Characterization of inflamed, acutely infarcted myocardial tissue by combined clinical FDG PET and CMR

185 Objectives The inflammatory response to acute myocardial infarction (MI) is emerging as a target for novel therapies aiming at improved healing. Cardiac magnetic resonance imaging (CMR) and PET provide multiple parameters for characterization of the biology of acutely infarcted, inflamed myocardium, but the interrelations are poorly understood. Methods CMR and 18FDG-PET/CT were performed in 9 pts within one wk after first MI. Heparin was administered before PET to enable inflammation imaging by suppressing myocardial glucose uptake. CMR was used for imaging of late contrast enhancement (LE), microvascular obstruction (MVO), edema and wall motion. Visual analysis was done using by a 5 point scoring system based on the AHA 17-segment model. Results FDG uptake was elevated in the hypoperfused infarct region in all pts. Linear regression analysis showed a significant correlation between global FDG-score, infarct size (r=0.758; p=0.03) and CKmax (r=0.764; p=0.05). FDG-score was significantly elevated in segments with LE vs without (1.7±0.3 vs 0.6±0.1; p=0.002), with MVO vs without (2.1±0.4 vs 0.9±0.01; p=0.01), and with edema vs without (1.6±0.3 vs 0.4±0.1; p=0.005). Among segments with LE, there was no difference in FDG score between those with/without MVO, or with/without edema. Conclusions Patients with acute MI show a high prevalence of increased FDG uptake in the infarct region under heparin-induced myocardial suppression, suggesting inflammation in regions with LE on CMR. MVO and edema coincide with FDG uptake but are not independently associated. Multimodality characterization of post-MI inflammation may provide multi-parametric endpoints for clinical studies of infarct healing.