Inflammation in carotid atherosclerotic plaque: A dynamic contrast-enhanced MR imaging study
Inflammation in carotid atherosclerotic plaque: A dynamic contrast-enhanced MR imaging study
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DOI：
10.1148/radiol.2412051336
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发表时间：
2006-11-01
期刊：
影响因子：
19.7
通讯作者：
Yuan, Chun
中科院分区：
文献类型：
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作者：
Kerwin, William S.;O'Brien, Kevin D.;Yuan, Chun
目的：前瞻性评估磁共振（MR）成像斑块增强与促炎心血管危险因素和斑块含量之间是否存在关联。材料和方法：本研究是在知情同意、HIPAA合规和机构审查委员会批准的情况下进行的。对30名计划行颈动脉内膜切除术的患者（29名男性，1名女性，平均年龄67.7岁+/- 10.7岁[标准差]）进行颈动脉斑块内造影剂动态测量。测量是基于以15秒间隔注射钆基造影剂获得的图像的动力学建模。斑块内随时间变化的信号强度被用来估计分数血浆体积（v(p)）和造影剂进入细胞外空间的转移常数（K-trans）。计算盲法MR测量和斑块组成的组织学测量之间的Pearson相关系数，包括巨噬细胞、新生血管、坏死核心、钙化、松散基质和致密纤维组织。计算心血管危险临床指标的相关系数或平均差异。结果：27例患者均获得可分析的MR图像和组织学结果。Ktrans的测定与巨噬细胞（r = 0.75, P < .001）、新生血管（r = 0.71, P < .001）和松散基质（r = 0.50, P = .01）含量相关。vp的测定与巨噬细胞（r = 0.54, P = 0.004）、新生血管（r = 0.68, P < 0.001）和松散基质（r = 0.42, P = 0.03）含量相关。对于临床参数，与非吸烟者相比，吸烟者高密度脂蛋白水平降低（r = -0.66, P < .001）和k -反式测量升高（平均0.134分钟（-1）vs 0.074分钟（-1）），仅与Ktrans相关；P = 0.01)。结论：Ktrans与炎症组织学标志物的相关性表明，Ktrans是斑块炎症的定量和非侵入性标志物，Ktrans与促炎心血管危险因素、高密度脂蛋白水平降低和吸烟的相关性进一步支持了这一观点。
Purpose: To prospectively evaluate if there is an association between plaque enhancement at magnetic resonance (MR) imaging and proinflammatory cardiovascular risk factors and plaque content.Materials and Methods: This study was performed with informed consent, HIPAA compliance, and institutional review board approval. Contrast agent dynamics within carotid plaques were measured in 30 patients (29 men, one woman; mean age, 67.7 years +/- 10.7 [standard deviation]) who were scheduled to undergo carotid endarterectomy. Measurements were based on kinetic modeling of images obtained at 15-second intervals during which a gadolinium-based contrast agent was injected. The time-varying signal intensities within the plaques were used to estimate the fractional plasma volume (v(p)) and transfer constant (K-trans) of contrast material into the extracellular space. Pearson correlation coefficients were computed between blinded MR measurements and histologic measurements of plaque composition, including macrophages, neovasculature, necrotic core, calcification, loose matrix, and dense fibrous tissue. Correlation coefficients or mean differences were computed regarding clinical markers of cardiovascular risk.Results: Analyzable MR images and histologic results were obtained in 27 patients. Measurements of Ktrans correlated with macrophage (r = 0.75, P < .001), neovasculature (r = 0.71, P < .001), and loose matrix (r = 0.50, P = .01) content. Measurements of vp correlated with macrophage (r = 0.54, P = .004), neovasculature (r = 0.68, P < .001), and loose matrix (r = 0.42, P = .03) content. For clinical parameters, significant associations were correlated with Ktrans only, with decreased high-density lipoprotein levels (r = -0.66, P < .001) and elevated K-trans measurements in smokers compared with nonsmokers (mean, 0.134 min(-1) vs 0.074 min(-1), respectively; P = .01).Conclusion: The correlations between Ktrans and histologic markers of inflammation suggest that Ktrans is a quantitative and non=invasive marker of plaque inflammation, which is further supported by the correlation of Ktrans with proinflammatory cardiovascular risk factors, decreased high-density lipoprotein levels, and smoking.