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(Circulation. 2004;110:894-896.)
© 2004 American Heart Association, Inc.

Editorial

Cardiac Metabolism as a Target for the Treatment of Heart Failure

Heinrich Taegtmeyer, MD, DPhil

From the Department of Internal Medicine, Division of Cardiology, University of Texas Health Science Center at Houston.

Correspondence to Heinrich Taegtmeyer, MD, DPhil, Division of Cardiology, University of Texas Health Science Center at Houston, 6431 Fannin, MSB 1.246, Houston TX 77030. E-mail Heinrich.Taegtmeyer@uth.tmc.edu

Key Words: Editorials • cardiomyopathy • insulin • metabolism • enzymes

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Few things in life are more irritating than failing to recognize the obvious. A case in point is energy substrate metabolism as a potential target of pharmacological agents for improving function of the failing heart. The complexities of hemodynamics, coronary flow, and cardiac structure obscure the simple fact that the heart is an efficient converter of energy. The reasoning is straightforward: In a series of highly regulated, enzyme-catalyzed reactions, heart muscle converts chemical energy into mechanical energy.¹ Although metabolism and function in the heart are inextricably linked (Figure), few investigators have considered energy substrate metabolism and the first law of thermodynamics (which states that all energy is conserved) as paradigms for the treatment of heart failure. However, interest in this area is growing.

View larger version (10K): [in this window] [in a new window]   Hypothesis of inextricable link between metabolism and function of heart. See text for further discussion.

See p 955

The Present Study in Perspective

A report in this issue of Circulation² joins a canon of papers from Richard Shannon’s laboratory in Pittsburgh describing metabolic derangements^3,4 and interventions⁵ in heart failure. In the present study, the authors show that recombinant glucagon-like peptide 1 (rGLP-1) dramatically improves left ventricular, systemic, and coronary flow hemodynamics in dogs with advanced dilated cardiomyopathy. The basis for this functional improvement appears to be related to the restoration of insulin sensitivity in the failing heart, but these are difficult studies to perform and the mechanism is unclear. The authors were unable to prove that direct metabolic effects on the heart were the cause for the improvement in myocardial . . . [Full Text of this Article]

Related Article:

Recombinant Glucagon-Like Peptide-1 Increases Myocardial Glucose Uptake and Improves Left Ventricular Performance in Conscious Dogs With Pacing-Induced Dilated Cardiomyopathy

Lazaros A. Nikolaidis, Dariush Elahi, Teresa Hentosz, Aaron Doverspike, Rhonda Huerbin, Lee Zourelias, Carol Stolarski, You-tang Shen, and Richard P. Shannon
Circulation 2004 110: 955-961. [Abstract] [Full Text]

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