Purpose: To evaluate T1-relaxation times of chronic myocardial infarction (CMI) using gadobutrol andgadopentetate dimeglumine (Gd-DTPA) over time and to determine the optimal imaging window forlate enhancement imaging with both contrast agents.Material and methods: Twelve patients with CMI were prospectively included and examined on a 1.5 Tmagnetic resonance (MR) system using relaxivity-adjusted doses of gadobutrol (0.15 mmol/kg) andGd-DTPA (0.2 mmol/kg) in random order. T1-relaxation times of remote myocardium (RM), infarctedmyocardium (IM), and left ventricular cavity (LVC) were assessed from short-axis TI scout imaging usingthe Look–Locker approach and compared intraindividually using a Wilcoxon paired signed-rank test(˛ < 0.05).Results: Within 3 min of contrast agent administration (CA), IM showed significantly lower T1-relaxationtimes than RM with both contrast agents, indicating beginning cardiac late enhancement. Differencesbetween gadobutrol and Gd-DTPA in T1-relaxation times of IM and RM were statistically not significantthrough all time points. However, gadobutrol led to significantly higher T1-relaxation times of LVC thanGd-DTPA from 6 to 9 min (220 ± 15 ms vs. 195 ± 30 ms p < 0.01) onwards, resulting in a significantly
greater �T1 of IM to LVC at 9–12 min (−20 ± 35 ms vs. 0 ± 35 ms, p < 0.05) and 12–15 min (−25 ± 45 msvs. −10 ± 60 ms, p < 0.05). Using Gd-DTPA, comparable �T1 values were reached only after 25–35 min.Conclusion: This study indicates good delineation of IM to RM with both contrast agents as early as 3 minafter administration. However, we found significant differences in T1 relaxation times with greater �T1IM–LVC using 0.15 mmol/kg gadobutrol compared to 0.20 mmol/kg Gd-DTPA after 9–15 min post-CAsuggesting earlier differentiability of IM and LVC using gadobutrol.
Cardiac late gadolinium enhancement (LGE) imaging is ahighly sensitive and specific method for assessment of myocardialinfarction, allowing direct imaging of myocardial necrosis andfibrosis with high spatial resolution and tissue contrast [1–3]. Theextent of LGE has a high prognostic value and may be used to pre-dict functional recovery, cardiovascular events, and response torevascularization or resynchronization therapy following myocar-dial infarction [4,5]. LGE is measured on T1-weighted imagesafter intravenous administration of T1-shortening extracellulargadolinium chelates [6], which have been shown to accumulate ininfarcted myocardium [7]. Accumulation in infarcted myocardiumis assumed to be a result of altered wash-in/wash-out kinetics and
an increased extracellular volume [1,8].
Most studies on LGE have been conducted with the firstapproved magnetic resonance (MR) imaging contrast agent,gadopentetate dimeglumine (Gd-DTPA) [2,6,8]. In the last decades,
everal other gadolinium-based MR contrast agents have beenpproved. They differ in their molecular structure, charge, ther-odynamic stability, pharmacokinetics, and T1 relaxivity [9,10].adobutrol is a nonionic macrocyclic extracellular contrast agent,ith a higher T1 relaxivity compared to the ionic, linear contrast
gent Gd-DTPA [9,11]. These contrast agents have been investi-ated in comparative studies in different organ systems to evaluateheir potential use for specific indications [12–14]. Recent com-arative studies evaluated different MR contrast agents also forardiac LGE imaging at a certain time point after administration12,15–19]. The contrast agents investigated in these studies wereenerally found to allow reliable differentiation between infarctedyocardium (IM) and remote myocardium (RM). In contrast, the
elineation of IM from the left ventricular cavity (LVC) proved toe challenging and varied significantly for some contrast agents15,18]. These observations indicate that the pharmacokinetics ofhe compared contrast agents in IM and LVC differ. Yet, IM-to-LVContrast is needed for delineating small subendocardial infarctsnd measuring infarct transmurality, which are strong prognosticarameters [20]. T1 relaxation times after contrast agent injectionetermine contrast in T1-weighted images. Unlike signal intensityeasurements, the T1 relaxation time is a quantitative measure
nd its absolute value after contrast agent application seems toe of clinical significance [21]. It relates to the extracellular vol-me fraction and is reduced in conditions with myocardial fibrosis30]. Therefore, we sought to determine the T1 relaxation times inM, IM, and LVC and the T1 relaxation time difference between IMnd RM (�T1 IM–RM) as well as IM and LVC (�T1 IM–LVC) overime after administration of Gd-DTPA and gadobutrol in order toetermine the optimal imaging time point for cardiac LGE imagingith the two contrast agents based on the T1 relaxation times and
o screen for systematic differences in post-contrast T1 relaxationimes.
