CARDIAC HIGH-ENERGY PHOSPHATE-METABOLISM IN PATIENTS WITH AORTIC-VALVE DISEASE ASSESSED BY P-31-MAGNETIC RESONANCE SPECTROSCOPY

Background: The purpose of this work was to determine the clinical and hemodynamic correlates of alterations in cardiac high-energy phosphat e metabolism in patients with aortic stenosis and with aortic incompet ence. Methods: Fourteen volunteers, 13 patients with aortic stenosis, and 9 patients with aortic incompetence were included. Patients underw ent echocardiography and left and right heart catheterization. P-31-MR spectra from the anterior myocardium were obtained with a 1.5 Tesla c linical MR system. Results: Aortic stenosis and aortic incompetence pa tients 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, p hosphocreatine/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 incomp etence, 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), bu t not with NYHA classes I and II (phosphocreatine/ATP 1.86 +/- 0.18), In aortic stenosis, phosphocreatine/ATP ratios decreased (1.13 +/- 0.0 3; 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 failur e in human myocardium, volume overload hypertrophy does not, but press ure overload does, induce significant impairment of cardiac high-energ y phosphate metabolism. In aortic valve disease, alterations of high-e nergy phosphate metabolism are related to the degree of heart failure.