Metabolism of the failing heart.
Our understanding of the pathogenesis and therapy of heart failure has evolved through three paradigms. Organ physiology, the first paradigm, focused therapy of heart failure on salt and water retention and vasoconstriction, which represent major circulatory responses to, cardiac pumping. The second paradigm of cell biochemistry led to the development of powerful inotropic agents designed to increase myocardial contractility. The third paradigm, gene expression (molecular biology), describes regulatory mechanisms that are both primitive and complex; in the setting of heart failure, this paradigm focuses on the roles of altered myocardial cell growth and composition in explaining the accelerated deterioration of the hypertrophied, failing heart. This review focuses on one aspect of the second paradigm: factors that contribute to a state of energy-starvation and the resulting functional consequences in the failing heart.
Katz
A M
AM
Department of Medicine, University of Connecticut, Farmington.
D000255:Adenosine Triphosphate / Q000378:metabolism; D004734:Energy Metabolism; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D016623:Ion Pumps / Q000378:metabolism; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism
D016623:Ion Pumps; D010725:Phosphocreatine; D000255:Adenosine Triphosphate