Hammer-Hansen Sophia, Leung Steve W, Hsu Li-Yueh, Wilson Joel R, Taylor Joni, Greve Anders M, Thune Jens Jakob, Køber Lars, Kellman Peter, Arai Andrew E
Laboratory for Advanced Cardiovascular Imaging, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland; Department of Medicine B, The Heart Center, Rigshospitalet, Copenhagen, Denmark.
Laboratory for Advanced Cardiovascular Imaging, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland; Department of Medicine and Radiology, Division of Cardiovascular Medicine, University of Kentucky, Lexington, Kentucky.
JACC Cardiovasc Imaging. 2017 Feb;10(2):130-139. doi: 10.1016/j.jcmg.2016.04.009. Epub 2016 Sep 21.
The aim of this study was to determine whether early gadolinium enhancement (EGE) by cardiac magnetic resonance (CMR) in a canine model of reperfused myocardial infarction depicts the area at risk (AAR) as determined by microsphere blood flow analysis.
It remains controversial whether only the irreversibly injured myocardium enhances when CMR is performed in the setting of acute myocardial infarction. Recently, EGE has been proposed as a measure of the AAR in acute myocardial infarction because it correlates well with T2-weighted imaging of the AAR, but this still requires pathological validation.
Eleven dogs underwent 2 h of coronary artery occlusion and 48 h of reperfusion before imaging at 1.5-T. EGE imaging was performed 3 min after contrast administration with coverage of the entire left ventricle. Late gadolinium enhancement imaging was performed between 10 and 15 min after contrast injection. AAR was defined as myocardium with blood flow <2 SD from remote myocardium determined by microspheres during occlusion. The size of infarction was determined with triphenyltetrazolium chloride.
There was no significant difference in the size of enhancement by EGE compared with the size of AAR by microspheres (44.1 ± 15.8% vs. 42.7 ± 9.2%; p = 0.61), with good correlation (r = 0.88; p < 0.001) and good agreement by Bland-Altman analysis (mean bias 1.4 ± 17.4%). There was no difference in the size of enhancement by EGE compared with enhancement on native T1 and T2 maps. The size of EGE was significantly greater than the infarct by triphenyltetrazolium chloride (44.1 ± 15.8% vs. 20.7 ± 14.4%; p < 0.001) and late gadolinium enhancement (44.1 ± 15.8% vs. 23.5 ± 12.7%; p < 0.001).
At 3 min post-contrast, EGE correlated well with the AAR by microspheres and CMR and was greater than infarct size. Thus, EGE enhances both reversibly and irreversibly injured myocardium.
本研究旨在确定在再灌注心肌梗死犬模型中,心脏磁共振成像(CMR)的早期钆增强(EGE)是否能描绘出通过微球血流分析确定的梗死危险区(AAR)。
在急性心肌梗死情况下进行CMR时,是否只有不可逆损伤的心肌会增强仍存在争议。最近,EGE已被提议作为急性心肌梗死中AAR的一种测量方法,因为它与AAR的T2加权成像相关性良好,但这仍需要病理验证。
11只犬在冠状动脉闭塞2小时并再灌注48小时后,于1.5-T场强下进行成像。在注射造影剂3分钟后进行EGE成像,覆盖整个左心室。在注射造影剂10至15分钟之间进行延迟钆增强成像。AAR定义为在闭塞期间通过微球测定的血流比远离梗死心肌的血流低2个标准差的心肌。用氯化三苯基四氮唑确定梗死面积。
与通过微球测定的AAR大小相比,EGE增强的大小无显著差异(44.1±15.8%对42.7±9.2%;p = 0.61),相关性良好(r = 0.88;p < 0.001),Bland-Altman分析显示一致性良好(平均偏差1.4±17.4%)。与T1和T2原始图像上的增强相比,EGE增强的大小无差异。EGE的大小显著大于氯化三苯基四氮唑确定的梗死面积(44.1±15.8%对20.7±14.4%;p < 0.001)和延迟钆增强面积(44.1±15.8%对23.5±12.7%;p < 0.001)。
在注射造影剂后3分钟,EGE与通过微球和CMR测定的AAR相关性良好,且大于梗死面积。因此,EGE增强了可逆性和不可逆性损伤的心肌。