Heparin Resistance, Measured by the Plasma Heparin Thrombin Time, in Patients on Long-term Anticoagulant Therapy with Phenylindanedione Following Coronary Occlusion

1960 ◽  
Vol 04 (02) ◽  
pp. 261-268
Author(s):  
T Holger-Madsen ◽  
M Schioler
Keyword(s):  
Comparative Study ◽  
Anticoagulant Therapy ◽  
Coronary Occlusion ◽  
Tolerance Test ◽  
Thrombin Time ◽  
Clotting Time ◽  
Heparin Resistance ◽  
History Of ◽  
Plasma Heparin

SummaryOf 74 patients with a history of coronary occlusion 42 received anticoagulant (phenylindanedione) therapy, while 32 were untreated. Both groups were investigated in a comparative study of prothrombin determination, heparin tolerance test, and plasma heparin thrombin time. By the latter method the clotting time with thrombin is determined on heparinized, platelet-poor citrated plasma. In several patients on anticoagulant therapy whose prothrombin-proconvertin level was well adjusted and whose heparin clotting time, as measured by the heparin tolerance test, was definitely prolonged in relation to normal, an increased heparin resistance might still be demonstrated in the form of a distinct shortening of the heparin thrombin time. In the majority of the treated patients the anticoagulant therapy had entailed a prolongation of the heparin clotting time as measured by the heparin tolerance test. As measured by the heparin thrombin time, however, the treatment was found to have had no influence on the heparin resistance, there being no difference between the frequency of shortened heparin thrombin time in the treated and in the untreated group.

On the Effect of Heparin at Various Concentrations with Particular Reference to Increased Heparin Resistance Measured by the Plasma Heparin Thrombin Time

1961 ◽  
Vol 06 (03) ◽  
pp. 573-579
Author(s):  
T Holger-Madsen
Keyword(s):  
Thrombin Time ◽  
Clotting Time ◽  
Heparin Concentration ◽  
Heparin Resistance ◽  
Plasma Heparin

SummaryThe heparin thrombin time was investigated in platelet-poor citrated plasma by determining the clotting time with thrombin after addition of heparin. At increasing heparin concentrations the heparin thrombin time was prolonged, reaching a maximum at a certain concentration. At higher concentrations the effect of heparin decreased, the heparin thrombin time getting shorter. At the highest concentrations there was again a full heparin effect, the heparin thrombin time being again prolonged to a maximum. In a study of plasma from patients with increased heparin resistance, in the form of a shortening of the heparin thrombin time in relation to normal, this was found to apply within all the studied ranges of heparin concentration.

Inherited Antithrombin Deficiency Causing Thrombophilia

1965 ◽  
Vol 13 (02) ◽  
pp. 516-530 ◽  
Author(s):  
O Egeberg
Keyword(s):  
Autosomal Dominant ◽  
Antithrombin Iii ◽  
Thrombin Time ◽  
Dominant Trait ◽  
Autosomal Dominant Trait ◽  
Antithrombin Deficiency ◽  
Heparin Resistance ◽  
High Incidence ◽  
History Of ◽  
Plasma Heparin

SummaryBlood coagulation systems were studied in members of a family with remarkably high incidence of thrombo - embolic diseases. Thrombotic episodes most often occurred as deep venous thrombosis in the legs, with the first attack at the age of 10-25 years.Pro coagulant factor activities were found within normal variation ranges.Plasma antithrombin III (progressive antithrombin) activity was abnormally low in members with history of thrombosis and in some of their children, with an average level of about 50 per cent of normal.Heparin resistance measured with plasma heparin thrombin time was increased in members with low antithrombin III, and plasma heparin cofactor activity was decreased.The results strongly support the explanation that antithrombin III and heparin cofactor are one and the same plasma substance, and that deficiency of this antithrombin can cause a severe tendency to thrombosis.The antithrombin deficiency seems to be inherited as an autosomal dominant trait.

