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1 Department of Radiology, San Raffaele Scientific Institute and Vita Salute San Raffaele University, Milan, Italy
2 Internal Medicine, Section of Nutrition/Metabolism, San Raffaele Scientific Institute, Milan, Italy
Correspondence to:
Dr A Esposito, San Raffaele Scientific Institute - Vita Salute San Raffaele University, Via Olgettina 60, Milan 20132, Italy; esposito.antonio@hsr.it
| The first 150 words of the full text of this article appear below. |
We are grateful to Petersen et al for their letter dealing with relevant concerns about left ventricular (LV) energy metabolism and myocardial fibrosis. Based on their previous experiments in rats with myocardial infarction (MI) induced by coronary ligation1 and on their unpublished data, Petersen et al strongly emphasise the fact that our correlative finding between the extension of late enhancement (LE) and the LV phosphocreatine (PCr)/ATP ratio in humans with hypertrophic cardiomyopathy (HCM)2 may not have a causative relationship. We have a few comments on the concern they raise.
First, we agree that biochemical analysis of gross scarring of infarction-induced lesions (25% of the left ventricle) may result in negligible amounts of ATP and probably of PCr as well1; however, in HCM the setting is different. In HCM a non-homogeneous pattern of fibrosis with a generalised increase in the normal structural skeletal framework (pericellular, intercellular and fascicular connective
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- Impaired left ventricular energy metabolism in hypertrophic cardiomyopathy is not due to fibrosis
- S E Petersen, H Watkins, and S Neubauer
Heart 2009 95: 505.[Extract] [Full Text] [PDF]
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