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Purpose: Acetylcarnitine can be assessed in vivo using proton MRS (1H‐MRS) with long TEs and this has been previously applied successfully in muscle. The aim of this study was to evaluate a 1H‐MRS technique for liver acetylcarnitine quantification in healthy humans before and after l‐carnitine supplementation. Method: Baseline acetylcarnitine levels were quantified using a STEAM sequence with prolonged TE in 15 healthy adults. Using STEAM with four different TEs was evaluated in phantoms. To assess reproducibility of the measurements, five of the participants had repeated 1H‐MRS without receiving l‐carnitine supplementation. To determine if liver acetylcarnitine could be changed after l‐carnitine supplementation, acetylcarnitine was quantified 2 h after intravenous l‐carnitine supplementation (50 mg/kg body weight) in the other 10 participants. Hepatic lipids were also quantified from the 1H‐MRS spectra. Results: There was good separation between the acetylcarnitine and fat in the phantoms using TE = 100 ms. Hepatic acetylcarnitine levels were reproducible (coefficient of reproducibility = 0.049%) and there was a significant (p < 0.001) increase in the relative abundance after a single supplementation of l‐carnitine. Hepatic allylic, methyl, and methylene peaks were not altered by l‐carnitine supplementation in healthy volunteers. Conclusion: Our results demonstrate that our 1H‐MRS technique could be used to measure acetylcarnitine in the liver and detect changes following intravenous supplementation in healthy adults despite the presence of lipids. Our techniques should be explored further in the study of fatty liver disease, where acetylcarnitine is suggested to be altered due to hepatic inflexibilities. [ABSTRACT FROM AUTHOR]

Purpose: Phosphorus spectroscopy (31P‐MRS) is a proven method to probe cardiac energetics. Studies typically report the phosphocreatine (PCr) to adenosine triphosphate (ATP) ratio. We focus on another 31P signal: inorganic phosphate (Pi), whose chemical shift allows computation of myocardial pH, with Pi/PCr providing additional insight into cardiac energetics. Pi is often obscured by signals from blood 2,3‐diphosphoglycerate (2,3‐DPG). We introduce a method to quantify Pi in 14 min without hindrance from 2,3‐DPG. Methods: Using a 31P stimulated echo acquisition mode (STEAM) sequence at 7 Tesla that inherently suppresses signal from 2,3‐DPG, the Pi peak was cleanly resolved. Resting state UTE‐chemical shift imaging (PCr/ATP) and STEAM 31P‐MRS (Pi/PCr, pH) were undertaken in 23 healthy controls; pH and Pi/PCr were subsequently recorded during dobutamine infusion. Results: We achieved a clean Pi signal both at rest and stress with good 2,3‐DPG suppression. Repeatability coefficient (8 subjects) for Pi/PCr was 0.036 and 0.12 for pH. We report myocardial Pi/PCr and pH at rest and during catecholamine stress in healthy controls. Pi/PCr was maintained during stress (0.098 ± 0.031 [rest] vs. 0.098 ± 0.031 [stress] P =.95); similarly, pH did not change (7.09 ± 0.07 [rest] vs. 7.08 ± 0.11 [stress] P =.81). Feasibility for patient studies was subsequently successfully demonstrated in a patient with cardiomyopathy. Conclusion: We introduced a method that can resolve Pi using 7 Tesla STEAM 31P‐MRS. We demonstrate the stability of Pi/PCr and myocardial pH in volunteers at rest and during catecholamine stress. This protocol is feasible in patients and potentially of use for studying pathological myocardial energetics. [ABSTRACT FROM AUTHOR]

Purpose We present a new Bloch-Siegert four Angle Saturation Transfer (BOAST) method for measuring the creatine kinase (CK) first-order effective rate constant kf in human myocardium at 7 tesla (T). BOAST combines a variant of the four-angle saturation transfer (FAST) method using amplitude-modulated radiofrequency pulses, phosphorus Bloch-Siegert [ABSTRACT FROM AUTHOR]