Fibrinogen New Orleans: An Inherited Variant with Abnormal Peptide Release

1979 ◽  
Author(s):  
S.I. Chavin ◽  
W.A. Andes ◽  
W.G. Beltran ◽  
W.J. Stuckey
Keyword(s):  
Laboratory Finding ◽  
Polyacrylamide Gel Electrophoresis ◽  
Complete Fusion ◽  
Thrombin Time ◽  
Clotting Time ◽  
Excessive Bleeding ◽  
Normal Limits ◽  
Peptide Release ◽  
Mother And Daughter ◽  
History Of

An inherited fibrinogen abnormality is described in a 30-year old woman with a history of several episodes of excessive bleeding. The initial laboratory finding was a prolonged thrombin time, and a comparable prolongation was present in the plasmas of her mother and daughter, but not of her father. The abnormal fibrinogen gave a reaction of complete fusion with normal fibrinogen in an Ouchterlony plate, and by immunoelectrophoresis, it had a slightly faster than normal anodal migration. The patient’s plasma and purified fibrinogen were able to prolong the clotting time of normal plasma. Using SDS-polyacrylamide gel electrophoresis, we have detected a marked delay in release of a major proportion of the A peptide and a lesser delay in release of the B peptide, after thrombin treatment. B peptide release appeared to be completed before that of A peptide release, in contrast to the situation with normal fibrinogen. Cross-linking of the resulting fibrin was delayed but eventually complete. The rate and extent of monomer aggregation, measured by spectrophotometry, were within normal limits.

Studies on the Anti-Heparin Activity of Serum

1962 ◽  
Vol 07 (01) ◽  
pp. 188-196 ◽  
Author(s):  
T Holger-Madsen
Keyword(s):  
Plasma Level ◽  
Normal Serum ◽  
Thrombin Time ◽  
Original Activity ◽  
Platelet Poor Plasma ◽  
Normal Platelet ◽  
Heparin Resistance ◽  
Heparin Activity ◽  
Plasma Heparin

SummaryThe anti-heparin activity of serum was investigated by adding serum to normal, platelet-poor plasma and determining the heparin thrombin time.BaSO4-adsorbed serum and serum from platelet-poor plasma proved to exert a considerably less marked anti-heparin activity than plain serum. Even in platelet-poor serum, adsorbed with BaSO4 some anti-heparin activity still remained, but by far the greater part of the original activity had disappeared. In some patients, in whom determination of the plasma heparin thrombin time has shown increased heparin resistance, the serum may also exert a greater anti-heparin activity than normal serum. In patients on anticoagulant therapy with phenylindanedione even a considerable lowering of the prothrombin-proconvertin plasma level did not entail any reduction in the anti-heparin activity of the serum as compared with normal serum.

Studies on Increased Heparin Resistance Measured by the Plasma Heparin Thrombin Time

1961 ◽  
Vol 06 (01) ◽  
pp. 125-143
Author(s):  
T Holger-Madsen
Keyword(s):  
Factor V ◽  
Thrombin Time ◽  
Freeze Thaw ◽  
Normal Plasma ◽  
Heparin Resistance ◽  
Tissue Thromboplastin ◽  
Plasma Heparin

SummaryIncreased heparin resistance was found to remain unchanged in BaSO4-adsorbed plasma, but disappeared following adsorption with large quantities of Al(OH)3. The factor V content in the plasma could be considerably reduced without any alteration in the heparin resistance. Antihaemophilic globulin exerted no influence upon the heparin thrombin time. Tissue thromboplastin in quantities sufficient to accelerate the clotting of recalcified plasma considerably, did not affect the heparin thrombin time. Plasma thromboplastin had no antiheparin effect. Increased heparin resistance was — although usually less marked — still demonstrable in most cases in plasma defibrinated with thrombin from patients with a greatly shortened heparin thrombin time, but not in cases of less pronounced shortening. Fibrinogen prepared by the freeze-thaw technique from normal plasma and patient plasma showed no difference in reactivity to heparin and thrombin. In experiments on plasma mixtures, a shortening of the heparin thrombin time was still demonstrable at the ratio 9 parts of normal plasma to 1 part of plasma from patients with greatly increased heparin resistance. The antithrombin content of plasma was not reduced in increased heparin resistance.

