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The Chemistry of ATP in the Failing Heart The Fundamentals

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Abstract

There is now compelling evidence that the [ATP] in both failed human myocardium and animal models of severe heart failure is as much as 25% lower than in normal myocardium. We also know that the tissue contents of phosphocreatine and creatine and the capacity of the creatine kinase reaction (Vmax) are also lower in the dysfunctional/failing heart. These observations increase our understanding of two important aspects of cardiac energetics: the kinetics of ATP synthesis and the thermodynamics of ATP utilization, i.e., the chemical driving force for the ATP-consuming reactions, ΔG∼P. In this chapter, we will first review the fundamentals of the chemistry of ATP synthesis in the heart and then summarize what is known about the energetics of the failing heart from the viewpoints of the kinetics of ATP synthesis and the thermodynamics of ATP utilization. We present a new model of the energetics of the failing heart and suggest that the loss of creatine from the failing heart protects the heart from an even greater loss of ATP.

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Authors and Affiliations

  1. NMR Laboratory for Physiological Chemistry, Division of Cardiovascular Medicine, Department of Medicine, Brigham & Women's Hospital and Harvard Medical School jingwall@rics.bwh.harvard.edu, USA

    Joanne S. Ingwall & Weiqun Shen

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  1. Joanne S. Ingwall
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  2. Weiqun Shen
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Ingwall, J.S., Shen, W. The Chemistry of ATP in the Failing Heart The Fundamentals. Heart Fail Rev 4, 221–228 (1999). https://doi.org/10.1023/A:1009857906567

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