. Methods
.1. Population
The study was conducted as an intraindividual comparison ofd-DTPA (Magnevist®, Bayer Healthcare, Berlin, Germany) andadobutrol (Gadovist®, Bayer Healthcare, Berlin, Germany) forardiac LGE imaging. Twelve patients with chronic myocardialnfarction were included for T1 relaxation time measurements.atients were examined on a 1.5 Tesla MR system (Siemens Mag-etom Avanto) using a 32-channel phased array surface coil. Allarticipants had glomerular filtration rates >60 ml/min/1.73 m2
estimated by the MDRD-formula). In two separate visits2–30 days apart), patients received 0.2 mmol/kg Gd-DTPA and.15 mmol/kg gadobutrol in random order. Contrast agents weredministered through a cubital vein catheter using an MRI-ompatible infusion system (Spectrum Solaris®), followed by a0 mL saline flush. Both the contrast agent and the saline flush were
njected at a flow rate of 2 mL/s. The Federal Institute for Drugsnd Medical Devices and the local ethics committee approved thisingle-center drug study. Informed written consent was obtainedrom all patients prior to enrolment in the study.
.2. MR imaging
From 0 to 15 min after contrast agent administration, TI scoutmaging (segmented inversion recovery TrueFISP, repetition time
TR) 23.49 ms, echo time (TE) 1.12 ms, flip angle 50, TI range5–1000 ms, step size 25 ms) was performed approximately every
min. At 15 min, a segmented inversion recovery gradient echo (IR-RE) sequence (2D T1-weighted fast low-angle shot (FLASH) 2D;
Radiology 83 (2014) 660–664 661
TR 9.4 ms, TE 4.4 ms, flip angle 30, readout bandwidth 140 Hz/Px,matrix 256 × 197, in-plane resolution 1.6 mm × 1.3 mm, slice thick-ness 6 mm, slice gap 20%, adapted inversion time) was acquired foridentifying sites of cardiac LGE. Thereafter, TI scout imaging wascontinued between 25 and 35 min.
2.3. Calculation of T1 relaxation times
Using dynamic regions of interest (ROI), an area of IM (infarct-type myocardial late enhancement localized on IR-GRE imaging),RM and LVC was encircled in all TI scout images and manuallyadjusted for regional wall movement during TI scout imaging(Fig. 1). T1 values were estimated by nonlinear regression of thesignal intensities to the TI times using the following equation:
SI(TI) = SI∗0[
1 − 2∗ exp(
− TIT1
)]
As a measure of tissue contrast, differences between the T1 relax-ation times of tissues were calculated (�T1 IM–RM and �T1IM–LVC).
2.4. Statistical analysis
Continuous values are given as means with standard devia-tions (SD). To compare T1 relaxation times intraindividually, resultswere stratified into six groups based on the TI scout imagingtime after contrast agent injection (0–3 min, 3–6 min, 6–9 min,9–12 min, 12–15 min and 25–35 min). This resulted in a total of 65valid intraindividual pairwise comparisons between both exami-nations, while seven pairs had to be excluded due to a missing TIscout in the corresponding time group. When more than one TIscout was acquired within any one of the six groups, the arith-metic mean of the T1 relaxation times was calculated. The meanT1 relaxation time for both contrast agents in all time groupsand the mean intraindividual differences between contrast agentswere calculated and compared using the Wilcoxon signed-rank test(two-sided p-values <0.05 were regarded as significant). All calcu-lations were performed using a commercially available softwarepackage (SPSS Statistics 19, IBM, Armonk, NY, USA).
