Cardiac phosphorus magnetic resonance spectroscopy (MRS) with surface coils promises better quantification at 3T due to improved signal-to-noise ratios and spectral resolution compared to 1.5T. However, Bloch equation and field analyses at 3T show that for efficient quantitative MRS protocols employing small-angle adiabatic (BIR4/BIRP) pulses the excitation-field is limited by RF power requirements and power deposition. When BIR4/BIRP pulse duration is increased to reduce power levels, T2-decay can introduce flip-angle dependent errors in the steady-state magnetization, causing errors in saturation corrections for metabolite quantification and in T1s measured by varying the flip-angle. A new dual-repetition-time (2TR) T1 method using frequency-sign-cycled adiabatic-half-passage pulses is introduced to alleviate power requirements, and avoid the problem related to T2 relaxation during the RF pulse. The 2TR method is validated against inversion-recovery in phantoms using a practical transmit/receive coil set designed for phosphorus MRS of the heart at depths of 9-10 cm with 4kW of pulse power. The T1s of phosphocreatine (PCr) and adenosine triphosphate (γ-ATP) in the calf-muscle (n=9) at 3T are 6.8±0.3s and 5.4±0.6s respectively. For heart (n=10) the values are 5.8±0.5s (PCr) and 3.1±0.6s (γ-ATP). The 2TR protocol measurements agreed with those obtained by conventional methods to within 10%.
Human cardiac phosphorus MR saturation transfer experiments to quantify creatine kinase forward rate constants (kf) have previously been performed at 1.5 T. Such experiments could benefit from increased signal‐to‐noise ratio (SNR) and spectral resolution at 3 T. At 1.5 T, the four‐angle saturation transfer method was applied with low‐angle adiabatic pulses and surface coils. However, low‐angle adiabatic pulses are potentially problematic above 1.5 T due to bandwidth limitations, power requirements, power deposition, and intrapulse spin‐spin relaxation. For localized metabolite spin‐lattice relaxation time (T1) measurements, a dual repetition time approach with adiabatic half‐passage pulses was recently introduced to solve these problems at 3 T. Because the saturation transfer experiment requires a T1 measurement performed while one reacting moiety is saturated, we adapt the dual repetition time approach to measure kf using a triple repetition time saturation transfer (TRiST) method. A new pulsed saturation scheme with reduced sensitivity to static magnetic field inhomogeneity and compatibility with cardiac triggering is also presented. TRiST measurements of kf are validated in human calf muscle against conventional saturation transfer and found to agree within 3%. The first 3‐T TRiST measurements of creatine kinase kf in the human calf (n = 6), chest muscle, and heart (n = 8) are 0.26 ± 0.04 s−1, 0.23 ± 0.03 s−1, and 0.32 ± 0.07 s−1, respectively, consistent with prior 1.5 T values. Magn Reson Med, 2010. © 2010 Wiley‐Liss, Inc.
Purpose: Accurate measurements of the RF power delivered during clinical MRI are essential for safety and regulatory compliance, avoiding inappropriate restrictions on clinical MRI sequences, and for testing the MRI safety of peripheral and interventional devices at known RF exposure levels. The goal is to make independent RF power measurements to test the accuracy of scanner-reported specific absorption rate (SAR) over the extraordinary range of operating conditions routinely encountered in MRI. Methods: A six channel, high dynamic range, real-time power profiling system was designed and built for monitoring power delivery during MRI up to 440 MHz. The system was calibrated and used in two 3 T scanners to measure power applied to human subjects during MRI scans. The results were compared with the scanner-reported SAR. Results: The new power measurement system has highly linear performance over a 90 dB dynamic range and a wide range of MRI duty cycles. It has about 0.1 dB insertion loss that does not interfere with scanner operation. The measurements of whole-body SAR in volunteers showed that scanner-reported SAR was significantly overestimated by up to about 2.2 fold. Conclusions: The new power monitor system can accurately and independently measure RF power deposition over the wide range of conditions routinely encountered during MRI. Scanner-reported SAR values are not appropriate for setting exposure limits during device or pulse sequence testing.
