Abstract
Changes in the kinetics of the creatine kinase (CK) shuttle are sensitive markers of cardiac energetics but are typically measured at rest and in the prone position. This study aims to measure CK kinetics during pharmacological stress at 3 T, with measurement in the supine position. A shorter “stressed saturation transfer” (StreST) extension to the triple repetition time saturation transfer (TRiST) method is proposed. We assess scanning in a supine position and validate the MR measurement against biopsy assay of CK activity. We report normal ranges of stress CK forward rate (kf CK) for healthy volunteers and obese patients.TRiST measures kf CK in 40 min at 3 T. StreST extends the previously developed TRiST to also make a further kf CK measurement during <20 min of dobutamine stress. We test our TRiST implementation in skeletal muscle and myocardium in both prone and supine positions. We evaluate StreST in the myocardium of six healthy volunteers and 34 obese subjects. We validated MR‐measured kf CK against biopsy assays of CK activity.TRiST kf CK values matched literature values in skeletal muscle (kf CK = 0.25 ± 0.03 s−1 vs 0.27 ± 0.03 s−1) and myocardium when measured in the prone position (0.32 ± 0.15 s−1), but a significant difference was found for TRiST kf CK measured supine (0.24 ± 0.12 s−1). This difference was because of different respiratory‐ and cardiac‐motion‐induced B0 changes in the two positions. Using supine TRiST, cardiac kf CK values for normal‐weight subjects were 0.15 ± 0.09 s−1 at rest and 0.17 ± 0.15 s−1 during stress. For obese subjects, kf CK was 0.16 ± 0.07 s−1 at rest and 0.17 ± 0.10 s−1 during stress. Rest myocardial kf CK and CK activity from LV biopsies of the same subjects correlated (R = 0.43, p = 0.03).We present an independent implementation of TRiST on the Siemens platform using a commercially available coil. Our extended StreST protocol enables cardiac kf CK to be measured during dobutamine‐induced stress in the supine position.
Highlights
The rate and flux of the creatine kinase (CK) exchange mechanism have been shown to be sensitive measures of heart failure(1), which is a prevalent and burdensome disease (2,3).The rate can be characterised by the pseudo first-order forward rate constant, kfCK.Phosphorus magnetic resonance spectroscopy (31P-MRS) enables non-invasive19 measurement of myocardial kfCK (4)
0.27±0.03 s-1) and myocardium when measured in the prone position (0.32±0.15 s-1), but a significant difference was found for TRiST kfCK measured supine (0.24±0.12 s-1)
Our extended stressed saturation transfer” (StreST) protocol enables cardiac kfCK to be measured during dobutamine-induced stress in the supine position
Summary
The rate and flux of the creatine kinase (CK) exchange mechanism have been shown to be sensitive measures of heart failure(1), which is a prevalent and burdensome disease (2,3). In addition to measuring kfCK in myocardium at rest, measuring kfCK during pharmacologically-induced stress would enable us to understand the effect of a perturbed CK mechanism in the stressed human heart (1,5). Schär et al introduced the triple repetition time saturation transfer (TRiST) sequence to 25 measure CK kinetics by 31P-MRS at 3T (6). A TRiST acquisition lasts 40 min (out of complete protocol totalling 84 min); it measures kfCK in a one-dimensional coronal stack of slices covering the heart and chest wall (7). 1D-localised kfCK measurement during inotropic stress was achieved by Weiss et al at 1.5 T using the four-angle saturation transfer (FAST) and the derived “FASTest” method (1,4). The 3T TRiST protocol offers an established measurement technique which can be included in a larger cardiac 1H MR protocol on the same scanner
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