Antithrombotic therapy in patients with known risk factors for thromboembolism.
In about 50% of the cases of spontaneous deep vein thrombosis a congenital deficiency of an inhibitor of coagulation or an insufficient fibrinolytic mechanism can be detected. In arterial thromboembolism a connection with hyperactive platelets or with a diminished availability of tissue plasminogen activator can be found in about 70%. However, in these cases the defect which provokes thrombosis is mostly acquired and is connected with hyperlipidemia and/or with atherosclerotic alterations of the vessel wall. A study on patients with thromboembolic tendency and detectable risk factors was carried out. A total of 470 patients could be observed for 2 years under an adequate antithrombotic prophylaxis. The occurrence of thromboembolic episodes 2 years prior to prophylaxis and 2 years under prophylaxis was compared. In venous cases thrombosis could be controlled almost completely by coumarins when the underlying cause was a deficient plasmatic inhibitor. In patients with diminished fibrinolysis there was only a partial effect of oral anticoagulants. A better result could be obtained when pentosan polysulfate was administered. In arterial thromboembolism the results of prophylaxis were less convincing. The efficacy of ASA in patients with an increased platelet function was only moderate. In addition, ASA hat to be discontinued in about 20% of the patients because of gastrointestinal problems. Pentosan polysulfate in patients with a diminished fibrinolytic capacity had a fairly good effect and resulted in a 60% reduction of thromboembolic manifestations. It is shown that an exact diagnosis of the underlying deficiency which is likely to cause thrombosis can also improve the efficacy and the specificity of prophylaxis.
Vinazzer
H
H
Coagulation Laboratory, Linz, Austria.
D000367:Age Factors; D020152:Antithrombin III Deficiency; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006023:Glycoproteins / Q000172:deficiency; D015844:Heparin Cofactor II / Q000172:deficiency; D006801:Humans; D010426:Pentosan Sulfuric Polyester / Q000627:therapeutic use; D010644:Phenprocoumon / Q000627:therapeutic use; D010958:Plasminogen / Q000172:deficiency; D020151:Protein C Deficiency; D017293:Protein S; D012307:Risk Factors; D013923:Thromboembolism / Q000235:genetics / Q000517:prevention & control*; D000979:alpha-2-Antiplasmin / Q000378:metabolism
D005343:Fibrinolytic Agents; D006023:Glycoproteins; D017293:Protein S; D000979:alpha-2-Antiplasmin; D010426:Pentosan Sulfuric Polyester; D015844:Heparin Cofactor II; D010958:Plasminogen; D010644:Phenprocoumon