title: Altered relative concentrations of high-energy phosphates in patients with uraemic cardiomyopathy measured by magnetic resonance spectroscopy.
abstract: BACKGROUND
  Premature sudden cardiovascular death is the commonest cause of death in end-stage renal disease (ESRD) patients and is associated with uraemic cardiomyopathy [left ventricular hypertrophy (LVH), systolic dysfunction (LVSD) or LV dilation]. High-energy phosphates (HEP), quantified using phosphorus-31 magnetic resonance spectroscopy, are reduced in patients with diabetes, heart failure and uraemia. Phosphocreatine:β adenosine triphosphate (PCr:ATP) ratio is an index of metabolic activity. We compared resting HEPs in ESRD patients and hypertensive patients (with and without LVH) who had normal renal function (LVH-only or normal myocardia). We also assessed associations of HEP levels with abnormalities of uraemic cardiomyopathy.
  
  
  METHODS
  Fifty-three ESRD and 30 hypertensive patients (18 with LVH, 12 with normal myocardia) underwent phosphorus magnetic resonance spectroscopy of their left ventricle. PCr:ATP ratios were calculated from (31)P-MR spectra obtained from long-axis views of the left ventricle.
  
  
  RESULTS
  There were no significant differences in age, LV mass, chamber sizes and ejection fraction between patient groups. PCr:ATP was significantly lower in ESRD patients compared to hypertensive patients, irrespective of the presence or absence of LVH (P = 0.01). In the ESRD group, PCr:ATP was significantly lower in patients with LVSD (P = 0.05) and LV dilation (P = 0.01). LVH was not associated with significant difference in PCr:ATP.
  
  
  CONCLUSIONS
  ESRD patients have lower HEP levels compared to hypertensive patients. Lower PCr:ATP ratio, indicating altered myocardial metabolic function in ESRD patients, is associated with features of uraemic cardiomyopathy.
authors.affiliation: Renal Research Group, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK. rajan.patel@glasgow.ac.uk
authors.forename: Rajan K
authors.initials: RK
authors.lastname: Patel
authors.forename: Patrick B
authors.initials: PB
authors.lastname: Mark
authors.forename: Gillian
authors.initials: G
authors.lastname: Macnaught
authors.forename: Kathryn K
authors.initials: KK
authors.lastname: Stevens
authors.forename: Emily P
authors.initials: EP
authors.lastname: McQuarrie
authors.forename: Tracey
authors.initials: T
authors.lastname: Steedman
authors.forename: Keith
authors.initials: K
authors.lastname: Gillis
authors.forename: Henry J
authors.initials: HJ
authors.lastname: Dargie
authors.forename: Alan G
authors.initials: AG
authors.lastname: Jardine
mesh_terms: D009202:Cardiomyopathies / Q000175:diagnosis* / Q000209:etiology*; D016022:Case-Control Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000150:complications; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000150:complications*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D010710:Phosphates / Q000032:analysis*; D010759:Phosphorus Isotopes / Q000378:metabolism; D011379:Prognosis; D014511:Uremia / Q000150:complications*
chemical_list: D010710:Phosphates; D010759:Phosphorus Isotopes