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Dilated cardiomyopathy: changing pathophysiological concepts and mechanisms of dysfunction
G W De Keulenaer1, D L Brutsaert
1The Department of Physiology and Medicine, University of Antwerp, Belgium. gillesdk@ruca.ua.ac.be
Insights
Heart failure is a complex condition driven by neurohormonal imbalances and paracrine processes, not just hemodynamics. Understanding these factors is crucial for effective treatment of heart failure and dilated cardiomyopathy.
Area of Science:
- Cardiology
- Molecular Biology
Background:
- Heart failure and dilated cardiomyopathy paradigms have shifted.
- These conditions are now viewed as complex, multifactorial diseases.
Purpose of the Study:
- To re-evaluate the understanding of heart failure and dilated cardiomyopathy.
- To emphasize the role of neurohormonal and paracrine processes.
Main Methods:
- Review of experimental observations over the past two decades.
- Analysis of current conceptual paradigms in heart failure research.
Main Results:
- Heart failure is governed by neurohormonal imbalances and intracardiac paracrine processes.
- Activated cardiac endothelial cells and cytokines mediate maladaptation and disease progression.
Conclusions:
- Therapeutic interventions for heart failure should consider neurohormonal, endothelial, and cytokine effects.
- Hemodynamic improvements alone do not fully explain treatment efficacy.
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.