• Cecilia Marini, Assuero Giorgetti, Alessia Gimelli, Annette Kusch, Nadia Sereni, Antonio L'abbate, Paolo Marzullo, and Gianmario Sambuceti.
• CNR Institute of Clinical Physiology, Via G.Moruzzi 1, 56124, Pisa, Italy. cmarini@ifc.cnr.it
• Eur. J. Nucl. Med. Mol. Imaging. 2005 Jun 1; 32 (6): 682-8.

PurposeThis 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).MethodsTwenty 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.ResultsDCM 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.ConclusionThese 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.

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