Dilated cardiomyopathy: Changing pathophysiological concepts and mechanisms of dysfunction

Experimental observations made over the past two decades have led to a prof ound shift in the conceptual paradigms about the syndrome of heart failure and dilated cardiomyopathy. As a consequence, heart failure is currently co nsidered a complex disease and is not merely characterized by hemodynamic d isturbances. It is now believed that the syndrome is governed and impelled by neurohormonal imbalances and intracardiac paracrine processes. The latte r processes are mediated by activated cardiac endothelial cells and cytokin es, creating a state of cardiac maladaption and leading to disease progress ion. Therapeutic interventions such as operative left ventricular volume re duction or mitral valve reconstruction should therefore no longer be solely interpreted in terms of hemodynamics (i.e., symptomatic improvements). Eff ects on neurohormonal, endothelial, and cytokine activities should be taken equally into account.