Purpose The translation of sophisticated phosphorus MR spectroscopy (31P-MRS) protocols to 7 Tesla (T) is particularly challenged by the issue of radiofrequency (RF) heating. Legal limits on RF heating make it hard to reliably suppress signals from skeletal muscle that can contaminate human cardiac 31P spectra at 7T. We introduce the first surface-spoiling crusher coil for human cardiac 31P-MRS at 7T. Methods A planar crusher coil design was optimized with simulations and its performance was validated in phantoms. Crusher gradient pulses (100 μs) were then applied during human cardiac 31P-MRS at 7T. Results In a phantom, residual signals were 50 ± 10% with BISTRO (B1-insensitive train to obliterate signal), and 34 ± 8% with the crusher coil. In vivo, residual signals in skeletal muscle were 49 ± 4% using BISTRO, and 24 ± 5% using the crusher coil. Meanwhile, in the interventricular septum, spectral quality and metabolite quantification did not differ significantly between BISTRO (phosphocreatine/adenosine triphosphate [PCr/ATP] = 2.1 ± 0.4) and the crusher coil (PCr/ATP = 1.8 ± 0.4). However, the specific absorption rate (SAR) decreased from 96 ± 1% of the limit (BISTRO) to 16 ± 1% (crusher coil). Conclusion A crusher coil is an SAR-efficient alternative for selectively suppressing skeletal muscle during cardiac 31P-MRS at 7T. A crusher coil allows the use of sequence modules that would have been SAR-prohibitive, without compromising skeletal muscle suppression. Magn Reson Med 75:962-972, 2016. © 2015 The Authors. Magnetic Resonance in Medicine Published by Wiley Periodicals, Inc. on behalf of International Society of Medicine in Resonance. [ABSTRACT FROM AUTHOR]

Purpose Phosphorus magnetic resonance spectroscopy (31P-MRS) affords unique insight into cardiac energetics but has a low intrinsic signal-to-noise ratio (SNR) in humans. Theory predicts an increased 31P-MRS SNR at 7T, offering exciting possibilities to better investigate cardiac metabolism. We therefore compare the performance of human cardiac 31P-MRS at 7T to 3T, and measure T1s for 31P metabolites at 7T. Methods Matched 31P-MRS data were acquired at 3T and 7T, on nine normal volunteers. A novel Look-Locker CSI acquisition and fitting approach was used to measure T1s on six normal volunteers. Results T1s in the heart at 7T were: phosphocreatine (PCr) 3.05 ± 0.41s, γ-ATP 1.82 ± 0.09s, α-ATP 1.39 ± 0.09s, β-ATP 1.02 ± 0.17s and 2,3-DPG (2,3-diphosphoglycerate) 3.05 ± 0.41s (N = 6). In the field comparison (N = 9), PCr SNR increased 2.8× at 7T relative to 3T, the Cramer-Ráo uncertainty (CRLB) in PCr concentration decreased 2.4×, the mean CRLB in PCr/ATP decreased 2.7× and the PCr/ATP SD decreased 2×. Conclusion Cardiac 31P-MRS at 7T has higher SNR and the spectra can be quantified more precisely than at 3T. Cardiac 31P T1s are shorter at 7T than at 3T. We predict that 7T will become the field strength of choice for cardiac 31P-MRS. Magn Reson Med 72:304-315, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

