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Systolische und diastolische Funktionsveränderungen bei der hypertensiven Herzkrankheit

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Endorganschädigungen der arteriellen Hypertonie — Konsequenzen für Diagnostik und Therapie

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Zusammenfassung

In den letzten Jahren sind zunehmend Erkenntnisse über strukturelle Anpassungsmechanismen des linken Ventrikels an eine chronisch erhöhte Nachlast, wie sie bei der arteriellen Hypertonie vorliegt, gewonnen worden. Ein erhöhter Blutdruck im systemischen Kreislauf führt zu einer chronisch zunehmenden Arbeitsbelastung des linken Ventriles. Hämodynamisch gesehen liegt der arteriellen Hypertonie anfangs ein vermehrtes Herzminutenvolumen (HMV) bei bereits unangemessen erhöhtem total peripherem Widerstand (TPW) zugrunde, im weiteren Verlaufkommt es dann zu einer Normalisierung des Herzminutenvolumens und stetigem Anstieg des arteriellen Gefäß Widerstandes. Bleibt die Hochdruckkrankheit unbehandelt, führt die chronische Nachlasterhöhung schließlich unter der vermehrten Arbeitsbelastung des Ventrikels zu einer terminalen Herzinsuffizienz. Ergebnisse der Framing-hamstudie zeigten, daß die arterielle Hypertonie neben der koronaren Herzkrankheit (KHK) die häufigste Ursache einer Herzinsuffizienz ist und einen unabhägigen Risikofaktor für das Entstehen einer Herzinsuffizienz darstellt [32, 37].

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Authors
  1. V.-E. Smith
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  2. J. K. Rockstroh
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Editors and Affiliations

  1. 4. Med. Klinik, Universität Erlangen-Nürnberg, Kontumazgarten 14-18, D-8500, Nürnberg 80, Germany

    Roland E. Schmieder

  2. Nibelungenstraße 9a, D-8000, München 19, Germany

    Hans-Michael Müller

  3. Section of Hypertension, Ochsner Clinic, 1514 Jefferson Highway, 70121, New Orleans, LA, USA

    Franz H. Messerli

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© 1991 Springer-Verlag Berlin Heidelberg

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Smith, VE., Rockstroh, J.K. (1991). Systolische und diastolische Funktionsveränderungen bei der hypertensiven Herzkrankheit. In: Schmieder, R.E., Müller, HM., Messerli, F.H. (eds) Endorganschädigungen der arteriellen Hypertonie — Konsequenzen für Diagnostik und Therapie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76361-8_12

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  • DOI: https://doi.org/10.1007/978-3-642-76361-8_12

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