title: Dilated cardiomyopathy: changing pathophysiological concepts and mechanisms of dysfunction.
abstract: Experimental observations made over the past two decades have led to a profound shift in the conceptual paradigms about the syndrome of heart failure and dilated cardiomyopathy. As a consequence, heart failure is currently considered a complex disease and is not merely characterized by hemodynamic disturbances. It is now believed that the syndrome is governed and impelled by neurohormonal imbalances and intracardiac paracrine processes. The latter processes are mediated by activated cardiac endothelial cells and cytokines, creating a state of cardiac maladaption and leading to disease progression. Therapeutic interventions such as operative left ventricular volume reduction or mitral valve reconstruction should therefore no longer be solely interpreted in terms of hemodynamics (i.e., symptomatic improvements). Effects on neurohormonal, endothelial, and cytokine activities should be taken equally into account.
authors.affiliation: The Department of Physiology and Medicine, University of Antwerp, Belgium. gillesdk@ruca.ua.ac.be
authors.forename: G W
authors.initials: GW
authors.lastname: De Keulenaer
authors.forename: D L
authors.initials: DL
authors.lastname: Brutsaert
mesh_terms: D002311:Cardiomyopathy, Dilated / Q000503:physiopathology* / Q000601:surgery; D016207:Cytokines / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology* / Q000601:surgery; D006352:Heart Ventricles / Q000503:physiopathology / Q000601:surgery; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D018377:Neurotransmitter Agents / Q000502:physiology; D019899:Paracrine Communication / Q000502:physiology; D011379:Prognosis
chemical_list: D016207:Cytokines; D018377:Neurotransmitter Agents