Pacher R
Klinischen Abteilung für Kardiologie, Universitätsklinik Innere Medizin II, Wien.
Wien Med Wochenschr. 1998;148(5):121-4.
Heart failure is defined as a malfunction of the cardiac muscle. The ongoing interaction between pump failure and the vasculature, however, results in symptoms due to malperfusion of the pulmonary and systemic circuit. As a consequence, biologic systems of pressure and volume control are activated. In the neurohumoral heart failure model the sympathetic nervous system, the renin system and endothelin all develop their own pathologic contribution to the disease process. Thereby the role of endothelin seems to be special since its production is particularly increased in advanced disease. Like angiotensin, endothelin has major proliferative properties to promote adverse vascular and myocardial growth. The finding of increasing neurohumoral activation as heart failure progresses and the role of plasma levels of neurohormones as predictors of mortality has rearranged the primary goal of therapy to suppress these deleterious neurohumoral systems as completely as possible. Though angiotensin converting enzyme inhibitors are currently first line therapy of heart failure, uncertainties remain concerning their mechanisms of action and - associated to that - optimal dosing.