By N. W. März, M. Nauck, H. Wieland (auth.), Dr. A. Geibel, Prof. Dr. H. Just, Dr. med. W. Kasper, Dr. S. Konstantinides (eds.)
The price of echocardiography within the diagnostic work-up of sufferers with suspected acute pulmonary embolism.- New advancements within the thrombolytic treatment of venous thrombosis.- Mechanism of blood coagulation. more moderen features of anticoagulant and antithrombotic therapy.- MR-angiography within the analysis of pulmonary embolism.- Scintigraphy-ventilation/perfusion scanning and imaging of the embolus.- scientific direction and diagnosis of acute pulmonary embolism.- The molecular mechanisms of inherited thombophilia.
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Additional info for Acute Pulmonary Embolism: A Challenge for Hemostasiology
Heller· 1. Seipel Medizinische Universitatsklinik Abteilung Innere Medizin III Otfried-Miiller-StraBe 10 72076 Tiibingen, Germany 27 Clinical implications of the new understanding of thrombophilia S. Moll, D. Gulba Summary Thrombophilia used to be viewed as a disorder caused by a single congenital thrombophilic abnormality with thrombosis often triggered by an exogenous risk situation. It is becoming clear, however, that it is often a compound state with several congenital and acquired thrombophilic abnormalities.
That homocysteinemia is also a risk factor for venous thromboembolism has only emerged in the last few years [19,30,37,75,91]. Falcon et al. compared a group of 80 young patients with venous thromboembolic disease with 51 controls and found a positive association between elevated homocysteine levels and venous thrombosis . , comparing 89 patients with deep vein thrombosis with 89 controls . Mandel et ai. found that patients with concurrent homocystinuria and factor V Leiden have an increased risk of thrombosis .
One of the best investigated markers is the tissue-type plasminogen activator (antigen). The test to examine this marker, which was frequently used in patients with coronary heart disease [5, 10], determines the mass concentration of the tissue-type plasminogen activator using an ELISA technique. The measurement includes active and inactive tissue-type plasminogen activator, mainly those inactivated by plasminogen activator inhibitor. The measurement of both compounds explains why there is a strong association with the plasminogen activator inhibitor levels and why in patients with coronary heart disease and a risk constellation this marker is increased, while the activity of tissue-type plasminogen activator was found to be normal or even decreased [5, 16,23,26].