Department of Radiology, Cambridge University Hospital NHS Foundation Trust, Cambridge, CB2 0QQ.
Magn Reson Imaging. 2012 Sep;30(7):1017-21. doi: 10.1016/j.mri.2012.02.018. Epub 2012 Apr 12.
Previous studies reporting relaxation times within atherosclerotic plaque have typically used dedicated small-bore high-field systems and small sample sizes. This study reports quantitative T(1), T(2) and T(2) relaxation times within plaque tissue at 1.5 T using spatially co-matched histology to determine tissue constituents.
Ten carotid endarterectomy specimens were removed from patients with advanced atherosclerosis. Imaging was performed on a 1.5-T whole-body scanner using a custom built 10-mm diameter receive-only solenoid coil. A protocol was defined to allow subsequent computation of T(1), T(2) and T(2) relaxation times using multi-flip angle spoiled gradient echo, multi-echo fast spin echo and multi-echo gradient echo sequences, respectively. The specimens were subsequently processed for histology and individually sectioned into 2-mm blocks to allow subsequent co-registration. Each imaging sequence was imported into in-house software and displayed alongside the digitized histology sections. Regions of interest were defined to demarcate fibrous cap, connective tissue and lipid/necrotic core at matched slice-locations. Relaxation times were calculated using Levenberg-Marquardt's least squares curve fitting algorithm. A linear-mixed effect model was applied to account for multiple measurements from the same patient and establish if there was a statistically significant difference between the plaque tissue constituents.
T(2) and T(2) relaxation times were statistically different between all plaque tissues (P=.026 and P=.002 respectively) [T(2): lipid/necrotic core was lower 47 ± 13.7 ms than connective tissue (67 ± 22.5 ms) and fibrous cap (60 ± 13.2 ms); T(2): fibrous cap was higher (48 ± 15.5 ms) than connective tissue (19 ± 10.6 ms) and lipid/necrotic core (24 ± 8.2 ms)]. T(1) relaxation times were not significantly different (P=.287) [T(1): Fibrous cap: 933 ± 271.9 ms; connective tissue (1002 ± 272.9 ms) and lipid/necrotic core (1044 ± 304.0 ms)]. We were unable to demarcate hemorrhage and calcium following histology processing.
This study demonstrates that there is a significant difference between qT(2) and qT(2) in plaque tissues types. Derivation of quantitative relaxation times shows promise for determining plaque tissue constituents.
以前报道动脉粥样硬化斑块内弛豫时间的研究通常使用专用的小口径高场系统和小样本量。本研究报告了在 1.5T 下使用空间匹配的组织学来确定组织成分的斑块组织内的定量 T(1)、T(2)和 T(2)弛豫时间。
从患有晚期动脉粥样硬化的患者中切除了 10 个颈动脉内膜切除术标本。使用定制的 10mm 直径的接收线圈在 1.5T 全身扫描仪上进行成像。定义了一个方案，允许使用多翻转角激发梯度回波、多回波快速自旋回波和多回波梯度回波序列分别计算 T(1)、T(2)和 T(2)弛豫时间。然后将标本进行组织学处理，并将其单独切成 2mm 块以进行后续配准。将每个成像序列导入内部软件，并与数字化组织学切片并排显示。在匹配的切片位置定义感兴趣区域以划定纤维帽、结缔组织和脂质/坏死核心。使用 Levenberg-Marquardt 最小二乘曲线拟合算法计算弛豫时间。应用线性混合效应模型来解释来自同一患者的多个测量值，并确定斑块组织成分之间是否存在统计学上的显著差异。
所有斑块组织的 T(2)和 T(2)弛豫时间均存在统计学差异（分别为 P=.026 和 P=.002）[T(2)：脂质/坏死核心较低，为 47 ± 13.7ms，低于结缔组织（67 ± 22.5ms）和纤维帽（60 ± 13.2ms）；T(2)：纤维帽较高（48 ± 15.5ms），高于结缔组织（19 ± 10.6ms）和脂质/坏死核心（24 ± 8.2ms）]。T(1)弛豫时间无显著差异（P=.287）[T(1)：纤维帽：933 ± 271.9ms；结缔组织（1002 ± 272.9ms）和脂质/坏死核心（1044 ± 304.0ms）]。我们无法在组织学处理后区分出血和钙。
本研究表明，斑块组织类型之间的 qT(2)和 qT(2)存在显著差异。定量弛豫时间的推导有望确定斑块组织成分。
