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Published online before print January 24, 2003, 10.1148/radiol.2263020151
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Characterization of Viable and Nonviable Myocardium at MR Imaging: Comparison of Gadolinium-based Extracellular and Blood Pool Contrast Materials versus Manganese-based Contrast Materials in a Rat Myocardial Infarction Model1

Sebastian Flacke, MD, John S. Allen, BA, Jon M. Chia, MS, James H. Wible, PhD, M. Peri Periasamy, PhD, Max D. Adams, PhD, I. Kofi Adzamli, PhD and Christine H. Lorenz, PhD

1 From the Center for Cardiovascular Magnetic Resonance, Department of Medicine, Cardiovascular Division, Washington University Medical School, St Louis, Mo (S.F., J.S.A., J.M.C., C.H.L.); and Imaging Division, Mallinckrodt, St Louis, Mo (J.H.W., M.P.P., M.D.A., I.K.A.). Received March 4, 2002; revision requested April 23; final revision received July 31; accepted August 14. S.F. supported by German Research Foundation grant FL-330. Address correspondence to S.F., Department of Radiology, University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany (e-mail: flacke@uni-bonn.de).



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Figure 1a. Graph shows T1 calculated as 1/T1 - 1/T1precontrast for (a) myocardium and (b) liver at various time points for gadolinium- and manganese-based MR imaging contrast agents. All three manganese-based contrast media reduced the T1 values of normal myocardium and liver. The peak reduction of T1 in the myocardium for MnCl2 ({blacksquare}) was observed 23 minutes after contrast agent injection, whereas the slower manganese release of MnCl2/Ca ({bullet}) and MP-680 ({blacktriangleup}) resulted in peak reduction of T1 at the end of the observation time. At the time the first T1 measurements were performed, approximately 20 minutes after injection of the contrast agents gadoversetamide ({triangleup}) and MP-2269 ({square}), the bulk of the gadolinium-based agents had already washed out of the myocardium and liver, with similar kinetics for both tissues.

 


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Figure 1b. Graph shows T1 calculated as 1/T1 - 1/T1precontrast for (a) myocardium and (b) liver at various time points for gadolinium- and manganese-based MR imaging contrast agents. All three manganese-based contrast media reduced the T1 values of normal myocardium and liver. The peak reduction of T1 in the myocardium for MnCl2 ({blacksquare}) was observed 23 minutes after contrast agent injection, whereas the slower manganese release of MnCl2/Ca ({bullet}) and MP-680 ({blacktriangleup}) resulted in peak reduction of T1 at the end of the observation time. At the time the first T1 measurements were performed, approximately 20 minutes after injection of the contrast agents gadoversetamide ({triangleup}) and MP-2269 ({square}), the bulk of the gadolinium-based agents had already washed out of the myocardium and liver, with similar kinetics for both tissues.

 


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Figure 2a. Graph shows CNR between (a) viable myocardium and blood and between (b) normal myocardium and infarct on inversion-recovery late-enhancement images with a fixed inversion time of 430 msec for the five groups of animals. For all manganese-based media, the contrast agent cleared from the blood pool rapidly. CNR ratios between viable myocardium and infarct were observed to have plateaued for MnCl2 ({blacksquare}) approximately 30 minutes after injection and for MP-680 ({blacklozenge}) and MnCl2/Ca ({bullet}) approximately 1 hour after injection. Gadoversetamide ({triangleup}), the extracellular agent, washed out of the blood rapidly, whereas MP-2269 ({square}) persisted in the blood pool for the duration of the imaging. Accumulation of gadoversetamide in the infarct area was apparent after 5 minutes, which led to a peak CNR between infarct and myocardium comparable with the peak CNR of manganese-based agents.

 


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Figure 2b. Graph shows CNR between (a) viable myocardium and blood and between (b) normal myocardium and infarct on inversion-recovery late-enhancement images with a fixed inversion time of 430 msec for the five groups of animals. For all manganese-based media, the contrast agent cleared from the blood pool rapidly. CNR ratios between viable myocardium and infarct were observed to have plateaued for MnCl2 ({blacksquare}) approximately 30 minutes after injection and for MP-680 ({blacklozenge}) and MnCl2/Ca ({bullet}) approximately 1 hour after injection. Gadoversetamide ({triangleup}), the extracellular agent, washed out of the blood rapidly, whereas MP-2269 ({square}) persisted in the blood pool for the duration of the imaging. Accumulation of gadoversetamide in the infarct area was apparent after 5 minutes, which led to a peak CNR between infarct and myocardium comparable with the peak CNR of manganese-based agents.

 


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Figure 3. Late-enhancement MR images (5.2/2.5; flip angle, 15°) obtained with various contrast agents. Sample images at various time points from injection of the contrast media from each group of animals are displayed in columns. In the three columns at left, images obtained with the three manganese-based contrast agents show the viable myocardium as bright, whereas the infarct has no contrast enhancement. In the two columns at right, images obtained with both gadolinium-based contrast agents show the infarct as bright. At 15 minutes after injection, the infarcted myocardium (arrows) can be seen in all groups. Specimens of the corresponding histologic sections stained with hematoxylin-eosin are displayed in the last row. The infarct can be seen at low magnification (x5) due to the wall thinning at the poorly stained region (arrowheads). Gd-DTPA BMEA = gadoversetamide.

 


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Figure 4. Graph shows estimation of infarct size by using late-enhancement MR imaging findings compared with histologic findings. The relative misestimation was calculated with a section-by-section comparison. The SD was not displayed if it was smaller than the icon size. {blacksquare} = MnCl2, {bullet} = MnCl2/Ca, {blacktriangleup} = MP-680, {triangleup} = Gadoversetamide, {square} = MP-2269.

 





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