Abstract 3029: Is Regionally Reduced Myocardial Catecholamine Uptake and Storage Capacity a Substrate for Post-Infarct Ventricular Tachycardia?
Background: Nuclear imaging has identified regionally-impaired sympathetic innervation in the normally-perfused border zone of some patients after myocardial infarction. This pattern has been proposed to reflect arrhythmogenic risk and may be used to guide therapy, but pathophysiologic mechanisms are still poorly understood.
Methods: Myocardial infarction was induced by mid LAD balloon occlusion in 5 farm pigs. PET imaging of tissue perfusion and presynaptic catecholamine uptake and storage was performed using N-13 ammonia and C-11 epinephrine 10–12 weeks later. MRI (cine mode, scar detection), and invasive electrophysiology(electroanatomic mapping, basket catheter, VT inducibility) were performed within 1 week of PET. Parameters were compared in 9 myocardial segments per animal.
Results: LVEF at imaging was 35±2%. At PET, all animals had at least one segment with a perfusion/ innervation matched defect(MD), consistent with the infarct area (9/45 segments), and at least another segment in the border zone with a mismatch of reduced innervation but normal perfusion (MM; 12/45 segments). MRI revealed no differences in wall thickness and thickening between MM and normal segments (N), while both were reduced in MD. MRI-defined scar transmurality was greatest in MD, but some nontransmural scar was also found in MM (3±12% of thickness for N vs 21±28 for MM vs 46±21 for MD; p=0.01). Electroanatomic mapping revealed areas of markedly-reduced voltage (<0.5mV) mostly in MD (0.2±0.6% of area for N vs 5.7±13.2 vs 28.4±32.5; p<0.01), but areas of moderately-reduced voltage (<1.5mV) were also detected in MM (4.2±12.1% of area for N vs 19.2±17.7 vs 54.2±27.8; p<0.01). Programmed stimulation induced 5 sustained monomorphic VTs from 4 pigs. The site of earliest activation of VT was located in a MM segment in 3/5 cases (chi square p=0.17).
Conclusions: Areas of reduced innervation but normal perfusion are clearly identified by PET in a model of post-infarct inducible ventricular tachycardia. These are characterized by small amounts of nontransmural scar at MRI and by reduced voltage at electroanatomic mapping, but inducible VT did not always emerge from there. Regional autonomic dysinnervation may contribute to the substrate of VT, but is not the single, critical factor.