Trial reportEuropean journal of nuclear medicine and molecular imaging2005
Extension of myocardial necrosis differently affects MIBG retention in heart failure caused by ischaemic heart disease or by dilated cardiomyopathy.
Trial report in European journal of nuclear medicine and molecular imaging, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Establishment of aAnnals of nuclear medicine · 2025Article
- Cardiac sympathetic dysfunction in left ventricular hypertrophy caused by arterial hypertension and degenerative aortic stenosis.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2022Article
- Prediction of sudden cardiac death in patients with chronic heart failure by regional washout rate in cardiac MIBG SPECT imaging.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2019Article
- Dual isotope and multidetector camera: The best choices for a specific end-point.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2017Article
- Association between left ventricular regional sympathetic denervation and mechanical dyssynchrony in phase analysis: a cardiac CZT study.European journal of nuclear medicine and molecular imaging · 2014Article
- The expanding role of left ventricular functional assessment using gated myocardial perfusion SPECT: the supporting actor is stealing the scene.European journal of nuclear medicine and molecular imaging · 2007Review
- Will innervation imaging predict ventricular arrhythmias in ischaemic cardiomyopathy?European journal of nuclear medicine and molecular imaging · 2006Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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