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DOI: 10.1055/s-2005-866773
© Georg Thieme Verlag Stuttgart · New York
Wenn die Myofilamente sensibel werden
Ca2+ -Sensitizer zur Therapie der HerzinsuffizienzSensitization of the myofilaments and its implication for treatment in human heart failurePublication History
eingereicht: 28.5.2004
akzeptiert: 3.2.2005
Publication Date:
05 April 2005 (online)

Die Herzinsuffizienz wird definiert als ein akutes oder chronisches Unvermögen des Herzens, bei Belastung oder/und in Ruhe dem Organismus das für den Stoffwechsel erforderliche Blutvolumen zur Verfügung zu stellen. Man unterscheidet systolische und diastolische Herzinsuffizienz. Die systolische Herzleistungsschwäche ist in der Kontraktionsphase gelegen: Das Herz ist nicht in der Lage, sich ausreichend zusammenzuziehen und Kraft zu entwickeln, um genügend Blut auszuwerfen und den Kreislauf auf den Weg zu bringen (z. B.: nach Herzinfarkt, Myokarditis oder bei pathologischen Veränderungen der Herzklappen). Bei der diastolischen Herzinsuffizienz liegt zunächst überhaupt keine Kontraktionsschwäche des Herzens vor, sondern das Herzmuskelgewebe kann in der Diastole nicht ausreichend erschlaffen.
Da die Anzahl der Patienten mit Herzinsuffizienz, die auf eine Herztransplantation warten, ansteigt [25], sind Therapien notwendig, die es diesen Patienten ermöglichen, die Zeit bis zur Herztransplantation zu überbrücken. Die pharmakologisch-therapeutische Unterstützung dieser Patienten ist jedoch limitiert. Ein wesentlicher Nachteil von positiv inotropen Substanzen, die über eine Erhöhung der intrazellulären Ca2+-Konzentration die Kontraktionskraft steigern, besteht darin, dass sie möglicherweise durch die Erhöhung der intrazellulären Ca2+-Konzentration eine Ca2+-Überladung der Zelle verursachen, die mit der Bildung von Nekrosen (Anstieg der Apoptoserate), Tachykardien und Arrhythmien einhergeht. Hinzu kommt, dass eine Kontraktionskraftsteigerung durch Erhöhung der intrazellulären Ca2+-Konzentration mit einer Erhöhung des kardialen Sauerstoffverbrauchs aufgrund der Zunahme des Energiebedarfs verbunden ist [20] - und dies in einer Situation, in der sich das Herz bereits schon in einem Sauerstoffversorgungsengpass befindet.
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Prof. Dr. Robert H. G. Schwinger
Klinik III für Innere Medizin, Labor für Herzmuskelphysiologie und Molekulare Kardiologie
Josef-Stelzmann-Straße 9
50924 Köln
Phone: 0221/4783138
Fax: 0221/4783746
Email: Robert.Schwinger@medizin.uni-koeln.de