Brain MR Spectroscopy Markers of Encephalopathy Due to Nonalcoholic Steatohepatitis.

BACKGROUND AND PURPOSE: In hepatic encephalopathy (HE), osmotic stressors promoting brain edema result in a compensatory drop in the astrocyte metabolite myo-inositol (mI). Identifying differences between nonalcoholic steatohepatitis (NASH) with and without HE and healthy controls using proton magnetic resonance spectroscopy (MRS) and evaluating hypoalbuminemia and hyperammonemia as osmotic stressors that predict the reduction of mI allow further understanding of mechanisms that promote brain edema in HE. The aim of this study was to assess brain edema in HE using characteristic MRS markers and serum albumin. METHODS: We evaluated between group differences among 19 NASH cirrhosis without HE (Crhs-HE) (age = 63 ± 8.7), 9 NASH cirrhosis with HE (Crhs+HE) (age = 63 ± 9.2), and 16 controls (age = 57.8 ± 11.7) using 1 H MRS. Glutamine (Gln/tCr) and serum albumin were evaluated as predictors of myo-inositol (mI/tCr) using linear regression. Statistical significance was set at P < .05 with adjustment for multiple comparisons. RESULTS: Brain mI/tCr was decreased, and Gln/tCr increased in Crhs+HE compared to Crhs-HE and controls in both brain regions (P < .001 for all). Evaluated together as joint predictors, serum albumin but not Gln/tCr significantly predicted mI/tCr in GM (P = .02 and P = .2, respectively) and PWM (P = .01 and P = .1, respectively). CONCLUSION: Low mI/tCr and increased Gln/tCr were characteristics of Crhs+HE. Low serum albumin was the strongest predictor of brain osmotic stress indicated by reduced mI/tCr, with no residual independent association seen for brain Gln/tCr concentration. This suggests that hypoalbuminemia in chronic liver disease may promote brain edema in HE.

Group delay method for MRI aortic pulse wave velocity measurements in clinical protocols with low temporal resolution: Validation in a heterogeneous cohort.

BACKGROUND: MRI assessment of aortic pulse wave velocity (PWV) helps predict the risk of vascular events, but the recommended phase contrast sampling rate is faster than what is utilized in most clinical sequences. There are many existing MRI databases obtained for assessment of cardiac output using lower temporal frequency sampling where information might be obtained about aortic stiffness (PWV). In this work, we sought to evaluate whether the Group Delay (GD) method can generate a reproducible measure of stiffness and describe expected age-related stiffening of the aortic arch using lower sampling rates in standard clinical sequences. METHODS: Phase contrast (PC) MRI was obtained on the ascending and descending aortic arch in a heterogeneous adult cohort (n = 23; 9 women) spanning over a wide range of ages (ages 24-89, mean 49.4 ± 18.4). Data was collected with standard cardiac MRI protocols for cardiac output evaluation (repetition time = 7.8 ms, views-per-segment = 4, encoding velocity = 200 cm/s). Pulse wave transit times (TT) were computed using the GD method, two other validated automated approaches (cross correlation TT Algorithm by Gaddum and Segment by Medviso), and the manual tangent method. Pressure waveforms from tonometry and flow waveforms from PC MRI were used to assess wave reflections. RESULTS: Group Delay and TT-Algorithm showed significant and high retest reproducibility (r = 0.86 for both) as well as high PWV correlation with age (r = 0.93, P-value < 0.00005 and r = 0.96, P-value < 0.00005 respectively) and with each other (r = 0.94, P-value < 0.00001, RMSE = 0.94 m/s). Arbitrary altering of the image acquisition trigger in the GD method introduced error of 10%-13%, but the TT-algorithm error range was 11%-25%. CONCLUSION: Group Delay enables reproducible assessment of transit time to derive PWV from low temporal resolution clinical cardiac MRI sequences that can also identify age-related stiffening.