by uremic plasma (B) seems to be corrected for uremic platelets in normal plasma (A).

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