Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA.
JACC Cardiovasc Imaging. 2012 Jun;5(6):596-603. doi: 10.1016/j.jcmg.2012.01.016.
The aim of this study was to determine whether cardiac magnetic resonance (CMR) in vivo T1 mapping can measure myocardial area at risk (AAR) compared with microspheres or T2 mapping CMR.
If T2-weighted CMR is abnormal in the AAR due to edema related to myocardial ischemia, then T1-weighted CMR should also be able to detect and accurately quantify AAR.
Dogs (n = 9) underwent a 2-h coronary occlusion followed by 4 h of reperfusion. CMR of the left ventricle was performed for mapping of T1 and T2 prior to any contrast administration. AAR was defined as regions that had a T1 or T2 value (ms) >2 SD from remote myocardium, and regions with microsphere blood flow (ml/min/g) during occlusion <2 SD from remote myocardium. Infarct size was determined by triphenyltetrazolium chloride staining.
The relaxation parameters T1 and T2 were increased in the AAR compared with remote myocardium (mean ± SD: T1, 1,133 ± 55 ms vs. 915 ± 33 ms; T2, 71 ± 6 ms vs. 49 ± 3 ms). On a slice-by-slice basis (n = 78 slices), AAR by T1 and T2 mapping correlated (R(2) = 0.95, p < 0.001) with good agreement (mean ± 2 SD: 0.4 ± 16.6% of slice). On a whole-heart analysis, T1 measurements of left ventricular mass, AAR, and myocardial salvage correlated to microsphere measures (R(2) = 0.94) with good agreement (mean ± 2 SD: -1.4 ± 11.2 g of myocardium). Corresponding T2 measurements of left ventricular mass, AAR, and salvage correlated to microsphere analysis (R(2) = 0.96; mean ± 2 SD: agreement 1.6 ± 9.2 g of myocardium). This yielded a median infarct size of 30% of the AAR (range 12% to 52% of AAR).
For determining AAR after acute myocardial infarction, noncontrast T1 mapping and T2 mapping sequences yield similar quantitative results, and both agree well with microspheres. The relaxation properties T1 and T2 both change in a way that is consistent with the presence of myocardial edema following myocardial ischemia/reperfusion.
本研究旨在确定心脏磁共振（CMR）体内 T1 映射是否可以与微球或 T2 映射 CMR 测量心肌危险区（AAR）。
如果由于与心肌缺血相关的水肿，AAR 中的 T2 加权 CMR 异常，那么 T1 加权 CMR 也应该能够检测到并准确量化 AAR。
狗（n = 9）经历了 2 小时的冠状动脉闭塞，随后进行 4 小时的再灌注。在任何对比剂给药之前，对左心室进行 CMR 以进行 T1 和 T2 映射。AAR 定义为 T1 或 T2 值（ms）比远程心肌高 2 个标准差的区域，以及在闭塞期间微球血流（ml/min/g）低于远程心肌 2 个标准差的区域。梗塞面积通过三苯基四唑氯化物染色确定。
与远程心肌相比，AAR 的弛豫参数 T1 和 T2 增加（平均值 ± SD：T1，1133 ± 55 ms 与 915 ± 33 ms；T2，71 ± 6 ms 与 49 ± 3 ms）。在逐层基础上（n = 78 层），T1 和 T2 映射的 AAR 相关性良好（R²=0.95，p<0.001），一致性好（平均值 ± 2 SD：0.4 ± 16.6%的切片）。在整个心脏分析中，左心室质量、AAR 和心肌挽救的 T1 测量值与微球测量值相关（R²=0.94），一致性好（平均值 ± 2 SD：-1.4 ± 11.2 g 心肌）。相应的左心室质量、AAR 和挽救的 T2 测量值与微球分析相关（R²=0.96；平均值 ± 2 SD：一致性 1.6 ± 9.2 g 心肌）。这导致梗塞面积中位数为 AAR 的 30%（范围为 AAR 的 12%至 52%）。
对于确定急性心肌梗死后的 AAR，非对比 T1 映射和 T2 映射序列产生相似的定量结果，并且与微球均具有良好的一致性。弛豫特性 T1 和 T2 都发生变化，这与心肌缺血/再灌注后心肌水肿的存在一致。
