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Pathophysiologie der Herzinsuffizienz

Pathophysiology of heart failure

  • Schwerpunkt: Herzinsuffizienz
  • Published:
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Zusammenfassung

Die Herzinsuffizienz ist ein klinisches Syndrom und die gemeinsame Endstrecke unterschiedlicher kardialer Erkrankungen. Sie wird von einer Aktivierung des Renin-Angiotensin-Aldosteron-Systems und des sympathischen Nervensystems begleitet. Aktuelle Forschungsergebnisse rücken maladaptive intrazelluläre Signaltransduktionswege, die verminderte Kapillarisierung des insuffizienten Myokards, eine gestörte Kalziumhomöostase, metabolische Veränderungen, Genpolymorphismen und den programmierten Zelltod in den Mittelpunkt des Interesses. Hierbei mussten tradierte Konzepte zum Beispiel zur Rolle der Hypertrophie aufgegeben werden. So resultiert ein zunehmend komplexes Bild, bei dem Veränderungen auf biochemischer, molekularer, metabolischer und zellulärer Ebene ineinander greifen. Basierend auf diesen neuen Konzepten sollten sich mittelfristig neue Therapieansätze der Herzinsuffizienz ergeben.

Abstract

Chronic heart failure is a clinical syndrome and the final common pathway of different cardiac diseases. Heart failure is accompanied by activation of the renin-angiotensin-aldosterone-system and the adrenergic nervous system. In addition, recent data emphasize important roles of maladaptive intracellular signaling pathways, decreased capillary density, altered calcium handling, metabolic changes, genetic polymorphisms, and programmed cell death in the failing heart. In this context, traditional pathophysiological concepts, e. g. concerning the role of cardiac hypertrophy, had to be given up. Thus, an increasingly complex scenario emerges with interdependent changes on the biochemical, molecular, metabolic, and cellular level. Novel therapeutic strategies may soon be based on these new pathophysiological concepts.

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Correspondence to K.C. Wollert.

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Kempf, T., Drexler, H. & Wollert, K. Pathophysiologie der Herzinsuffizienz. Internist 48, 899–908 (2007). https://doi.org/10.1007/s00108-007-1929-3

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  • DOI: https://doi.org/10.1007/s00108-007-1929-3

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