Key result
Cardiac high-energy phosphate metabolism, measured by phosphocreatine/ATP ratio, was significantly reduced in patients with aortic valve disease compared to volunteers (1.64 vs 2.02; p=0.011).
Why the study?
The clinical and hemodynamic correlates of alterations in cardiac high-energy phosphate metabolism in patients with aortic stenosis and aortic incompetence remained to be determined.
Does pressure or volume overload in aortic valve disease alter cardiac high-energy phosphate metabolism compared to healthy volunteers?
Observational (n=36)
Does pressure or volume overload in aortic valve disease alter cardiac high-energy phosphate metabolism compared to healthy volunteers?
Pressure overload from aortic stenosis, but not volume overload from aortic incompetence, induces significant impairment of cardiac high-energy phosphate metabolism, which correlates with the degree of heart failure.
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. 31 P-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.
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Neubauer et al. (1997) conducted an observational in Aortic valve disease (n=36). 31P-Magnetic Resonance Spectroscopy vs. Healthy volunteers was evaluated on Phosphocreatine/ATP ratio (p=0.011). Cardiac high-energy phosphate metabolism, measured by phosphocreatine/ATP ratio, was significantly reduced in patients with aortic valve disease compared to volunteers (1.64 vs 2.02; p=0.011).
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