3. Results
3.1. T1 relaxation times in remote and infarcted myocardium andleft ventricular cavity
The T1 relaxation times for RM, IM, and LVC at all time points aregiven in Table 1 and illustrated over time in Fig. 2. In RM, initial T1relaxation times at 0–3 min were 225 ± 25 ms and 245 ± 40 ms inGd-DTPA- and gadobutrol-enhanced images, respectively (Table 1).Thereafter, T1 times showed a steady increase with both contrastagents without any significant difference between the two contrastagents at any time point (p > 0.05; Table 1), indicating wash-out ofthe contrast agent from RM. Due to the circulating contrast agent,LVC showed T1 relaxation times of 115 ± 15 ms and 125 ± 15 msfor Gd-DTPA and gadobutrol, respectively, at 0–3 min. Likewise, T1relaxation times of LVC showed a steady incline over time due torenal excretion. Significantly shorter T1 relaxation times were mea-sured in LVC with Gd-DTPA compared to gadobutrol from 6 to 9 minonwards (p < 0.01; Table 1), indicating stronger enhancement of theLVC with use of Gd-DTPA from this time onwards.
IM showed T1 relaxation times of 160 ± 40 ms and 180 ±40 ms,respectively, in Gd-DTPA- and gadobutrol-enhanced images
0–3 min after administration (Table 1). T1 relaxation times of IMshowed a steady incline over time and were lower than T1 relax-ation times of RM at all times with both contrast agents, indicating“delayed” enhancement of IM beginning as early as 0–3 min after
662 P. Doeblin et al. / European Journal of Radiology 83 (2014) 660–664
Fig. 1. Top: Representative slides from TI-Scout imaging of an anterior myocardial infarction at 15 min post CA application with Gd-DTPA and gadobutrol. Bottom: Y-axissignal intensity (SI), X-axis inversion time (TI [ms]). The inversion pulse at TI = 0 (not shown) inverts the tissue magnetization and thereby the tissue signal intensity. Thereafter,the tissues recover their original signal intensity depending on their T1 relaxation time. Signal intensity measurements were performed at intervals of 25 ms from 85 msto ∼1000 ms. The T1 relaxation time was estimated by fitting the data to the equation SI = SI0 × |1 − 2 exp(−TI/T1)|. Signal intensities were measured by means of manuallyadjusted regions of interests in IM (infarcted myocardium; blue), RM (remote myocardium; red), and LVC (left ventricular cavity; green). SI0, Baseline Signal Intensity; TI,inversion time.
Table 1Comparison of T1 relaxation times using gadobutrol and Gd-DTPA in infarcted myocardium, remote myocardium, and left ventricular cavity; Wilcoxon signed-rank test.
Time after contrast agent administration
0–3 min 3–6 min 6–9 min 9–12 min 12–15 min 25–35 minN 10 10 11 11 12 11
ontrast agent administration and persisting until the end of thebservation period at 25–35 min (Fig. 2).
In order to characterize accurately the optimal time point ofardiac LGE for both contrast agents with regard to contrast ofM to RM and contrast of IM to LVC, �T1 values were calcu-ated (Table 2). Mean intraindividual �T1 IM–RM was −65 ± 30 mst 0–3 min for both contrast agents and decreased further overime. Mean intraindividual �T1 IM–LVC started at 45 ± 35 ms and5 ± 35 ms for Gd-DTPA and gadobutrol, respectively. The meanT1 IM–LVC turned negative with Gd-DTPA after 12 min com-
ared with 6 min for gadobutrol. Indeed, at 9–12 and 12–15 min,he absolute �T1 IM–LVC was significantly greater with gadobutrolompared to Gd-DTPA, indicating better IM-to-LVC contrast withadobutrol.
