J Nucl Med. 2007; 48 (Supplement 2):54P
Cardiovascular: Basic Science
PET and SPECT |
Relationship between sympathetic dysinnervation and invasive electrophysiology in a pig model of post-infarct ventricular tachycardia
Tetsuo Sasano1,
M. Roselle Abraham1,
Kuan-Cheng Chang1,
Robert Dannals2,
Daniel Holt2,
John Hilton2,
Albert Lardo1,
Eduardo Marban1 and
Frank Bengel2
1 Cardiology; ;
2 Nuclear Medicine, Johns Hopkins University, Baltimore, Maryland
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Objectives: Sympathetic innervation can be impaired in the normally perfused borderzone of myocardial infarction. The resulting reduction of catecholamine reuptake may contribute to myocardial overexposure to the neurotransmitter and thus reflect arrhythmogenic risk. The aim of this study was to characterize the interaction between dysinnervation, electrophysiology and arrhythmia inducibility in a standardized animal model. Methods: Myocardial infarction (MI) was induced by mid LAD balloon occlusion in 11 farm pigs. PET imaging of perfusion and presynaptic catecholamine uptake and storage was performed using N-13 ammonia and C-11 epinephrine 4-10 weeks later. Using polarmap analysis, regional (9 myocardial segments) and global abnormalities were defined by comparison with a normal database (n=9 pigs). Cine MRI and invasive electrophysiology (electroanatomical mapping (EAM), VT induction) were performed within 1 week of PET. Results: All pig had anteroseptal MI with an ejection fraction (EF) of 32.7±3.8%. A perfusion defect (PD, defined as NH3 uptake <2sd) was detected in 34/99 segments. In the 20 of the remaining segments, an innervation/perfusion mismatch (MM), defined as >1.5 sd reduction of epinephrine retention when compared to perfusion, was detected. At EAM, MM segments were characterized as having small amount of reduced (<1.5mV) voltage area (26.7±30.5%). Programmed stimulation induced 8 sustained monomorphic VTs in 7 of 11 pigs. Globally, VT inducible animals had larger MM areas (9.4±3.6 vs. 3.8±2.2 % of LV, p=0.020) compared to non-inducible pigs, but showed no difference in EF and infarct size. Regionally, the site of earliest activation of VT was located in a MM segment in 6 of 8 cases (chi square p=0.002). Diastolic fragmented potential was recorded in 6 sites, and was located mostly in PD (5/6) but not in MM segments. Conclusions: Dysinnervated but normally perfused myocardium is present after experimental myocardial infarction. These areas are characterized by mildly reduced voltage at EAM, associated with the exit of VT reentry circuit, and larger in inducible VT animals. Sympathetic dysinnervation is thus considered a substrate of VT after MI.
