QUANTITATION OF SIZE OF RELATIVE MYOCARDIAL PERFUSION DEFECT BY SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY
QUANTITATION OF SIZE OF RELATIVE MYOCARDIAL PERFUSION DEFECT BY SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY
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DOI：
10.1161/01.cir.70.6.1048
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发表时间：
1984-01-01
期刊：
影响因子：
37.8
通讯作者：
RITCHIE, JL
中科院分区：
文献类型：
--
作者：
CALDWELL, JH;WILLIAMS, DL;RITCHIE, JL
一种半自动的方法定量的大小相对心肌灌注缺损的单光子发射计算机断层扫描（SPECT）图像进行了验证。在体内的图像缺陷的大小，表示为所涉及的左心室的百分比，通过这种方法确定的与在19只狗的体外的缺陷的解剖尺寸进行了比较。为了在最佳条件下测试该方法，首先在9只狗的左心室心肌中通过左心房注射99mTc标记的大聚集白蛋白颗粒，在急性闭塞1条冠状动脉后。缺损体积定义为一系列动物中计数低于正常冠状动脉供血心肌中计数分布2个或更多SD的左心室心肌体积。SPECT测量的相对体内缺损体积为26.46 ± 0.99。左心室容积的12.7%（平均值±. SD），与之相比，体外相对缺损尺寸为33.3 ±。心肌样本计数结果显示左心室容积为13.7%（P = NS，无显著性）。两种测量值之间有密切的相关性（r = 0.92）。然而，SPECT未识别出涉及< 5%心肌的心肌相对缺损体积。还确定了针对缺损区内的相对流量减少或相对减少的灌注体积加权的缺损体积。SPECT的估计值与体外相对减少灌注量的估计值之间的相关性也很高（r = 0.94）。然后在模拟临床成像情况的条件下，通过将201 Tl静脉注射到10只静息犬中，对该方法进行评价。通过SPECT测定的体内相对缺损体积为29.38 ± 0.001。左心室体积的13.3%，而体外相对缺损体积为35.09 ± 0.1%。左室心肌容积的10.73%（P = 0.09）。两者的相关系数为0.70。断层相对减少灌注体积占11.4 ±。左心室容积的7.8%，而左心室容积的16.9 ±。9.3%（P = 0.003）。SPECT和相对减少灌注量的解剖估计之间的相关性很高（r = 0.88）。相对心肌灌注缺损的大小显然可以通过单光子断层扫描准确定量。所描述的技术可能被证明是有用的，在体内的干预措施，旨在改变心肌梗死的大小，在缺血性心肌的程度的测定或在诊断评估可疑的冠状动脉疾病的患者。
A semiautomatic method for quantitating the size of relative myocardial perfusion defects from single-photon emission computed tomographic (SPECT) images was validated. The size of the image defect in vivo, expressed as percent of involved left ventricle, as determined by this method was compared with the anatomic size of the defect in vitro in 19 dogs. To test the method under optimal conditions, the left ventricular myocardium was first labeled in 9 dogs, by left atrial injection of 99mTc-labeled macroaggregated albumin particles oafter acute occlusion of 1 coronary artery. The defect volume was defined as the volume of the left ventricular myocardium for which counts fell 2 or more SD below the distribution of counts in the myocardium supplied by a normal coronary artery in a series of animals. The relative in vivo defect volume by SPECT occupied 26.46 .+-. 12.7% of the left ventricular volume (mean .+-. SD), compared with a relative defect size in vitro of 33.3 .+-. 13.7% (P = NS, not significant) of left ventricular volume as determined by well counting of myocardial samples. There was a close correlation between the 2 measurements (r = 0.92). However, myocardial relative defect volumes involving < 5% of myocardium were not identified by SPECT. The defect volume weighted for the relative reduction in flow within the defect zone or the relative reduced perfusion volume was also determined. The correlation between the estimates by SPECT and those made in vitro for relative reduced perfusion volume was also high (r = 0.94). The method was then evaluated under conditions simulating the clinical imaging situation by injecting 201Tl i.v. into 10 resting dogs. Relative defect volume in vivo by SPECT was 29.38 .+-. 13.3% of left ventricular volume compared with a relative defect volume in vitro of 35.09 .+-. 10.73% of left ventricular myocardial volume (P = 0.09). The correlation between the 2 was 0.70. The tomographic relative reduced perfusion volume occupied 11.4 .+-. 7.8% of the left ventricular volume compared with 16.9 .+-. 9.3% (P = 0.003) for the measure in vitro. Correlation between the SPECT and anatomic estimates of relative reduced perfusion volume was high (r = .88). The size of a relative myocardial perfusion defect apparently can be accurately quantitated by single-photon tomography. The techniques described may prove useful in the assessment in vivo of interventions directed at altering myocardial infarct size, in the determination of extent of ischemic myocardium or in the diagnostic evaluation of patients with suspected coronary artery disease.