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Download Acute Pulmonary Embolism: A Challenge for Hemostasiology by N. W. März, M. Nauck, H. Wieland (auth.), Dr. A. Geibel, PDF

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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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 [37]. , comparing 89 patients with deep vein thrombosis with 89 controls [19]. Mandel et ai. found that patients with concurrent homocystinuria and factor V Leiden have an increased risk of thrombosis [75].

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].

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