At clinical MRI field strengths (1.5 and 3 T), quantitative maps of the longitudinal relaxation time T1 of the myocardium reveal diseased tissue without requiring contrast agents. Cardiac T1 maps can be measured by Look-Locker inversion recovery sequences such as ShMOLLI at 1.5 and 3 T. Cardiovascular MRI at a field strength of 7 T has recently become feasible, but doubts have remained as to whether magnetization inversion is possible in the heart due to subject heating and technical limitations. This work extends the repertoire of 7 T cardiovascular MRI by implementing an adiabatic inversion pulse optimized for use in the heart at 7 T. A 'ShMOLLI+IE' adaptation of the ShMOLLI pulse sequence has been introduced together with new postprocessing that accounts for the possibility of incomplete magnetization inversion. These methods were validated in phantoms and then used in a study of six healthy volunteers to determine the degree of magnetization inversion and the T1 of normal myocardium at 7 T within a 22-heartbeat breathhold. Using a scanner with 16 × 1 kW radiofrequency outputs, inversion efficiencies ranging from −0.79 to −0.83 (intrasegment means; perfect 180° would give −1) were attainable across the myocardium. The myocardial T1 was 1925 ± 48 ms (mean ± standard deviation). Magn Reson Med, 70:1038-1046, 2013. © 2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Purpose Quantitative mapping of the native T1 of the heart using the modified look-locker inversion recovery (MOLLI) technique provides high quality diagnostic information without requiring contrast agents. Previous work has considered the effects of T2 relaxation on MOLLI T1 measurements, finding that the T1 measured by MOLLI is biased, and that Saturation-recovery single-Shot Acquisition generates a more precise T1. However, despite detailed experiments and simulation the exact relaxation times observed in vivo remain unexplained, but might be due to magnetization transfer (MT). Methods We used an MT simulation based on the Bloch-McConnell equations to evaluate the most common MOLLI and saturation-recovery single-shot acquisition sequence variants. Results For myocardial tissue we find that the T1 measured by saturation-recovery single-shot acquisition is insensitive to MT and T2, whereas MT reduces the T1 measured by MOLLI (>10%) in addition to the effects due to T2 relaxation. Conclusions The consequences of this T1 underestimation by MOLLI are relevant. Increases in the actual T1 and T2 and decreases in MT will all result in an increase in T1 measured by MOLLI. Myocardial infarction demonstrates increased native T1 and T2 and decreased MT, indicating that these biases enhance the sensitivity of MOLLI to detect this and possibly other cardiovascular disease states. Magn Reson Med 70:664-670, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Phase-contrast magnetic resonance imaging is a technique that allows for characterization of regional cardiac function and for measuring transmural myocardial velocities in human hearts with high temporal and spatial resolution. The application of this technique (also known as tissue phase mapping) to murine hearts has been very limited so far. The aim of our study was to implement and to optimize tissue phase mapping for a comprehensive assessment of murine transmural wall motion. Baseline values for regional motion patterns in mouse hearts, based on the clinically used American Heart Association's 17-segment model, were established, and a detailed motion analysis of mouse heart for the entire cardiac cycle (including epicardial and endocardial motion patterns) is provided. Black-blood contrast was found to be essential to obtain reproducible velocity encoding. Tissue phase mapping of the mouse heart permits the detailed assessment of regional myocardial velocities. While a proof-of-principle application in a murine ischemia-reperfusion model was performed, future studies are warranted to assess its potential for the investigation of systolic and diastolic functions in genetically and surgically manipulated mouse models of human heart disease. Magn Reson Med, 2012. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The mouse is the predominant animal model to study the effect of gene manipulations. Imaging techniques to define functional effects on the heart caused by genomic alterations are becoming increasingly routine in mice, yet methods for in vivo investigation of metabolic phenotypes in the mouse heart are lacking. In this work, cardiac 1H-MRS was developed and applied in mouse hearts in vivo using a single-voxel technique (PRESS). In normal C57Bl/6J mice, stability and reproducibility achieved by dedicated cardiac and respiratory gating was demonstrated by measuring amplitude and zero-order phase changes of the unsuppressed water signal. Various cardiac metabolites, such as creatine, taurine, carnitine, or intramyocardial lipids were successfully detected and quantified relative to the total water content in voxels as small as 2 μl, positioned in the interventricular septum. The method was applied to a murine model of guanidinoacetate N-methyltransferase (GAMT) deficiency, which is characterized by substantially decreased myocardial creatine levels. Creatine deficiency was confirmed noninvasively in myocardium of anesthetized GAMT-/- mice. This is the first study to report the application of cardiac 1H-MRS in mice in vivo. Magn Reson Med 52:1029-1035, 2004. © 2004 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Experimental studies demonstrated persistently increased 23Na content in nonviable myocardium post-myocardial infarction (MI). We hypothesized that nonviable myocardium in humans would show elevated 23Na content at all stages of infarct development, and therefore could be imaged with 23Na MRI. Ten patients were examined on days 4, 14, and 90 after infarction, and five of these patients participated in a 12-month follow-up. Double angulated short-axis cardiac 23Na images were obtained with the use of a 23Na surface coil and an ECG-triggered, 3D gradient-echo sequence. 1H T2-weighted imaging ( N = 9) was performed on days 4, 14, and 90. Wall motion was assessed by cine MRI, and the infarct size was determined by late enhancement on day 90. The 23Na signal intensity (SI) of infarcted myocardium was expressed as the percentage increase over 23Na SI of noninfarcted myocardium. All of the patients showed an area of elevated SI on 23Na and 1H T2-weighted images that correlated with wall motion abnormalities and late enhancement. 23Na SI was highest on day 4. It then decreased until day 90, but remained elevated (39% ± 18%, 31% ± 17%, 28% ± 13% on days 4, 14, and 90, respectively, P = 0.001). No further decrease was found 1 year after infarction (25% ± 7%, P = 0.89 vs. day 90). 1H T2-weighted SI decreased between days 4 and 14, but on day 90 only six of nine patients had a residual elevated SI. Thus, 23Na SI is elevated in nonviable infarction at all time points following MI, and 23Na MRI may become a suitable technique for imaging nonviable myocardium in humans. Magn Reson Med 52:545-551, 2004. © 2004 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]