Heparin Resistance in Acute Coronary Occlusion Measured by the Plasma Heparin Thrombin Time

1960 ◽  
Vol 23 (4) ◽  
pp. 195-207 ◽  
Author(s):  
T. Holger-Madsen
1960 ◽  
Vol 04 (02) ◽  
pp. 261-268
Author(s):  
T Holger-Madsen ◽  
M Schioler

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.


1962 ◽  
Vol 07 (01) ◽  
pp. 188-196 ◽  
Author(s):  
T Holger-Madsen

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.


1961 ◽  
Vol 06 (01) ◽  
pp. 125-143
Author(s):  
T Holger-Madsen

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.


1961 ◽  
Vol 06 (03) ◽  
pp. 573-579
Author(s):  
T Holger-Madsen

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.


1965 ◽  
Vol 13 (02) ◽  
pp. 516-530 ◽  
Author(s):  
O Egeberg

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.


1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.


2021 ◽  
Vol 33 ◽  
pp. 100767
Author(s):  
H. Pendell Meyers ◽  
Alexander Bracey ◽  
Daniel Lee ◽  
Andrew Lichtenheld ◽  
Wei J. Li ◽  
...  

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