Partial Characterization of an Autoantibody Recognizing the Secondary Binding Site(s) of Thrombin in a Patient with Recurrent Spontaneous Arterial Thrombosis

1992 ◽  
Vol 67 (02) ◽  
pp. 193-199 ◽  
Author(s):  
J M Costa ◽  
J N Fiessinger ◽  
L Capron ◽  
M Aiach
Keyword(s):  
Catalytic Activity ◽  
Binding Site ◽  
Arterial Thrombosis ◽  
Thrombin Time ◽  
Clotting Time ◽  
Heparin Cofactor Ii ◽  
Human Thrombin ◽  
History Of

SummaryA patient with an 18 year history of recurrent arterial thrombosis and no evidence of atherosclerosis or embolism of cardiac origin presented with a prolonged thrombin clotting time when performed with human thrombin. The bovine thrombin clotting time was only slightly prolonged. During 30 months of follow-up, the thrombin time fluctuated, but remained prolonged. The patient has been treated with an oral anticoagulant for the past 8 years, with no thrombotic recurrence.The inhibitor activity was due to the presence of polyclonal IgGs which bound to thrombin-Sepharose. The influence of IgGs purified from the patient’s serum was compared to the influence of normal IgGs in several systems exploring the catalytic activity of thrombin and the binding of the enzyme to macromolecular substrates through secondary binding site(s). We found that the IgGs did not impair the catalytic activity toward small synthetic substrates, but inhibited the binding of thrombin to fibrinogen, thrombomodulin and heparin cofactor II. Such proteins are known to require a secondary binding site of thrombin to interact with the enzyme.The anti-thrombin antibody might have resulted from an abnormal generation of thrombin. This would be the consequence of the process favouring thrombosis. Alternatively, the autoantibody might have favoured thrombosis primarily, by impairing natural antithrombotic mechanisms triggered by thrombin.

scholarly journals Long-term prognosis in patients with acute myocardial infarction and newly detected glucose abnormalities: predictive value of oral glucose tolerance test and HbA1c

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Stelios Karayiannides ◽  
Catarina Djupsjö ◽  
Jeanette Kuhl ◽  
Claes Hofman-Bang ◽  
Anna Norhammar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Predictive Value ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
History Of ◽  
Long Term Prognosis

Abstract Background Disturbances of glucose metabolism can be diagnosed by an oral glucose tolerance test (OGTT) and by glycated haemoglobin (HbA1c). The aim of this study was to investigate the association between newly detected disturbances of glucose metabolism and long-term prognosis after acute myocardial infarction (AMI) and to compare the predictive value of an OGTT and HbA1c. Methods Patients under the age of 80 years with no known history of diabetes admitted for AMI at the Department of Cardiology, Danderyd University Hospital, Stockholm, Sweden, from January 1st, 2006 until December 31st, 2013, were investigated with an OGTT and a HbA1c before discharge and were classified as having normal glucose tolerance (NGT), prediabetes or diabetes according to American Diabetes Association (ADA) criteria. Using nationwide, all-inclusive registers, patients were followed for the incidence of combined event [CE (first of myocardial infarction, heart failure, ischaemic stroke or mortality)] for a mean follow-up time of 4.8 years. Cox regression analysis was used to calculate Hazard Ratios (HR) and their 95% confidence intervals (CI). Results Of the 841 patients who were investigated with both an OGTT and a HbA1c, 139 (17%) patients had NGT, 398 (47%) had prediabetes and 304 (36%) had diabetes according to OGTT. The corresponding figures using HbA1c were 320 (38%), 461 (55%) and 60 (7%). Patients with newly discovered diabetes were older and had a higher body mass index compared to those with NGT. OGTT was not predictive for CE. In contrast, prediabetes identified by a HbA1c was associated with an increased risk for CE (HR 1.31; 95% CI 1.05–1.63) compared to normoglycaemia. When comparing the prognostic value of different glucose and HbA1c cut-offs, only a HbA1c ≥ 39 mmol/mol was significantly associated with CE (HR 95% CI; 1.30:1.05–1.61). Conclusion In this single-centre study, in a recent contemporary cohort, we found that around two thirds of the patients admitted with AMI with no known history of diabetes had disturbed glucose metabolism, in accordance with previous studies. HbA1c in the prediabetes range, but not OGTT, added predictive value on the long-term outcome, in a cohort to whom a pathologic OGTT result was communicated with lifestyle advice.

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