Zusammenfassung
Unser Verständnis für die pathogenetischen Mechanismen, die der chronisch stabilen Angina, der instabilen Angina und der Prinzmetal-Angina zugrundeliegen, ist in den letzten Jahren gewachsen. Es besteht jetzt generelles Einvernehmen darüber, daß dynamische Koronarstenosen zu diesen ischämischen Syndromen beitragen [15, 24, 25]. Dynamische Stenosen können durch einen Anstieg im koronaren Gefäß-tonus, durch eine koronare Thrombose oder durch eine Kombination dieser beiden Mechanismen verursacht werden. Die thrombotische Komponente steuert zu den Angina-Syndromen das Merkmal der Instabilität und die Tendenz bei, sich bis hin zum Myokardinfarkt weiterzuentwickeln [18, 32]. Es gilt heute als allgemein akzeptiert, daß eine gelegentliche Zunahme des Gefäßtonus in einer epikardialen Koronararterie nicht nur die Ursache der Prinzmetal-Angina ist, sondern auch eine pathogenetische Komponente in anderen, häufigeren Angina-Syndromen sein mag [15, 18, 24, 25, 32, 50, 771 Obwohl die Begriffe „koronarer Spasmus“ und „koronare Vasokonstriktion“ häufig in der medizinischen Literatur synonym benutzt werden, um eine Zunahme des koronaren Gefäßtonus anzuzeigen, ist eine Unterscheidung zwischen diesen beiden Begriffen notwendig. Der Unterschied zwischen einem koronaren Spasmus, wie er bei der Prinzmetal-Angina gesehen wird, und der koronaren Vasokonstriktion, die häufig bei chronisch stabiler Angina beobachtet wird, ist nicht nur ein Unterschied des Schweregrades, sondern er scheint auch unterschiedliche zugrundeliegende Mechanismen zu reflektieren.
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© 1990 Dr. Dietrich Steinkopff Verlag, GmbH & Co. KG, Darmstadt
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Kaski, J.C., Maseri, A. (1990). Klinische Bedeutung des koronaren Vasomotorentonus bei Myokardischämie. In: Heusch, G. (eds) Pathophysiologie und rationale Pharmakotherapie der Myokardischämie. Steinkopff. https://doi.org/10.1007/978-3-642-72437-4_10
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