RATIONALE AND OBJECTIVES: The aim of this prospective study was to explore muscular metabolism in arterial occlusive disease (AOD) by dynamic phosphorus-31 (31P) magnetic resonance spectroscopy (MRS). METHODS: The authors examined 56 patients with AOD. Acquisition of up to 60 consecutive phosphorus spectra of the quadriceps muscle was done by "time series" in 36 seconds each. In this way, the authors achieved uninterrupted monitoring of muscle metabolism during rest, exhaustion, and recovery. During 31P MRS, the volunteers performed an isometric and an isotonic exercise until exhaustion of the quadriceps muscle. Spectroscopic results of 56 patients with AOD were correlated with clinical and angiographic findings and were compared with spectroscopic results of 10 age-matched healthy volunteers. RESULTS: There were no significantly differing spectroscopic results between patients and volunteers at rest, except for an elevated ratio phosphomonoester (PME)/beta-adenosine triphosphate (ATP) in patients with AOD (0.66 +/- 0.19 versus 0.48 +/- 0.09). Despite a sixfold duration of both of the exercises until exhaustion in healthy volunteers, exercise-induced changes of inorganic phosphate (P1)/phosphocreatine (PCr), PME/beta-ATP, and pH were similar in healthy volunteers and patients with AOD. Compared with maximal exercise-induced values of Pi/PCr, acidosis was relatively increased in AOD, resulting in a steeper slope of linear regression line (-0.33 +/- 0.06 versus -0.14 +/- 0.06) between these parameters. Recovery rate of Pi/PCr was markedly prolonged in AOD (time of half recovery: 80 seconds versus 25 seconds [isometric exercise] and 70 seconds versus 37 seconds [isotonic exercise]), whereas recovery rate of pH was not significantly slowed down in our patients (192 seconds versus 166 seconds [isometric exercise] and 234 seconds versus 220 seconds [isotonic exercise]). CONCLUSIONS: Dynamic 31P MRS provides a direct judgment of muscular metabolism, which is not only influenced by macro-, but also by microangiopathia. Results of 31P MRS suggest a reduced mitochondrial oxidative phosphorylation in AOD.
RATIONALE AND OBJECTIVES: The aim of this prospective study was to explore muscular metabolism in arterial occlusive disease (AOD) by dynamic phosphorus-31 (31P) magnetic resonance spectroscopy (MRS). METHODS: The authors examined 56 patients with AOD. Acquisition of up to 60 consecutive phosphorus spectra of the quadriceps muscle was done by "time series" in 36 seconds each. In this way, the authors achieved uninterrupted monitoring of muscle metabolism during rest, exhaustion, and recovery. During 31PMRS, the volunteers performed an isometric and an isotonic exercise until exhaustion of the quadriceps muscle. Spectroscopic results of 56 patients with AOD were correlated with clinical and angiographic findings and were compared with spectroscopic results of 10 age-matched healthy volunteers. RESULTS: There were no significantly differing spectroscopic results between patients and volunteers at rest, except for an elevated ratio phosphomonoester (PME)/beta-adenosine triphosphate (ATP) in patients with AOD (0.66 +/- 0.19 versus 0.48 +/- 0.09). Despite a sixfold duration of both of the exercises until exhaustion in healthy volunteers, exercise-induced changes of inorganic phosphate (P1)/phosphocreatine (PCr), PME/beta-ATP, and pH were similar in healthy volunteers and patients with AOD. Compared with maximal exercise-induced values of Pi/PCr, acidosis was relatively increased in AOD, resulting in a steeper slope of linear regression line (-0.33 +/- 0.06 versus -0.14 +/- 0.06) between these parameters. Recovery rate of Pi/PCr was markedly prolonged in AOD (time of half recovery: 80 seconds versus 25 seconds [isometric exercise] and 70 seconds versus 37 seconds [isotonic exercise]), whereas recovery rate of pH was not significantly slowed down in our patients (192 seconds versus 166 seconds [isometric exercise] and 234 seconds versus 220 seconds [isotonic exercise]). CONCLUSIONS: Dynamic 31PMRS provides a direct judgment of muscular metabolism, which is not only influenced by macro-, but also by microangiopathia. Results of 31PMRS suggest a reduced mitochondrial oxidative phosphorylation in AOD.
Authors: David C Isbell; Stuart S Berr; Alicia Y Toledano; Frederick H Epstein; Craig H Meyer; Walter J Rogers; Nancy L Harthun; Klaus D Hagspiel; Arthur Weltman; Christopher M Kramer Journal: J Am Coll Cardiol Date: 2006-05-15 Impact factor: 24.094
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