Beanlands R S, deKemp R, Scheffel A, Nahmias C, Garnett E S, Coates G, Johansen H L, Fallen E
Division of Cardiology, E. S. Garnett Medical Imaging Research Centre, McMaster University Medical Centre, Ottawa, Ontario, Canada.
J Am Coll Cardiol. 1997 Mar 1;29(3):537-43. doi: 10.1016/s0735-1097(96)00561-x.
The hypothesis of this study was that evaluation of myocardial flow and metabolism using nitrogen-13 (N-13) ammonia kinetic modeling with dynamic positron emission tomographic (PET) imaging could identify regions of myocardial scar and viable myocardium as defined by fluorine-18 fluorodeoxyglucose (F-18 FDG) PET.
Uptake of most perfusion tracers depends on both perfusion and metabolic retention in tissue. This characteristic has limited their ability to differentiate myocardial scar from viable tissue. The kinetic modeling of N-13 ammonia permits quantification of blood flow and separation of the metabolic component of its uptake, which may permit differentiation of scar from viable tissue.
Sixteen patients, > 3 months after myocardial infarction, underwent dynamic N-13 ammonia and F-18 FDG PET imaging. Regions of reduced and normal perfusion were defined on static N-13 ammonia images. Patients were classified into two groups (group I [ischemic viable], n = 6; group II [scar], n = 10) on the basis of percent of maximal F-18 FDG uptake in hypoperfused segments. Nitrogen-13 ammonia kinetic modeling was applied to dynamic PET data, and rate constants were determined. Flow was defined by K1; volume of distribution (VD = K1/k2) of N-13 ammonia was used as an indirect indication of metabolic retention.
Fluorine-18 FDG uptake was reduced in patients with scar compared with normal patients with ischemic viable zones (ischemic viable 93 +/- 27% [mean +/- SD]; scar 37 +/- 16%, p < or = 0.01). Using N-13 ammonia kinetic modeling, flow and VD were reduced in the hypoperfused regions of patients with scar (ischemic viable flow: 0.65 +/- 0.20 ml/min per g, scar: 0.36 +/- 0.16 ml/min per g, p < or = 0.01; VD: 3.9 +/- 1.3 and 2.0 +/- 1.07 ml/g, respectively, p < or = 0.01). For detection of viable myocardium in these patients, the sensitivity and specificity were 100% and 80% for N-13 ammonia PET flow > 0.45 ml/min per g; 100% and 70% for VD > 2.0 ml/g; and 100% and 90% for both flow > 0.45 ml/min per g and VD > 2.0 ml/g, respectively. The positive and negative predictive values for the latter approach were 86% and 100%, respectively.
In this cohort, patients having regions with flow < or = 0.45 ml/min per g or VD < or = 2.0 ml/g had scar. Viable myocardium had both flow > 0.45 ml/min per g and VD > 2.0 ml/g. Nitrogen-13 ammonia kinetic modeling permits determination of blood flow and metabolic integrity in patients with previous myocardial infarction and can help differentiate between scar and ischemic but viable myocardium.
本研究的假设是，使用氮 - 13（N - 13）氨动力学模型结合动态正电子发射断层扫描（PET）成像来评估心肌血流和代谢，能够识别出如氟 - 18氟脱氧葡萄糖（F - 18 FDG）PET所定义的心肌瘢痕区域和存活心肌。
大多数灌注示踪剂的摄取取决于组织中的灌注和代谢滞留。这一特性限制了它们区分心肌瘢痕和存活组织的能力。N - 13氨的动力学模型允许对血流进行定量，并分离其摄取的代谢成分，这可能有助于区分瘢痕和存活组织。
16例心肌梗死后3个月以上的患者接受了动态N - 13氨和F - 18 FDG PET成像。在静态N - 13氨图像上定义灌注降低和正常的区域。根据灌注不足节段中最大F - 18 FDG摄取百分比，将患者分为两组（I组[缺血性存活心肌]，n = 6；II组[瘢痕]，n = 10）。将N - 13氨动力学模型应用于动态PET数据，并确定速率常数。血流由K1定义；N - 13氨的分布容积（VD = K1/k2）用作代谢滞留的间接指标。
与具有缺血性存活区域的正常患者相比，瘢痕患者的F - 18 FDG摄取降低（缺血性存活心肌：93±27%[平均值±标准差]；瘢痕：37±16%，p≤0.01）。使用N - 13氨动力学模型，瘢痕患者灌注不足区域的血流和VD降低（缺血性存活心肌血流：0.65±0.20 ml/min per g，瘢痕：0.36±0.16 ml/min per g，p≤0.01；VD：分别为3.9±1.3和2.0±1.07 ml/g，p≤0.01）。对于这些患者中存活心肌的检测，当N - 13氨PET血流>0.45 ml/min per g时，敏感性和特异性分别为100%和80%；当VD>2.0 ml/g时，敏感性和特异性分别为100%和70%；当血流>0.45 ml/min per g且VD>2.0 ml/g时，敏感性和特异性分别为100%和90%。后一种方法的阳性预测值和阴性预测值分别为86%和100%。
在该队列中，血流≤0.45 ml/min per g或VD≤2.0 ml/g的区域的患者有瘢痕。存活心肌的血流>0.45 ml/min per g且VD>2.0 ml/g。N - 13氨动力学模型能够确定既往心肌梗死患者的血流和代谢完整性，并有助于区分瘢痕与缺血但存活的心肌。
