联合应用Neuro DSA、Agatston Calcium Score和CTP技术对颈动脉粥样硬化患者的综合影像评价
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摘要
目的:应用64层CT血管造影对颈动脉粥样硬化斑块的类型、分布及所致血管狭窄等影像特征进行初步分析,探讨64层CT血管造影对颈动脉斑块影像特征评价的价值及临床意义。
     材料和方法:对临床可疑颈动脉粥样硬化的患者行64排CT血管造影检查,后循环及颅内血管病变均排除在外(经CTA、DSA或MRA证实);狭窄程度的判断采用NASCET标准。分析不同类型颈动脉斑块在各年龄组及各血管节段的分布、斑块类型与临床症状与狭窄程度的关系、钙化的临床意义以及斑块的并发改变。
     结果:116例患者中共发现377个斑块,其中软斑块138个,钙化性斑块115个,以钙化为主的混合性斑块29个,以软组织为主的混合性斑块95个,软斑块发生率36.60%,斑块钙化发生率63.40%;发生于颈总动脉起始部23例,颈总动脉105例,颈动脉分叉部150例,颈内动脉81例,颈外动脉18例。轻、中、重度狭窄及闭塞的发病率分别为57.56%、24.67%、11.94%及5.83%。<50岁与>70岁年龄组间发生的斑块类型具有统计学差异(P=0.005,P<0.01);颈总动脉与颈总动脉分叉部及颈内动脉发生斑块类型具有统计学差异(P=0.000,P<0.01)。颈动脉狭窄程度与斑块类型及发生血管节段相关,但无统计学意义(P>0.05);将斑块类型、狭窄程度、发生血管节段等因素进行逐步回归分析,发现血管闭塞与临床症状正相关(B=1.080,P<0.05),而钙化性斑块与临床症状负相关(B=-0.688,P<0.05);对颈动脉分叉部的逐步回归分析发现也得出相同结论。
     结论:64层CT血管造影不仅可初步评价颈动脉斑块的影像特征,还可以准确测量斑块所致的血管狭窄;联合评价斑块类型、狭窄程度及发生血管节段、斑块内钙化可对临床脑血管事件作出预测。
     目的:应用64层CT血管造影对颈动脉钙化的影像学特征进行分析,探讨钙化在不同年龄组及不同血管节段的分布趋势以及钙化所致的血管狭窄的程度,并探讨64层CT血管造影对颈动脉钙化评价的临床意义。材料和方法:116例患者行64排CT血管造影检查,后循环及颅内血管病变均排除在本研究之外(经CTA、DSA或MRA证实),回顾性分析颈动脉斑块钙化的影像特征及临床意义。
     结果:116例患者共发现377个斑块,其中钙化性斑块115例,颈动脉斑块钙化的发生率为63.40%。不同年龄组间斑块钙化率有统计学差异(P=0.004,P<0.01),小于50岁年龄组斑块钙化发生率很低,随年龄增加,斑块钙化比率明显上升。不同血管节段钙化的发生率如下:颈总动脉起始部60.87%,颈总动脉27.62%,分叉部84%,颈内动脉和颈外动脉分别为69.14%和77.78%,颈动脉分叉部钙化率明显高于其他血管节段;颈总动脉、分叉部及颈内动脉斑块钙化率有明显统计学差异(P=0.000,P<0.01)。在轻度、中度、重度狭窄及闭塞组中钙化的发生率分别为46.51%、33.33%、26.67%及0.00%,但仅有轻度与重度狭窄组间斑块钙化率有统计学差异(P=0.013,P<0.05);斑块钙化与狭窄程度非线性相关,钙化常引起轻中度狭窄。钙化在斑块内的分布与临床症状相关但无明显的统计学差异。单纯钙化性斑块在症状组与无症状组中分布有明显的统计学差异,斑块钙化率在两组间也有统计学差异(P=0.013,P<0.05)。将斑块类型、狭窄程度、发生血管节段等因素进行逐步回归分析,发现钙化与临床症状负相关(B=-0.688,P<0.05)。
