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Hypertrophic cardiomyopathy due to sarcomeric gene mutations is characterized by impaired energy metabolism irrespective of the degree of hypertrophy

Jenifer G. Crilley, MRCP^*,*, Ernest A. Boehm, PhD, Edward Blair, MRCP, Bheeshma Rajagopalan, PhD, FRCP^*, Andrew M. Blamire, PhD^*, Peter Styles, PhD^*, William J. McKenna, FRCP^||, Ingegerd Östman-Smith, FRCP, Kieran Clarke, PhD and Hugh Watkins, MD, PhD, FRCP

^* MRC Biochemical and Clinical Magnetic Resonance Unit, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom
Department of Paediatric Cardiology, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford, United Kingdom
BHF Molecular Cardiology Group, Department of Biochemistry, University of Oxford, South Parks Road, Oxford, United Kingdom
^|| Department of Cardiological Sciences, St. George’s Hospital Medical School, London, United Kingdom

View larger version (14K): [in a new window]   Figure 1 Phosphocreatine/adenosine triphosphate (PCr/ATP) data for all familial hypertrophic cardiomyopathy (HCM) subjects and controls, HCM subjects without left ventricular hypertrophy (LVH), and subjects in each disease-gene group. Filled circles = HCM patients; open circles = controls; filled squares = subjects without LVH; open triangles = beta-myosin heavy chain (ß-MHC); filled triangles = cardiac troponin T (cTnT); open squares = myosin-binding protein C (MyBPC). p < 0.001 for all HCM patients vs. controls, HCM subjects without LVH vs. controls, and for each disease-gene group vs. controls; p = not significant between each disease-gene group.

View larger version (16K): [in a new window]   Figure 2 Scatterplot showing lack of correlation between max wall thickness and phosphocreatine/adenosine triphosphate (PCr/ATP). Open triangles = beta-myosin heavy chain; filled triangles = cardiac troponin T; open squares = myosin-binding protein C.