REPERFUSED MYOCARDIAL INFARCTIONS ON T-1- AND SUSCEPTIBILITY-ENHANCED MRI - EVIDENCE FOR LOSS OF COMPARTMENTALIZATION OF CONTRAST-MEDIA

REPERFUSED MYOCARDIAL INFARCTIONS ON T-1- AND SUSCEPTIBILITY-ENHANCED MRI - EVIDENCE FOR LOSS OF COMPARTMENTALIZATION OF CONTRAST-MEDIA
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DOI:
10.1002/mrm.1910310105
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发表时间:
1994-01-01
影响因子:
3.3
通讯作者:
HIGGINS, CB
HIGGINS, CB
中科院分区:
医学3区
文献类型:
--
作者:
SAEED, M;WENDLAND, MF;HIGGINS, CB

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本研究的目的是表征磁共振成像对比剂的敏感性,自旋回波T-2加权成像的再灌注心肌梗死。我们对该模型的兴趣集中在预期的要求上,即这些药物在组织中被区室化,导致自旋回波图像上的信号丢失,这种情况可能不存在于再灌注的梗死心肌中。因此,在给予造影剂之前,对9只大鼠进行2小时的左冠状动脉闭塞,然后进行3 +/- 0.5小时的再灌注。采集了三组MR图像:(a)中心室基线轴向图像,均为T1加权(TR/TE = 300/20)和T-2加权(TR/TE = 1500/60);(B)给予T-1增强剂Gd-DTPA-BMA后的T-1加权图像(0.2 mmol/kg),以记录造影剂被递送至再灌注梗死;和(c)施用敏感剂Dy-DTPA-BMA(1.0 mmol/kg)后的T-2加权图像。钆增强的T-1图像显示再灌注梗死区域与未梗死心肌相比信号强度大大增强,表明造影剂被输送到梗死区。镝增强的T-2图像将损伤描述为相对于正常心肌中的信号耗尽的持续信号强度区域,与造影剂导致信号丢失的失败一致。在未增强的T2加权图像(33 +/- 5%)、钆增强的T1加权图像(36 +/- 5%)和死后染色(30 +/- 6%)中观察到类似的梗死面积;在这些数据的比较中注意到强相关性(r > 0.9)。镝增强图像显示出较小区域的差异信号,推测为梗死(20 +/-5%,P < 0.05),与其他测量值的相关性较弱(r < 0.75)。我们的结论是,小梗死描绘的镝增强图像是一个分区的真正的梗死,心肌坏死是足够先进的代理是均匀分布在所有的组织室,防止T-2* 依赖性相位损失自旋回波图像。
The purpose of this study was to characterize the contrast caused by a susceptibility MRI contrast agents, on spin echo T-2-weighted imaging of reperfused myocardial infarction. Our interest in this model focused on the expected requirement that such agents be compartmentalized in the tissue to cause signal loss on spin echo images, a condition which may not be present in reperfused infarcted myocardium. Accordingly, nine rats were subjected to 2 h of left coronary artery occlusion followed by 3 +/- 0.5 h of reperfusion prior to administration of contrast media. Three sets of MR images were acquired: (a) baseline axial images at the midventricle, both T-1-weighted (TR/TE = 300/20) and T-2-weighted (TR/TE = 1500/60); (b) T-1-weighted images after administering a T-1-enhancing agent, Gd-DTPA-BMA (0.2 mmol/kg), to document that contrast media is delivered to the reperfused infarction; and (c) T-2-weighted images after administering the susceptibility agent, Dy-DTPA-BMA (1.0 mmol/kg). Gadolinium-enhanced T-1 images depicted reperfused infarction as regions with greatly enhanced signal intensity compared with uninfarcted myocardium, indicating that contrast agent was delivered to the infarcted zone. Dysprosium-enhanced T-2 images depicted the injury as a region of persistent signal intensity relative to depletion of signal in normal myocardium, consistent with failure of the contrast agent to cause signal loss. Similar infarction sizes were observed for unenhanced T-2- weighted images (33 +/- 5%), gadolinium-enhanced T-1-weighted images (36 +/- 5%) and postmortem staining (30 +/- 6%); strong correlations (r > 0.9) were noted in comparisons of these data. Dysprosium-enhanced images exhibited a smaller region of differential signal presumed to be infarction (20 +/- 5%, P < 0.05) and weak correlations (r < 0.75) with the other measurements. We conclude that the smaller infarction depicted on dysprosium-enhanced images is a subregion of the true infarction in which myocardial necrosis is sufficiently advanced that the agent is homogeneously distributed throughout all tissue compartments, preventing T-2*-dependent phase loss on spin echo images.