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Re: Impaired left ventricular energy metabolism in Hypertrophic Cardiomyopathy is not due to fibrosis

Esposito et al address an important pathophysiological question, i.e., whether altered cardiac energy metabolism in hypertrophic cardiomyopathy (HCM) is primary or secondary, due to fibrosis (1). The authors conclude that “the inverse relation observed between LE extension (LE = late enhancement a measure of fibrosis) and the alteration of PCr/ATP-ratio (PCr = phosphocreatine; ATP = adenosinetriphosphate) suggests that the impairment of myocardial energy metabolism, detected by 31P-MRS (MRS=magnetic resonance spectroscopy) in HCM patients, 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 fact in contrast to experimental data previously published. Using HPLC measurements in rat hearts (2), we showed that myocardial scar tissue contains negligible amounts of ATP (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 cannot contain PCr if it contains no ATP. In line with this, we also have unpublished data showing that myocardial scar contains negligible amounts of PCr. These experimental data strongly suggest that any signal measured in the HCM patients, whether they show fibrosis or not, must almost exclusively come from the remaining cardiomyocytes and not from the scar. In conclusion, the authors demonstrate an inverse relationship of the PCr/ATP-ratio and myocardial fibrosis, but their data do not support their conclusion, i.e. that altered myocardial energetics in HCM occur secondary to fibrosis.