[Pathophysiology of heart failure today].
METHODS
In chronic heart failure mechanisms which regulate myocardial contractility are defective (Frank-Starling mechanism, force-frequency-relationship, beta-adrenergic responsiveness). Neuroendocrine mechanisms induce the progression of left ventricular dysfunction to chronic heart failure (renin-angiontensin-aldosterone system, endothelin system, sympathetic nervous system). Angiotensin II and norepinephrine induce programmed cell death (apoptosis) in myocardial cells, thereby contributing to the progression of left ventricular function to heart failure.
Established principles for treatment are based on the antagonism of these neuroendocrine mechanisms. New concepts like augmentation of myocardial regeneration by stem cells are an attractive perspective for innovative treatments of heart failure. The characterization of the underlying mechanisms can offer potential new strategies of the treatment of these malignant condition.
Böhm
Michael
M
Medizinische Universitätsklinik und Poliklinik, Innere Medizin III, Homburg/Saar. boehm@med-in.uni-saarland.de
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000473:pathology; D009490:Neurosecretory Systems / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000502:physiology