Department of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118, USA.
Circ Cardiovasc Imaging. 2010 May;3(3):323-32. doi: 10.1161/CIRCIMAGING.109.918524. Epub 2010 Mar 1.
The ability to identify atherosclerotic plaques with a high risk for sudden disruption before stroke or myocardial infarction would be of great utility. We used a rabbit model of controlled atherothrombosis to test whether in vivo MRI can noninvasively distinguish between plaques that disrupt after pharmacological triggering (vulnerable) and those that do not (stable).
Atherosclerosis was induced in male New Zealand White (n=17) rabbits by cholesterol diet and endothelial denudation of the abdominal aorta. After baseline (pretrigger) MRI with and without gadolinium contrast, the rabbits underwent 2 pharmacological triggerings to induce atherothrombosis, followed by another MRI 48 hours later (post-triggering). Atherosclerosis was identified by the pretriggered images in all rabbits, and thrombosis was identified in 9 of 17 animals (53%) by post-trigger MRI. After the animals were euthanized, 95 plaques were analyzed; 28 (29.5%) had thrombi (vulnerable) and 67 did not (stable) (70.5%). Pretriggered MRI revealed comparable stenosis in stable and vulnerable plaques, but vulnerable plaques had a larger plaque area (4.8+/-1.6 versus 3.0+/-1.0 mm(2); P=0.01), vessel area (9.2+/-3.0 versus. 15.8+/-4.9 mm(2); P=0.01), and higher remodeling ratio (1.16+/-0.2 versus 0.93+/-0.2; P=0.01) compared with stable plaques. Furthermore, vulnerable plaques more frequently exhibited (1) positive remodeling (67.8% versus 22.3%; P=0.01), in which the plaque is hidden within the vessel wall instead of occluding the lumen; and (2) enhanced gadolinium uptake (78.6% versus 20.9%; P=0.01) associated with histological findings of neovascularization, inflammation, and tissue necrosis.
We demonstrate that in vivo MRI at 3.0 T detects features of vulnerable plaques in an animal model of controlled atherothrombosis. These findings suggest that MRI may be used as a noninvasive modality for localization of plaques that are prone to disruption.
在中风或心肌梗塞之前，能够识别具有高破裂风险的动脉粥样硬化斑块将具有巨大的实用价值。我们使用兔动脉粥样硬化模型来测试体内 MRI 是否能够无创地区分在药物触发后破裂的斑块（易损斑块）和未破裂的斑块（稳定斑块）。
通过给予雄性新西兰白兔（n=17）高胆固醇饮食和腹主动脉内皮剥脱，在兔中诱导动脉粥样硬化。在进行有和没有钆对比剂的基线（预触发）MRI 后，兔子接受了 2 次药物触发以诱导动脉粥样硬化，随后在 48 小时后进行另一次 MRI（触发后）。在所有兔子中，通过预触发图像识别出了动脉粥样硬化，通过触发后 MRI 在 17 只动物中的 9 只（53%）中识别出了血栓。动物安乐死后，分析了 95 个斑块；28 个（29.5%）有血栓（易损斑块），67 个没有（稳定斑块）（70.5%）。预触发 MRI 显示稳定斑块和易损斑块的狭窄程度相当，但易损斑块的斑块面积更大（4.8+/-1.6 比 3.0+/-1.0 mm(2)；P=0.01），血管面积更大（9.2+/-3.0 比 15.8+/-4.9 mm(2)；P=0.01），重塑比率更高（1.16+/-0.2 比 0.93+/-0.2；P=0.01）。此外，易损斑块更频繁地表现出（1）正性重塑（67.8%比 22.3%；P=0.01），其中斑块隐藏在血管壁内而不是阻塞管腔；（2）增强的钆摄取（78.6%比 20.9%；P=0.01），与新生血管、炎症和组织坏死的组织学发现相关。
我们证明，在 3.0T 的体内 MRI 能够检测到控制动脉粥样硬化血栓形成动物模型中易损斑块的特征。这些发现表明，MRI 可能可作为一种无创的方法，用于定位易破裂的斑块。
