Extension of myocardial necrosis differently affects MIBG retention in heart failure caused by ischaemic heart disease or by dilated cardiomyopathy.
OBJECTIVE
This study aims to investigate the relationship between cardiac sympathetic nervous function (CSNF) and myocardial perfusion/function in patients with heart failure (HF) due to dilated cardiomyopathy (DCM) or ischaemic heart disease (CAD).


METHODS
Twenty patients (10 DCM, 10 CAD, 17 males, age 69+/-5 years) with NYHA class IIIb HF were studied. CSNF was evaluated by early/delayed (123)I-metaiodobenzylguanidine (MIBG) uptake and regional washout (WO). Myocardial perfusion and function were evaluated by (99m)Tc-tetrofosmin gated single-photon emission tomography (G-SPECT) using a 20-segment model for 400 segments. In each segment, regional MIBG WO was computed as (count density in early images-count density in delayed images/count density in early images)x100.


RESULTS
DCM and CAD showed similar summed rest perfusion score (6.7+/-5 vs 9.5+/-5, p=NS) and mean ejection fraction values (29+/-7% vs 30+/-9%, p=NS). By contrast, the summed thickening score was higher in DCM than in CAD patients (26+/-7 vs 17+/-6, p<0.05). QGS analysis identified akinesis/dyskinesis in 129/137 (94%) severely hypoperfused segments which were considered as damaged. According to the underlying aetiology of HF, marked differences in regional MIBG WO were observed. In fact, within the CAD group, regional MIBG WO was lower in reference than in damaged segments (38+/-21% vs 46+/-19%, p<0.05). By contrast, in DCM patients, regional MIBG WO was faster in reference than in damaged segments (49+/-18% vs 41+/-30%, p<0.05). When the two groups were directly compared, regional MIBG WO from damaged areas was similar irrespective of the underlying disease, while it was faster in DCM than in CAD patients from reference segments.


CONCLUSIONS
These data confirm the hypothesis that the presence of myocardial necrosis in HF due to CAD and the consequent loss of neuronal endings cause alterations in regional MIBG WO different from those observed in DCM.
Marini
Cecilia
C
CNR Institute of Clinical Physiology, Via G.Moruzzi 1, 56124, Pisa, Italy. cmarini@ifc.cnr.it
Giorgetti
Assuero
A
Gimelli
Alessia
A
Kusch
Annette
A
Sereni
Nadia
N
L'abbate
Antonio
A
Marzullo
Paolo
P
Sambuceti
Gianmario
G
D019797:3-Iodobenzylguanidine / Q000493:pharmacokinetics*; D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism*; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism*; D006321:Heart / Q000000981:diagnostic imaging / Q000294:innervation; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism*; D009206:Myocardium / Q000473:pathology; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index
D019275:Radiopharmaceuticals; D019797:3-Iodobenzylguanidine