title: Cardiac high-energy phosphate metabolism in patients with aortic valve disease assessed by 31P-magnetic resonance spectroscopy.
abstract: BACKGROUND
  The purpose of this work was to determine the clinical and hemodynamic correlates of alterations in cardiac high-energy phosphate metabolism in patients with aortic stenosis and with aortic incompetence.
  
  
  METHODS
  Fourteen volunteers, 13 patients with aortic stenosis, and 9 patients with aortic incompetence were included. Patients underwent echocardiography and left and right heart catheterization. 31P-MR spectra from the anterior myocardium were obtained with a 1.5 Tesla clinical MR system.
  
  
  RESULTS
  Aortic stenosis and aortic incompetence patients had similar New York Heart Association (NYHA) classes (2.77 +/- 0.12 vs 2.44 +/- 0.18), ejection fractions (normal), left ventricular (LV) end-diastolic pressures, and LV wall thickness. In volunteers, phosphocreatine/adenosine triphosphate (ATP) ratios were 2.02 +/- 0.11. For all patients, phosphocreatine/ATP was significantly reduced (1.64 +/- 0.09; *p = 0.011 vs volunteers). Phosphocreatine/ATP decreased to 1.55 +/- 0.12 (*p = 0.008) in aortic stenosis, while in aortic incompetence, phosphocreatine/ATP only showed a trend for a reduction (1.77 +/- 0.12; p = 0.148). For all patients, phosphocreatine/ATP decreased significantly only with NYHA class III (1.51 +/- 0.09; *p = 0.001), but not with NYHA classes I and II (phosphocreatine/ATP 1.86 +/- 0.18). In aortic stenosis, phosphocreatine/ATP ratios decreased (1.13 +/- 0.03; *p = 0.019) only when LV end-diastolic pressures were > 15 mm Hg or when LV diastolic wall stress was > 20 kdyne cm-2 (1.13 +/- 0.03; *p = 0.024).
  
  
  CONCLUSIONS
  For a similar clinical degree of heart failure in human myocardium, volume overload hypertrophy does not, but pressure overload does, induce significant impairment of cardiac high-energy phosphate metabolism. In aortic valve disease, alterations of high-energy phosphate metabolism are related to the degree of heart failure.
authors.affiliation: Department of Medicine, Würzburg University, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Neubauer
authors.forename: M
authors.initials: M
authors.lastname: Horn
authors.forename: T
authors.initials: T
authors.lastname: Pabst
authors.forename: K
authors.initials: K
authors.lastname: Harre
authors.forename: H
authors.initials: H
authors.lastname: Strömer
authors.forename: G
authors.initials: G
authors.lastname: Bertsch
authors.forename: J
authors.initials: J
authors.lastname: Sandstede
authors.forename: G
authors.initials: G
authors.lastname: Ertl
authors.forename: D
authors.initials: D
authors.lastname: Hahn
authors.forename: K
authors.initials: K
authors.lastname: Kochsiek
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D000368:Aged; D001022:Aortic Valve Insufficiency / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D001024:Aortic Valve Stenosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006439:Hemodynamics; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010710:Phosphates / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D010761:Phosphorus Radioisotopes
chemical_list: D010710:Phosphates; D010761:Phosphorus Radioisotopes; D010725:Phosphocreatine; D000255:Adenosine Triphosphate