Feinendegen L E, Henrich M M, Kuikka J T, Thompson K H, Vester E G, Strauer B
Institute of Medicine, Research Centre Jülich, Germany.
J Nucl Cardiol. 1995 Jan-Feb;2(1):42-52. doi: 10.1016/s1071-3581(05)80007-8.
Myocardial lipid metabolism appears abnormal in dilated cardiomyopathy (DCM). A dual-tracer approach with two different fatty acid analogs may allow us to observe such alteration in vivo. 15-(Ortho-123I-phenyl)-pentadecanoic acid (oPPA) and 15-(para-123I-phenyl)-pentadecanoic acid (pPPA) have similar kinetics in circulation, diffusion, and transport. However, pPPA in normal myocardium undergoes beta-oxidation and may also be lost from myocardial cells through back-diffusion; oPPA is hardly catabolized and normally retained mainly in the cytosolic lipid pool. Use of both pPPA and oPPA in the dual-tracer approach focuses observation on the turnover of myocardial lipids (with pPPA) that is scaled against loss of fatty acid through back-diffusion into circulation (with oPPA).
Fifteen patients with idiopathic DCM and five control subjects were given oPPA and pPPA sequentially for dynamic planar scintigraphy. Uptake and elimination rates were determined for both substrates from three myocardial regions per individual; the corresponding six elimination rate constants and the three differences between them were analyzed for significant alterations in patients from control values. At least 66% of the patients had a significant alteration in myocardial lipid turnover in three types of patterns: (1) increased beta-oxidation, (2) decreased beta-oxidation, and (3) increased back-diffusion, in part associated with decreased beta-oxidation. Even with the limited number of patients and control subjects, the pattern of abnormality of lipid turnover in DMC appeared to be consistent individually but heterogeneous in the patient group. Moreover, a highly significant increase in beta-oxidation was observed for the posterolateral region of the myocardium compared with the anteroseptal and apical regions in control subjects and patients.
The dual-tracer approach uncovered in vivo that in at least two thirds of the patients with DCM myocardial lipid turnover was significantly altered compared with control values.
扩张型心肌病（DCM）患者的心肌脂质代谢似乎存在异常。采用两种不同脂肪酸类似物的双示踪法或许能让我们在体内观察到这种改变。15-（邻-123I-苯基）-十五烷酸（oPPA）和15-（对-123I-苯基）-十五烷酸（pPPA）在循环、扩散和转运方面具有相似的动力学特性。然而，正常心肌中的pPPA会经历β氧化，也可能通过反向扩散从心肌细胞中流失；oPPA几乎不被分解代谢，通常主要保留在胞质脂质池中。在双示踪法中同时使用pPPA和oPPA，将观察重点放在心肌脂质的周转（使用pPPA）上，该周转以脂肪酸通过反向扩散进入循环（使用oPPA）的损失为参照。
15例特发性DCM患者和5例对照受试者先后接受oPPA和pPPA进行动态平面闪烁显像。测定每个个体三个心肌区域两种底物的摄取和消除率；分析相应的六个消除速率常数以及它们之间的三个差值相对于对照值在患者中是否有显著改变。至少66%的患者心肌脂质周转存在三种类型的显著改变：（1）β氧化增加，（2）β氧化减少，（3）反向扩散增加，部分与β氧化减少有关。即使患者和对照受试者数量有限，DMC患者脂质周转的异常模式在个体中似乎是一致的，但在患者组中具有异质性。此外，与对照受试者和患者的前间隔及心尖区域相比，心肌后外侧区域的β氧化显著增加。
双示踪法在体内发现，至少三分之二的DCM患者心肌脂质周转与对照值相比有显著改变。
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