BackgroundIt has been hypothesized that the supply of chemical energy may be insufficient to fuel normal mechanical pump function in heart failure (HF). The creatine kinase (CK) reaction serves as the heart’s primary energy reserve, and the supply of adenosine triphosphate (ATP flux) it provides is reduced in human HF. However, the relationship between the CK energy supply and the mechanical energy expended has never been quantified in the human heart. This study tests whether reduced CK energy supply is associated with reduced mechanical work in HF patients.MethodsCardiac mechanical work and CK flux in W/kg, and mechanical efficiency were measured noninvasively at rest using cardiac pressure-volume loops, magnetic resonance imaging and phosphorus spectroscopy in 14 healthy subjects and 27 patients with mild-to-moderate HF.ResultsIn HF, the resting CK flux (126 ± 46 vs. 179 ± 50 W/kg, p < 0.002), the average (6.8 ± 3.1 vs. 10.1 ± 1.5 W/kg, p <0.001) and the peak (32 ± 14 vs. 48 ± 8 W/kg, p < 0.001) cardiac mechanical work-rates, as well as the cardiac mechanical efficiency (53% ± 16 vs. 79% ± 3, p < 0.001), were all reduced by a third compared to healthy subjects. In addition, cardiac CK flux correlated with the resting peak and average mechanical power (p < 0.01), and with mechanical efficiency (p = 0.002).ConclusionThese first noninvasive findings showing that cardiac mechanical work and efficiency in mild-to-moderate human HF decrease proportionately with CK ATP energy supply, are consistent with the energy deprivation hypothesis of HF. CK energy supply exceeds mechanical work at rest but lies within a range that may be limiting with moderate activity, and thus presents a promising target for HF treatment.Trial registrationClinicalTrials.gov Identifier: NCT00181259.Electronic supplementary materialThe online version of this article (10.1186/s12968-018-0491-6) contains supplementary material, which is available to authorized users.
The creatine kinase (CK) reaction is central to muscle energetics, buffering ATP levels during periods of intense activity via consumption of phosphocreatine (PCr). PCr is believed to serve as a spatial shuttle of high-energy phosphate between sites of energy production in the mitochondria and sites of energy utilization in the myofibrils via diffusion. Knowledge of the diffusion coefficient of PCr (D PCr) is thus critical for modeling and understanding energy transport in the myocyte, but DPCr has not been measured in humans. Using localized phosphorus magnetic resonance spectroscopy, we measured D PCr in the calf muscle of 11 adults as a function of direction and diffusion time. The results show that the diffusion of PCr is anisotropic, with significantly higher diffusion along the muscle fibers, and that the diffusion of PCr is restricted to a ϳ28-m pathlength assuming a cylindrical model, with an unbounded diffusion coefficient of ϳ0.69 ϫ 10 Ϫ3 mm 2 /s. This distance is comparable in size to the myofiber radius. On the basis of prior measures of CK reaction kinetics in human muscle, the expected diffusion distance of PCr during its half-life in the CK reaction is ϳ66 m. This distance is much greater than the average distances between mitochondria and myofibrils. Thus these first measurements of PCr diffusion in human muscle in vivo support the view that PCr diffusion is not a factor limiting high-energy phosphate transport between the mitochondria and the myofibrils in healthy resting myocytes. myocyte; energy metabolism; creatine kinase shuttle; human studies PHOSPHOCREATINE (PCr) serves as the main short-term energy reserve in muscle, heart, and brain. PCr generates ATP to fuel cellular processes, including ion transport and muscular contraction, via the creatine kinase (CK) reaction. The CK reaction reversibly transfers a phosphoryl group between PCr and ATP, with unphosphorylated Cr and ADP as the other reactants and k as the forward pseudo-first-order rate constant of the reaction: PCr ϩ ADP ϩ H ϩ ↔ k ATP ϩ Cr . It was long ago hypothesized that the CK reaction serves as an intracellular energy shuttle, facilitating the transfer of high-energy phosphate from sites of de novo ATP creation in the mitochondria to sites of energy utilization, such as the myofibrils (4, 29, 45). The energy transfer mechanism in this PCr shuttle hypothesis involves 1) the creation of PCr at the mitochondria from the reverse CK reaction, 2) the diffusion of PCr to the point of use (including possible recycling through CK in the cytosol), and 3) the regeneration of ATP from ADP and PCr via the forward CK reaction to supply the needed energy (Fig. 1). Provided that the rate of ATP production via CK is manyfold higher than that generated by oxidative phosphorylation, the CK reaction could serve as a temporal-spatial energy buffer, supplying ATP when and where it is needed during periods of acute demand and/or stress.Since PCr diffusion is central to the PCr shuttle hypothesis, knowledge of its diffusion coefficient (D PCr ) is ...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.