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Glykoprotein-IIb/IIIa-Hemmer und ADP-Antagonisten

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Gerinnungsaktive Therapie beim akuten Koronarsyndrom
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Zusammenfassung

Zelluläre Hämostase und plasmatische Gerinnung sind funktionell eng miteinander verbunden (Abb. 1). So exponieren aktivierte Plättchen an ihrer Oberfläche prokoagulatorische Aktivität, die die Thrombin-und anschließende Fibrinbildung verstärkt. Thrombin ist nicht nur das Schlüsselenzym der plasmatischen Gerinnung, sondern auch ein äußerst potenter Plättchenstimulator, wobei zur Plättchenstimulation weniger als 1/10 der Thrombinkonzentration genügt, die zur Gerinnung führt. Das bedeutet zum einen, daß immer dann, wenn es zur Gerinnung kommt, auch Plättchen aktiviert werden. Andererseits kann in Gegenwart eines Thrombinhemmstoffes, wie z. B. Hirudin, auch bei einer starken Gerinnungshemmung noch genügend Thrombin entstehen, um Plättchen zu aktivieren und die zelluläre Hämostase sicherzustellen.

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Patscheke, H. (2000). Glykoprotein-IIb/IIIa-Hemmer und ADP-Antagonisten. In: Hach-Wunderle, V., Neuhaus, KL. (eds) Gerinnungsaktive Therapie beim akuten Koronarsyndrom. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59667-4_3

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  • DOI: https://doi.org/10.1007/978-3-642-59667-4_3

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-66379-9

  • Online ISBN: 978-3-642-59667-4

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