OBJECTIVE: The objective of the present study was to determine the detectability of metabolic alterations in patients with peripheral arterial occlusive disease (PAOD) using proton MR spectroscopy (hydrogen-1 MR spectroscopy). SUBJECTS AND METHODS: Twenty-seven people were included in this study: 10 patients with PAOD and a pain-free walking distance of less than 200 m served as the patient group and 17 young healthy subjects served as a control group. Hydrogen-1 MR spectroscopy was performed on a 1.5-T scanner using an extremity coil and a point-resolved spectroscopy (PRESS) sequence (TR/TE, 1,500/30; 256 repetitions). For the patient group, a voxel was localized in the gastrocnemius muscle of the diseased leg. The data were processed using standard 1H MR spectroscopy tools. The identification of resonances detected on all MR spectra was made: intramyocellular lipids at 1.2 ppm, extramyocellular lipids at 1.6 ppm, lactate at 4.1 ppm, glucose with two main peaks at 3.4 and 3.8 ppm, choline at 3.2 ppm, and creatine at 3.0 and 3.9 ppm. To avoid operator bias, three spectral intensities were measured after correcting baseline and phase of MR spectra each time. The creatine signal was used as an internal reference; thus, all spectra were scaled relative to creatine. We compared the resultant intensity ratios between the two groups using the Mann-Whitney U test. RESULTS: The lactate-creatine quotient was higher in the patient group, with a ratio of 1.6, than in the control group, with a ratio of 0.6. The glutamate-creatine ratio was higher in the patient group than in the control group (1.3 vs 0.8, respectively). All other ratios were higher in the control group. The best ratio for differentiating between healthy subjects and patients with PAOD was the glucose-lactate ratio. The patient group had a glucose-lactate quotient of 5.4, whereas the control group had a glucose-lactate quotient of 21.5 (p = 0.001). CONCLUSION: Proton MR spectroscopy has the potential to allow identification of patients who have PAOD on the basis of altered muscle metabolism.
OBJECTIVE: The objective of the present study was to determine the detectability of metabolic alterations in patients with peripheral arterial occlusive disease (PAOD) using proton MR spectroscopy (hydrogen-1 MR spectroscopy). SUBJECTS AND METHODS: Twenty-seven people were included in this study: 10 patients with PAOD and a pain-free walking distance of less than 200 m served as the patient group and 17 young healthy subjects served as a control group. Hydrogen-1 MR spectroscopy was performed on a 1.5-T scanner using an extremity coil and a point-resolved spectroscopy (PRESS) sequence (TR/TE, 1,500/30; 256 repetitions). For the patient group, a voxel was localized in the gastrocnemius muscle of the diseased leg. The data were processed using standard 1H MR spectroscopy tools. The identification of resonances detected on all MR spectra was made: intramyocellular lipids at 1.2 ppm, extramyocellular lipids at 1.6 ppm, lactate at 4.1 ppm, glucose with two main peaks at 3.4 and 3.8 ppm, choline at 3.2 ppm, and creatine at 3.0 and 3.9 ppm. To avoid operator bias, three spectral intensities were measured after correcting baseline and phase of MR spectra each time. The creatine signal was used as an internal reference; thus, all spectra were scaled relative to creatine. We compared the resultant intensity ratios between the two groups using the Mann-Whitney U test. RESULTS: The lactate-creatine quotient was higher in the patient group, with a ratio of 1.6, than in the control group, with a ratio of 0.6. The glutamate-creatine ratio was higher in the patient group than in the control group (1.3 vs 0.8, respectively). All other ratios were higher in the control group. The best ratio for differentiating between healthy subjects and patients with PAOD was the glucose-lactate ratio. The patient group had a glucose-lactate quotient of 5.4, whereas the control group had a glucose-lactate quotient of 21.5 (p = 0.001). CONCLUSION: Proton MR spectroscopy has the potential to allow identification of patients who have PAOD on the basis of altered muscle metabolism.