Zusammenfassung
Bei herzinsuffizienten Patienten findet sieh eine Aktivierung des sympathoadrenergen Systems. Hinweise auf die Aktivierung dieses zentralen neurohumoralen Systems ergeben sich sowohl aus dem klinischen Bild der Patienten als auch aus der Messung der sympathischen neuronalen Aktivität und der Bestimmung der Kateeholaminfreisetzung. Die Höhe der Plasmanoradrenalinkonzentration korreliert mit dem Schweregrad der Herzinsuffizienz und ist als prognostischer Indikator den hämodynamischen Parametern überlegen.
Die Ursachen der erhöhten sympathischen Aktivität bei Herzinsuffizienz sind bisher nicht eindeutig geklärt. Diskutiert werden:
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1.
eine Störung der Barorezeptorempfindlichkeit und der zentralen Kreislaufreflexe,
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2.
eine Aktivierung des Sympathikus durch andere vasopressorische Systeme (z.B. das Renin-Angiotensin-System) und
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2.
eine verminderte Elimination der Katecholamine.
Die sympathische Aktivierung kann kurzfristig zur Rekompensation einer schweren Herzinsuffizienz beitragen. Eine längerfristige sympathische Aktivierung gilt aber als wesentlicher pathophysiologischer Faktor für die Progression der Herzinsuffizienz. Diese Einschätzung beruht auf der Beobachtung, daß eine sympathoadrenerge Aktivierung den Energiemangel der noch aktiven Myokardzellen verstärkt und damit zum weiteren Absterben von Myokardzellen führt. Außerdem gibt es Hinweise, daß die sympathische Stimulation ein wichtiger Faktor in der Genese von Rhythmusstörungen bei herzinsuffizienten Patienten ist und daß sie zur Hypertrophie des Herzmuskels beiträgt.
Erste Untersuchungen zeigen günstige Wirkungen einer niedrig dosierten ß-Blockade bei der Herzinsuffizienz.
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Richardt, G., Schömig, A. (1992). Pathophysiologie — Adrenerges System: sympathische Aktivität. In: Dietz, R. (eds) Herzinsuffizienz. Aktuelle Therapieprinzipien in Kardiologie und Angiologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77021-0_12
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