Impaired catecholamine handling in the viable infarct border zone may play an important role in ventricular remodeling and lethal arrhythmia. We sought to get further biologic insights into cardiac sympathetic neuronal pathology after myocardial infarction, using multiple tomographic imaging techniques.In a porcine model of myocardial infarction (n = 13), PET and MR imaging were performed after 4-6 wk and integrated with electrophysiologic testing and postmortem histology.PET with the physiologic neurotransmitter (11)C-epinephrine, which is sensitive to metabolic degradation unless it is stored and protected in neuronal vesicles, identified a defect exceeding the perfusion defect (defined by (13)N-ammonia; defect size in all animals, 42 ± 12 vs. 35

作者：Riikka, Lautamaki；Tetsuo, Sasano；Takahiro, Higuchi；Stephan G, Nekolla；Albert C, Lardo；Daniel P, Holt；Robert F, Dannals；M Roselle, Abraham；Frank M, Bengel

来源：Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2015 年 56卷 3期