Zusammenfassung
Bei der Autopsie von Patienten, bei denen sich nach einem thrombotischen Verschluß einer Koronararterie ein tödlich verlaufender Myokardinfarkt entwickelt hat, stellt der Pathologe im Normalfall eine hochgradige Atherosklerose am Ort der Läsion fest. Dieser Zusammenhang ist seit mehr als einem halben Jahrhundert bekannt, und er gilt auch weiterhin. Die ersten Untersucher erkannten, daß der Mechanismus der verursachenden Läsion komplex ist. Trotz dieser Erkenntnis führte die Annahme, Hauptursache seien Lipidablagerungen, zu dem weithin vertretenen Konzept der Atherosklerose als unabhängigem Krankheitsprozeß, bis er durch eine Thrombose kompliziert wird. Langsam setzt sich die Einsicht durch, daß dieses Konzept zu stark vereinfacht und daß nicht zum Verschluß führende Episoden einer Thrombusbildung — nicht nur beim Myokardinfarkt und anderen ischämischen Syndromen, sondern auch in der Pathogenese der Atherosklerose selbst — eine wichtige Rolle spielen. Das heißt, der Thrombus, welcher letztlich das Lumen vollständig verschließt und sich als Myokardinfarkt oder plötzlicher Herztod manifestiert, kann als Endpunkt einer Kette kleinerer thrombotischer Ereignisse verstanden werden. Hierbei kann sich der Thrombus auf der Lumenoberfläche oder innerhalb der Intima oder an beiden Stellen gleichzeitig gebildet haben. Im folgenden wird besonders auf die komplexen Wechselwirkungen zwischen Atherosklerose und Thrombose eingegangen.
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Fulton, W.F.M. (1987). Koronaratherosklerose, Fissurbildung der Plaque und Thrombose. In: de Bono, D.P., Brochier, M.L., Hugenholtz, P.G., Kübler, W., Verstraete, M. (eds) Thrombolytische Therapie des akuten Herzinfarkts. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72754-2_2
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