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(Circulation. 2005;112:3218-3221.)
© 2005 American Heart Association, Inc.

Editorial

Modulation of Myocardial Energetics

Emerging Evidence for a Therapeutic Target in Cardiovascular Disease

David A. Morrow, MD, MPH; Michael M. Givertz, MD

From the TIMI Study Group (D.A.M.) and Advanced Heart Disease Program (M.M.G.), Cardiovascular Division (D.A.M., M.M.G.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

Correspondence to David A. Morrow, MD, MPH, TIMI Study Group, 350 Longwood Ave, First Floor, Boston, MA 02115. E-mail dmorrow@partners.org

Key Words: Editorials • angina • fatty acids • heart failure • ion channels

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

	Introduction

 
The traditional paradigm for heart failure management centered on mitigating the hemodynamic changes that occur in response to the failing heart. Subsequently, pharmacological modulation of neurohormonal activation and more recently cardiac resynchronization have been shown to reverse ventricular remodeling and to slow disease progression. Despite these advances in therapy, successful treatment of heart failure remains challenging, with rates of hospitalization in the United States exceeding 1 million per year and the annual number of heart failure–related deaths increasing steadily.¹ Unfortunately, the history of drug development for heart failure has been marked by many disappointments, most notably the excess mortality associated with oral positive inotropes that were targeted at improving hemodynamics. In addition, more recent interventions aimed at interrupting endothelin and cytokine signaling or reducing oxidative stress have yet to fulfill hopes for novel biological therapies. Thus, new therapeutic strategies are needed to alter the natural history of the disease and to slow or reverse current epidemiological trends. The report by Lee and colleagues² in this issue of Circulation points toward the promise of an alternative approach based on favorably influencing the efficiency of myocardial energetics, thereby increasing cardiac performance without depending on changes in oxygen consumption or improvement in hemodynamics.

Article p 3280

	Modulation of Myocardial Cellular Energetics

 
The study of agents aimed at enhancing myocardial energy efficiency has focused principally on shifting myocardial substrate use toward more oxygen-efficient pathways.³ Although the complete oxidation of fatty acids to CO₂ yields more adenosine triphosphate (ATP) per molecule of CO₂ produced than does complete oxidation of glucose, . . . [Full Text of this Article]

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