J Nucl Med. 2007; 48 (Supplement 2):2P
Cardiovascular: Special Sessions
Cardiovascular Young Investigator Symposium |
Myocardial sympathetic innervation and regional strain in a porcine model of chronic myocardial infarction
Tetsuo Sasano1,
M. Roselle Abraham1,
Kuan-Cheng Chang1,
Robert Dannals2,
Holt Daniel2,
John Hilton2,
Albert Lardo1,
Nael Osman3,
Eduardo Marban1 and
Frank Bengel2
1 Cardiology; ;
2 Nuclear Medicine; ;
3 Radiology, Johns Hopkins University, Baltimore, Maryland
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Objectives: Ischemic damage of myocardial sympathetic innervation may contribute to regional contractile dysfunction and facilitate ventricular remodelling. We sought to study the relationship between neuronal integrity and strain pattern in a multi-modality imaging study using a standardized animal model. Methods: Myocardial infarction was induced by mid LAD balloon occlusion in 6 farm pigs. Dynamic PET imaging of perfusion and presynaptic catecholamine uptake and storage was performed using N-13 ammonia and C-11 epinephrine 4-6 weeks later. An additional 3T MRI scan was done within 1 week of PET, and grid tagging was performed to determine circumferential strain using dedicated 2D analysis software (HARP, Diagnosoft, CA). Regional results were compared in 8 myocardial segments per animal (apex was not covered by MRI and thus excluded). Results: Average ejection fraction was 34.6±9.3%. When compared to a normal database, 24 segments (50%) showed normal perfusion and innervation, 14 showed concordantly reduced perfusion and innervation (scar), and 10 showed a mismatch with reduced perfusion but preserved innervation. Regional epinephrine retention showed a negative correlation with peak circumferential strain (PS), endsystolic strain (ESS), and time to peak strain (TP) (R=-0.476, -0.481, -0.467 respectively, p<0.01 for all). Regional perfusion also revealed negative correlations with PS, ESS, and TP (R=-0.473, -0.466, -0.579 respectively, p<0.01 for all). At multivariate stepwise regression, only epinephrine retention was an independent determinant of PS and ESS as measures of systolic function, while perfusion was an independent determinant of TP as a measure of regional dyssynchrony (p<0.001 for both). Conclusions: These results support a close relationship between sympathetic dysinnervation and impaired contractile performance. Ischemic damage of sympathetic neuronal integrity may contribute to the development and progression of heart failure after myocardial infarction.
