A rapid, proton magnetic resonance spectroscopy method to evaluate human myocardial lipid levels in a single breath-hold at 3 T using a commercial whole-body system is presented. During a 10 s breath-hold, water unsuppressed and suppressed spectra were acquired by two phased array coils using a short-echo time spectroscopic stimulated echo (STEAM) sequence electrocardiogram-triggered to mid-diastole. Lipid-to-water ratios were obtained in the septum of 15 healthy volunteers, (0.46 ± 0.19)%. These results agreed well with ratios obtained from averaged spectra acquired in seven multiple breath-holds, (0.45 ± 0.20)%, providing increased signal-to-noise ratio but requiring longer acquisition times. Excellent correlation was found between the two methods (r = 0.94, P < 0.05). Reproducibility of 1H MRS for measuring myocardial lipid levels in a short breath-hold was acceptable in five repeated measurements within the same subject (coefficient of variation = 19%). Thus, single breath-hold proton spectroscopy allows reliable and quick quantification of myocardial lipids at 3 T. Magn Reson Med, 2011. © 2011 Wiley-Liss, Inc.

BackgroundAndroid fat distribution (abdominal obesity) is associated with insulin resistance, hepatic steatosis, and greater secretion of large very low‐density lipoprotein (VLDL) particles in men. Since abdominal obesity is becoming increasingly prevalent in women, we aimed to investigate the relationship between android fat and hepatic lipid metabolism in pre‐ and postmenopausal women.Methods and ResultsWe used a combination of stable isotope tracer techniques to investigate intrahepatic fatty acid synthesis and partitioning in 29 lean and 29 abdominally obese women (android fat/total fat 0.065 [0.02 to 0.08] and 0.095 [0.08 to 0.11], respectively). Thirty women were premenopausal aged 35 to 45 and they were matched for abdominal obesity with 28 postmenopausal women aged 55 to 65. As anticipated, abdominal obese women were more insulin resistant with enhanced hepatic secretion of large (404±30 versus 268±26 mg/kg lean mass, P<0.001) but not small VLDL (160±11 versus 142±13). However, postmenopausal status had a pronounced effect on the characteristics of small VLDL particles, which were considerably triglyceride‐enriched (production ratio of VLDL 2‐ triglyceride:apolipoprotein B 30±5.3 versus 19±1.6, P<0.05). In contrast to postmenopausal women, there was a tight control of hepatic fatty acid metabolism and triglyceride production in premenopausal women, whereby oxidation (r s=−0.49, P=0.006), de novo lipogenesis (r s=0.55, P=0.003), and desaturation (r s=0.48, P=0.012) were closely correlated with abdominal obesity‐driven large VLDL‐triglyceride secretion rate.ConclusionsIn women, abdominal obesity is a major driver of hepatic large VLDL particle secretion, whereas postmenopausal status was characterized by increased small VLDL particle size. These data provide a mechanistic basis for the hyperlipidemia observed in postmenopausal obesity.

No abstract

No abstract

No abstract