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Cardiovascular: Basic ScienceNew Approaches Using SPECT, PET and Hybrid Imaging |
1 Johns Hopkins U, Baltimore, Maryland
122
Objectives: After myocardial infarction(MI),sympathetic nerve damage exceeds scar and promotes ventricular arrhythmia.We aimed to study the biology of neuronal damage using 3 tracers with different kinetic properties in a model of chronic MI.
Methods: A 2-day PET protocol was employed using GE Discovery Rx VCT in 7 pigs,4-6 weeks after reperfused MI.On day 1,perfusion was measured with N13-ammonia(NH3),followed by dynamic imaging with C11-epinephrine(EPI;vesicular storage with no significant washout in healthy subjects).On day 2,C11-hydroxyephedrine(HED;neuronal uptake with no significant washout)and C11-phenylephrine(PHEN;vesicular leakage with washout)were employed.Using polarmap analysis tracer retention and washout rates were compared globally and regionally in NH3-defined infarct(<60% uptake of maximum), borderzone(50-70%) and remote region(>70%).
Results: Pigs had LV dysfunction(EF 40.2±5.9%)and some had inducible VT. For all 3tracers,defect size exceeded perfusion defect(45±7%LV for EPI,43±7% for HED,48±5% for PHEN vs 39±8% for ammonia),and relative regional retention was below perfusion in borderzone,but not in infarct and remote areas. EPI showed global washout(1.2±0.3%/min),which was comparable to PHEN(1.1±0.3%/min),and absent with HED(-.6±.2%/min; p<.01).Regionally, EPI washout was 17/27% higher in the borderzone than in infarct/remote area.
Conclusions: In our model,neuronal damage in the infarct borderzone is mostly due to absolute denervation,as evidenced by reduced uptake of all 3 catecholaminergic tracers.Abnormally increased global and regional epinephrine washout suggests an additional component of impaired vesicular storage/increased catecholamine turnover which may represent reversible impairments and thus be a target of therapeutic intervention.
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