4. Discussion
T1 relaxation rates are a tissue-inherent constant and depen-dent on the magnetic field strength. Gadolinium-based MR contrastagents lead to hyperintensity on T1-weighted images by short-ening the T1 relaxation times of surrounding hydrogen atoms.Accumulation of extracellular contrast agents causes cardiac lateenhancement in tissues with an increased extracellular volumesuch as fibrotic or necrotic myocardium [23,24]. �T1 between tis-sues is a measure of the resulting tissue contrast. While the true T1
relaxation rate is constant, most measuring approaches have a sys-tematic bias [25,26,28]. However, T1 relaxation rates allow a moreaccurate and comparable view between different institutions thanmere SI measurements. Different methods for the measurement of
P. Doeblin et al. / European Journal of Radiology 83 (2014) 660–664 663
Fig. 2. Boxplots of the estimated T1 relaxation times of all subjects, over a time span of 35 min after Gd-DTPA and Gadobutrol injection. RM: remote myocardium; LVC: leftventricular cavity; IM: infarcted myocardium; DI: Diagnostic Imaging Window.
Table 2T1 relaxation time differences with gadobutrol and Gd-DTPA from 0–3 min to 25–35 min after contrast agent administration; Wilcoxon signed-rank test.
Time after contrast agent administration
0–3 min 3–6 min 6–9 min 9–12 min 12–15 min 25–35 minN 10 10 11 11 12 11
1 relaxation times exist. We measured T1 relaxation time using aodification of the approach initially proposed by Look and Locker
27], which is an established and reliable method for the estimationf T1 relaxation times [25,26].
In this study, we intraindividually compared T1 relaxation timesf IM, RM, and LVC over a time span of 35 min after intravenousdministration of either 0.2 mmol/kg Gd-DTPA or 0.15 mmol/kgadobutrol. We found significant differences between the two con-rast agents with regard to T1 relaxation times of the LVC, but notM or RM. This resulted in a significantly greater �T1 IM–LVC withadobutrol compared to Gd-DTPA from 9 to 15 min after admin-stration, indicating higher contrast of IM to LVC in this imaging
indow using gadobutrol. These findings are consistent with theNR and CNR measurements of an overlapping population pub-ished elsewhere.
T1 relaxation times of LVC and RM show a steep initial and alow continuous rise with both contrast agents, representing theiexponential decay of the two-compartment model postulatedor plasma gadolinium kinetics [29]. In IM, there is no steep ini-ial incline and a slower rise in T1 relaxation times compared to
VC and RM, possibly representing the trapped compartment ofhe three compartment model postulated for gadolinium kinetics innfarcted myocardium [29]. For both contrast agents, T1 relaxationimes of RM were consistently higher than the respective values
0.213 0.026 0.028 0.090
for IM and LVC, starting within a few minutes of contrast agentadministration and lasting through the whole observation periodof 35 min. This implies that differentiation of RM and IM is possi-ble over a wide range of time points after contrast administration.The T1 relaxation times of IM and LVC, on the other hand, showedmostly similar values with slightly higher values for LVC at latertime points, especially with gadobutrol. �T1 IM–LVC values weresignificantly higher for 0.15 mmol/kg gadobutrol than 0.2 mmol/kgGd-DTPA at 9–12 and 12–15 min. This seems to be attributableto overall higher T1 relaxation times in LVC for 0.15 mmol/kggadobutrol from 6 to 9 min onwards. As a result, T1 relaxationtimes of infarcted myocardium and ventricular lumen reached theircrossing point earlier in time when examined with gadobutrol,indicating that gadobutrol might produce earlier and better delin-eation of the endocardial border in infarcted myocardial regions.Thus LGE imaging with 0.15 mmol/kg gadobutrol could be per-formed as early as 9–12 min after contrast agent administration,while a delay of at least 15–25 min appears to be necessary for reli-able differentiation with 0.2 mmol/kg Gd-DTPA. When interpretingT1 weighted sequences obtained earlier than 15 min after appli-
cation of 0.2 mmol/kg Gd-DTPA, routine comparison with pre-CAimaging should be performed to avoid missing small subendo-cardial infarcts due to the similar T1 relaxation times of IM andLVC.
