In vivo 1H NMR spectra of small volumes-of-interest (VOI) were localized in human soleus muscle (8 ml) and compared with volume selective spectra of subcutaneous fat tissue and femoral yellow bone marrow (2 ml). All examinations were performed by the double spin echo (PRESS) localization technique. To provide comparability, spectra of different tissues were recorded using identical sequence timing. Clearly improved resolution of the lipid signals of muscle tissue was obtained using long echo times TE > 200 ms. The spectra of muscle tissue exhibit lipid signals that stem from two compartments with a difference of their resonance frequencies of about 0.2 ppm (Larmor frequency difference 12-13 Hz at 1.5 T). The existence of two fatty acid compartments is supported by measurements of the relaxation times and line shape analysis. Both compartments contain fatty acids or triglycerides with similar composition. Probably one compartment corresponds to fat cells within muscle tissue, the other compartment with lower Larmor frequency is located within muscle cells.
31P NMR spectroscopy detects alterations of myocardial metabolism in asymptomatic patients with HCM. These alterations may contribute to the understanding of the pathophysiology and natural history of the disease.
31P MRS examinations of the brain of 10 healthy volunteers were performed to determine T2 of the coupled ATP signals by use of the localized 90 degrees-TE/2-2662-TE/2-acq frequency selective spin echo sequence for elimination of phase and intensity distortions. The T2 relaxation times obtained are much longer than usually assumed: gamma-ATP: 89 +/- 9 ms; alpha-ATP: 84 +/- 6 ms; beta-ATP: 62 +/- 3 ms.
Friedreich's ataxia is a neurodegenerative disease frequently associated with hypertrophic cardiomyopathy. We have determined mitochondrial ATP, phosphocreatine, and intracellular inorganic phosphate levels by 31P nuclear magnetic resonance spectroscopy in the heart of 11 Friedreich's ataxia patients and 11 healthy controls. For the first time, to our knowledge, we showed a significant correlation between the extent of myocardial energy deficiency and the degree of myocardial hypertrophy. When combining our results with previous works on Friedreich's ataxia, these novel findings suggest that energy metabolism is most likely the cause and hypertrophy the effect in Friedreich's ataxia.
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