Review |
From Brigham and Womens Hospital (J.S.I.), Harvard Medical School, Boston, Mass; and Johns Hopkins Hospital and University School of Medicine (R.G.W.), Cardiology Division, Baltimore, Md.
Correspondence to Robert G. Weiss, MD, Johns Hopkins Hospital and University School of Medicine, Cardiology Division, 600 North Wolfe St, Carnegie 584, Baltimore, MD 21287-6568. E-mail rweiss{at}jhmi.edu
This Review is part of a thematic series on Unanswered Questions in Heart Failure, which includes the following articles:
Is Depressed Contractility Centrally Involved in Heart Failure?
What is the Role of ß-Adrenergic Signaling in Heart Failure?
What Mechanisms Underlie Diastolic Dysfunction in Heart Failure?
Is the Failing Heart Energy Starved?
What Causes Sudden Death in Heart Failure?
Is Abnormal Cell Growth and Hypertrophy the Cause of Heart Failure?
Steven Houser Guest Editor
The requirement of chemical energy in the form of ATP to support systolic and diastolic work of the heart is absolute. Because of its central role in cardiac metabolism and performance, the subject of this review on energetics in the failing heart is ATP. We briefly review the basics of myocardial ATP metabolism and describe how this changes in the failing heart. We present an analysis of what is now known about the causes and consequences of these energetic changes and conclude by commenting on unsolved problems and opportunities for future basic and clinical research.
Key Words: adenosine triphosphate phosphocreatine creatine kinase familial hypertrophic cardiomyopathy heart failure
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