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Also, our findings outline the influence of the choice of contrastgent and time of acquisition on T1 relaxation time measurements.herefore, when interpreting absolute post-CA T1 relaxation times,ontrast agent and time of acquisition must be standardized. Weuspect differences in the pharmacokinetics of both contrast agentss one possible cause of the discrepancy, yet this should be con-rmed in further research.
To the best of our knowledge, this is the first evaluation ofhe time course of T1 relaxation times after administration ofadobutrol. These data are in agreement with previous findingsf higher IM-to-LVC contrast-to-noise-ratio with 0.15 mmol/kgadobutrol compared to 0.2 mmol/kg Gd-DTPA in IR-GRE imaging15]. Bauner et al. reported T1 relaxation times of 239 ± 74 ms in IM,80 ± 59 ms in RM, and 261 ± 50 ms in LVC 15 min after administra-ion of 0.15 mmol/kg gadobutrol, which is also in good agreementith our values for gadobutrol at 12–15 min [30]. Schlosser et al.
ompared 0.2 mmol/kg Gd-DTPA and Gd-BOPTA intraindividuallyn 15 patients with chronic myocardial infarctions. Our T1 relax-tion times in IM, RM, and LVC for 0.2 mmol/kg Gd-DTPA are close tohe values reported by Schlosser et al. over a time course of 20 min,gain indicating good reproducibility despite the small sample sizes18]. Furthermore, Schlosser et al. demonstrated consistently neg-tive �T1 IM–LVC values with Gd-DTPA after 20 min, which is alsooncordant with our data. Schlosser et al. concluded an advantagef Gd-DTPA in localizing small subendocardial infarcts in compar-son to Gd-BOPTA, which has a significantly lower �T1 IM–LVCecause it binds to plasma albumin [18]. In our intraindividuallyontrolled setting, consistently negative �T1 IM–LVC values wereound at earlier time points using gadobutrol compared to Gd-TPA. This suggests that 0.15 mmol/kg gadobutrol allows betterelineation of subendocardial infarcts at earlier time points than.2 mmol/kg Gd-DTPA.
Our study is limited by the low number of subjects. Yet, thentraindividual design and the high temporal resolution improvehe statistical power. Additional determination of unenhanced T1elaxation rates would have allowed more sophisticated analyses.urthermore, we cannot exclude that the differences we foundight be attributable to the use of a lower dose of gadobutrol.owever, the optimal dose of gadobutrol for cardiac delayednhancement imaging has not yet been determined. Our stan-ard of reference was Gd-DTPA at a dose of 0.2 mmol/kg [6].ue to its higher ex vivo relaxivity (r1), we adjusted the dose ofadobutrol as described elsewhere [15,16]. Reported r1 values of.1 L mmol−1 s−1 for Gd-DTPA and 5.2 L mmol−1 s−1 for gadobutrolex vivo, 37 ◦C, human plasma, 1.5 Tesla) result in a relaxivity-djusted dose of ∼0.15 mmol/kg of gadobutrol [10].
In conclusion, this study is the first to compare T1 relaxationimes of IM and LVC over time with gadobutrol and Gd-DTPA.ur results indicate good delineation of IM to RM with both con-
rast agents as early as 3 min after administration. However, theT1 IM–LVC was greater with 0.15 mmol/kg gadobutrol than with
.20 mmol/kg Gd-DTPA after 9 to 15 min, suggesting earlier differ-ntiability of IM and LVC using gadobutrol.
onflict of interest
None declared.
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