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Impaired left ventricular energy metabolism in hypertrophic cardiomyopathy is not due to fibrosis
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK
Correspondence to:
Dr S E Petersen, Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK; steffen.petersen@cardiov.ox.ac.uk
| The first 150 words of the full text of this article appear below. |
To the editor: Esposito et al deal with an important pathophysiological question—that is, whether altered cardiac energy metabolism in hypertrophic cardiomyopathy (HCM) is primary or secondary, due to fibrosis.1 The authors conclude that the inverse relation seen between LE extension (LE, late enhancement a measure of fibrosis) and the alteration of phosphocreatine (PCr) suggests that the impairment of myocardial energy metabolism, detected by 31P magnetic resonance spectroscopy in patients with HCM, may be related to the presence of fibrosis rather than to a primary myocardial alteration. However, this conclusion is not supported by the data presented and is in contrast to experimental data previously published.
Using high-performance liquid chromatography measurements in rat hearts,2 we showed that myocardial scar tissue contains negligible amounts of ATP (mean (SD) 0.2 (0.1) nmol/mg protein, <1% of levels in normal myocardium). Furthermore, ATP is an essential requirement for PCr synthesis, and therefore, cardiac tissue
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- The authors’ response:
- A Esposito, F De Cobelli, G Perseghin, and A Del Maschio
Heart 2009 95: 505.[Extract] [Full Text] [PDF]
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