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Cardiovascular Research Advance Access first published online on November 5, 2008
This version [Corrected Proof] published online on November 26, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn301
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Energy metabolism in heart failure and remodelling

Joanne S. Ingwall*

NMR Laboratory for Physiological Chemistry, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, Room 247, Boston, MA 02115, USA

* Corresponding author. Tel: +1 617 732 6994; fax: +1 617 732 6990. E-mail address: jingwall{at}rics.bwh.harvard.edu

Myocytes of the failing heart undergo impressive metabolic remodelling. The time line for changes in the pathways for ATP synthesis in compensated hypertrophy is: flux through the creatine kinase (CK) reaction falls as both creatine concentration ([Cr]) and CK activity fall; increases in [ADP] and [AMP] lead to increases in glucose uptake and utilization; fatty acid oxidation either remains the same or decreases. In uncompensated hypertrophy and in other forms of heart failure, CK flux and fatty acid oxidation are both lower; any increases in glucose uptake and utilization are not sufficient to compensate for overall decreases in the capacity for ATP supply and [ATP] falls. Metabolic remodelling is under transcriptional and post-transcriptional control. The lower metabolic reserve of the failing heart contributes to impaired contractile reserve.

KEYWORDS Energetics; Heart failure; Metabolic remodelling; Familial hypertrophic cardiomyopathy; Adenosine triphosphate

Time for primary review: 34 days


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