Frank S Prato1, John Butler2, Jane Sykes2, Lynn Keenliside2, Kimberley J Blackwood3, R Terry Thompson4, James A White5, Yoko Mikami5, Jonathan D Thiessen6, Gerald Wisenberg7. 1. Lawson Health Research Institute, London, Ontario, Canada Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada Medical Imaging, University of Western Ontario, London, Ontario, Canada frank.prato@lawsonimaging.ca. 2. Lawson Health Research Institute, London, Ontario, Canada. 3. Lawson Health Research Institute, London, Ontario, Canada Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada Medical Imaging, University of Western Ontario, London, Ontario, Canada Stephenson Cardiovascular MR Centre, Libin Cardiovascular Institute, University of Calgary, Alberta, Canada; and Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada. 4. Lawson Health Research Institute, London, Ontario, Canada Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada Medical Imaging, University of Western Ontario, London, Ontario, Canada. 5. Stephenson Cardiovascular MR Centre, Libin Cardiovascular Institute, University of Calgary, Alberta, Canada; and. 6. Lawson Health Research Institute, London, Ontario, Canada Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada. 7. Lawson Health Research Institute, London, Ontario, Canada Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada.
Abstract
UNLABELLED: Inflammation that occurs after acute myocardial infarction plays a pivotal role in healing by facilitating the creation of a supportive scar. (18)F-FDG, which is taken up avidly by macrophages, has been proposed as a marker of cell-based inflammation. However, its reliability as an accurate indicator of inflammation has not been established, particularly in the early postinfarction period when regional myocardial perfusion is often severely compromised. METHODS: Nine adult dogs underwent left anterior descending coronary occlusion with or without reperfusion. Animals were imaged between 7 and 21 d after infarction with PET/MR imaging after bolus injection of gadolinium-diethylenetriaminepentaacetic acid (DTPA), bolus injection of (18)F-FDG, bolus injection of (99)Tc-DTPA to simulate the distribution of gadolinium-DTPA (which represents its partition coefficient in well-perfused tissue), and injection of (111)In-labeled white blood cells 24 h earlier. After sacrifice, myocardial tissue concentrations of (18)F, (111)In, and (99)Tc were determined in a well counter. Linear regression analysis evaluated the relationships between the concentrations of (111)In and (18)F and the dependence of the ratio of (111)In/(18)F to the apparent distribution volume of (99m)Tc-DTPA. RESULTS: In 7 of 9 animals, (111)In increased as (18)F increased with the other 2 animals, showing weak negative slopes. With respect to the dependence of (111)In/(18)F with partition coefficient, 4 animals showed no dependence and 4 showed a weak positive slope, with 1 animal showing a negative slope. Further, in regions of extensive microvascular obstruction, (18)F significantly underestimated the extent of the presence of (111)In. CONCLUSION: In the early post-myocardial infarction period, (18)F-FDG PET imaging after a single bolus administration may underestimate the extent and degree of inflammation within regions of microvascular obstruction.
UNLABELLED: Inflammation that occurs after acute myocardial infarction plays a pivotal role in healing by facilitating the creation of a supportive scar. (18)F-FDG, which is taken up avidly by macrophages, has been proposed as a marker of cell-based inflammation. However, its reliability as an accurate indicator of inflammation has not been established, particularly in the early postinfarction period when regional myocardial perfusion is often severely compromised. METHODS: Nine adult dogs underwent left anterior descending coronary occlusion with or without reperfusion. Animals were imaged between 7 and 21 d after infarction with PET/MR imaging after bolus injection of gadolinium-diethylenetriaminepentaacetic acid (DTPA), bolus injection of (18)F-FDG, bolus injection of (99)Tc-DTPA to simulate the distribution of gadolinium-DTPA (which represents its partition coefficient in well-perfused tissue), and injection of (111)In-labeled white blood cells 24 h earlier. After sacrifice, myocardial tissue concentrations of (18)F, (111)In, and (99)Tc were determined in a well counter. Linear regression analysis evaluated the relationships between the concentrations of (111)In and (18)F and the dependence of the ratio of (111)In/(18)F to the apparent distribution volume of (99m)Tc-DTPA. RESULTS: In 7 of 9 animals, (111)In increased as (18)F increased with the other 2 animals, showing weak negative slopes. With respect to the dependence of (111)In/(18)F with partition coefficient, 4 animals showed no dependence and 4 showed a weak positive slope, with 1 animal showing a negative slope. Further, in regions of extensive microvascular obstruction, (18)F significantly underestimated the extent of the presence of (111)In. CONCLUSION: In the early post-myocardial infarction period, (18)F-FDG PET imaging after a single bolus administration may underestimate the extent and degree of inflammation within regions of microvascular obstruction.
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