Can the inflammatory response be evaluated using18F-FDG within zones of microvascular obstruction after myocardial infarction?

Abstract

Inflammation that occurs after acute myocardial infarction plays a pivotal role in healing by facilitating the creation of a supportive scar. 18F-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 18F-FDG, bolus injection of 99Tc-DTPA to simulate the distribution of gadolinium-DTPA (which represents its partition coefficient in well-perfused tissue), and injection of 111In-labeled white blood cells 24 h earlier. After sacrifice, myocardial tissue concentrations of 18F, 111In, and 99Tc were determined in a well counter. Linear regression analysis evaluated the relationships between the concentrations of 111In and 18F and the dependence of the ratio of 111In/18F to the apparent distribution volume of 99mTc-DTPA. Results: In 7 of 9 animals, 111In increased as 18F increased with the other 2 animals, showing weak negative slopes. With respect to the dependence of 111In/18F 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, 18F significantly underestimated the extent of the presence of 111In. Conclusion: In the early post-myocardial infarction period, 18F-FDG PET imaging after a single bolus administration may underestimate the extent and degree of inflammation within regions of microvascular obstruction.