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Cardiovascular Research Advance Access [Accepted Manuscript] published online on November 5, 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, Ph.D.

Department of Medicine, Division of Cardiovascular Medicine, Brigham and Women's Hospital and, Harvard Medical School, Boston MA

Contact Information: Joanne S. Ingwall, PhD, NMR Laboratory for Physiological Chemistry, 221 Longwood Avenue, Room 247, Boston, MA 02115, jingwall{at}rics.bwh.harvard.edu, 617-732-6994 phone 617-732-6990 fax

Myocytes of the failing heart undergo impressive metabolic remodeling. 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 remodeling is under transcriptional and post-transcriptional control. The lower metabolic reserve of the failing heart contributes to impaired contractile reserve.

Time for primary review: 34 Days


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