Marini Cecilia, Giorgetti Assuero, Gimelli Alessia, Kusch Annette, Sereni Nadia, L'abbate Antonio, Marzullo Paolo, Sambuceti Gianmario
CNR Institute of Clinical Physiology, Via G.Moruzzi 1, 56124, Pisa, Italy.
Eur J Nucl Med Mol Imaging. 2005 Jun;32(6):682-8. doi: 10.1007/s00259-004-1735-2. Epub 2005 Mar 4.
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).
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.
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.
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.
本研究旨在探讨扩张型心肌病(DCM)或缺血性心脏病(CAD)所致心力衰竭(HF)患者的心脏交感神经功能(CSNF)与心肌灌注/功能之间的关系。
对20例纽约心脏协会(NYHA)心功能IIIb级的HF患者(10例DCM,10例CAD,17例男性,年龄69±5岁)进行研究。通过早期/延迟(123)I-间碘苄胍(MIBG)摄取及局部洗脱(WO)评估CSNF。使用20节段模型对400节段进行(99m)Tc-替曲膦门控单光子发射断层扫描(G-SPECT),以评估心肌灌注和功能。在每个节段中,局部MIBG洗脱率计算为(早期图像计数密度-延迟图像计数密度/早期图像计数密度)×100。
DCM和CAD患者的静息灌注总分值相似(6.7±5对9.5±5,p=无显著性差异),平均射血分数值也相似(29±7%对30±9%,p=无显著性差异)。相比之下,DCM患者的增厚总分值高于CAD患者(26±7对17±6,p<0.05)。QGS分析在129/137(94%)严重灌注不足的节段中识别出运动不能/运动障碍,这些节段被视为受损节段。根据HF的潜在病因,观察到局部MIBG洗脱存在显著差异。事实上,在CAD组中,正常节段的局部MIBG洗脱率低于受损节段(38±21%对46±19%,p<0.05)。相比之下,在DCM患者中,正常节段的局部MIBG洗脱比受损节段更快(49±18%对41±30%,p<0.05)。当直接比较两组时,无论潜在疾病如何,受损区域的局部MIBG洗脱相似,而DCM患者正常节段的洗脱比CAD患者更快。
这些数据证实了以下假设,即CAD所致HF中存在心肌坏死以及随之而来的神经末梢丧失,导致局部MIBG洗脱的改变不同于DCM中观察到的情况。