Chronic heart failure is characterised by neuroendocrine activation as an attempt of the body to maintain pump function of the heart and blood pressure for the perfusion of peripheral tissues. While this neuroendocrine activation is beneficial in the short term, it induces maladaptive remodeling of the heart with continuous deterioration of left ventricular function. Accordingly, pharmacological treatment of patients with heart failure aims at protecting the heart from this neuroendocrine activation, which is represented in particular by the sympathetic nervous and the renin-angiotensin-aldosterone systems. While this concept is based on evidence from numerous large randomised placebo-controlled studies in patients with systolic heart failure, about half of the patients with heart failure have preserved systolic function, and most studies antagonising neuroendocrine activation were not successful in these latter patients. Here, we review the pathophysiological changes that occur in patients with heart failure and provide an overview on the mechanisms and clinical evidence of currently applied pharmacological treatment in patients with systolic heart failure.
Disclosure: Christoph Maack received speaker honoraria from Pfizer, Berlin Chemie, Bayer and Servier. Michael Böhm received speaker honoraria from Servier, Pfizer, Novartis, Medtronic, St. Jude and Bo
