Zusammenfassung
In der Regel liegt den akuten Koronarsyndromen die Ruptur einer atherosklerotischen Plaque zugrunde. Über die Exposition von Kollagen und von v.-Willebrand-Faktor kommt es zur Adhäsion von Thrombozyten über den Glykoprotein-Ib-Rezeptor sowie zur nachfolgenden Aktivierung und Aggregation der Thrombozyten über den Glykoprotein-IIb/IIIa-Rezeptor.
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Rupprecht, H.J. (2000). Stellenwert von Heparin, niedermolekularem Heparin und Hirudin bei akutem Koronarsyndrom. 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_5
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DOI: https://doi.org/10.1007/978-3-642-59667-4_5
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