     结论:总之CTA可清晰显示斑块内钙化的形态、分布及其导致血管狭窄程度,同时可定量测量血管狭窄;对钙化的颈动脉斑块是否引发临床症状应综合考虑患者年龄、发生的血管节段、引起的狭窄程度及钙化的程度及分布方能做出准确预测。通过钙化的定性分析有助于临床对颈动脉斑块进行筛查并预测脑缺血事件发生。
     目的:联合应用Agatston Calcium Score和Neuro DSA技术定量、定性分析颈动脉钙化,探讨二者联合应用是否可作为一个有效工具指导治疗及颈动脉钙化积分的临床意义。
     材料和方法:收集一侧或两侧颈动脉钙化患者68例(年龄67.6±10.2岁;男:女=57:1),所有病例均行Siemens 64 CTA检查,参考NASCET标准,应用NuroDSA技术对血管狭窄分析,增强前数据被传入Agaston Calcium Score软件行钙化分析。
     结果:无论是否考虑狭窄和年龄的协同作用,症状组患者与无症状组患者相比具有更高的总钙化体积、钙化当量及钙化积分,但症状组患者与无症状组患者间总钙化体积、钙化当量及钙化积分未达到统计学差异。三个狭窄组间和三个年龄组间总钙化体积、钙化当量及钙化积分均有统计学差异;在重度与轻度狄窄组间、中度与轻度狭窄组间均具有明显的统计学差异(P<0.001);50-69岁与大于70岁年龄组间上述钙化参数具有明显的统计学差异(P<0.001)。将总钙化体积、钙化当量、钙化积分、一侧颈内动脉狭窄程度及年龄和性别进行逐步回归分析,仅有一侧颈内动脉狭窄程度与临床症状正相关(B=0.568,P=0.010)。一侧颈动脉球部及同侧颈内动脉的狭窄程度均与总钙化体积具有轻度但明显相关性(r_(bifurcation)=0.322,r_(ICA)=0.418,P<0.01)。无症状组发现217个独立钙化,而症状组仅发现120独立钙化。在症状组和无症状组间所有独立钙化的特性均无统计学差异,但症状组钙化特性显示其更不均质。对钙化在斑块内的分布分析发现,在症状组和无症状组间钙化的分布形式无统计学差异。
     结论:颈动脉钙化积分可作为一个无创性的新方法评价颈动脉粥样硬化负荷,帮助临床决定治疗方案,对斑块内钙化的定量和定性分析可帮助临床评价斑块的稳定性、预测临床症状的发生及对高危病人进行危险分层。
     目的:单侧颈内动脉狭窄或闭塞患者是否存在脑血流灌注异常及其在随后发生的脑缺血事件中的作用尚不清楚,应用CT灌注成像对上述患者脑血流灌注改变的评价较少且结论不一。本研究应用64层CT灌注成像对单侧颈内动脉狭窄(大于50%)或闭塞患者的脑灌注改变进行评价;探讨不同解剖部位及不同灌注参数对灌注异常改变的意义及CT灌注成像对可能发生脑缺血事件的高危人群的筛查价值。
     材料和方法:25例一侧颈内动脉狭窄(大于50%)或闭塞患者进行了64层螺旋CT灌注检查,所有病例均经CTA、DSA或MRA证实且颅内动脉无明显狭窄及闭塞。参照北美症状性颈动脉内膜切除术(NASCET)标准在本研究中将患者分为中度狭窄(50%-69%)、重度狭窄(70%-99%)及闭塞组。按颅内动脉血流分布手动镜面测量两侧大脑半球8个解剖部位的绝对灌注值并计算两侧半球的相对灌注值。对组内两侧的绝对灌注值比较采用Student's t-test和Mann-Whitneytest,组间相对灌注值比较采用One-way ANOVA和Kruskal-Wallis test。
     结果:(1)彩色参数图显示,闭塞组、重度狭窄组、中度狭窄组所有解剖部位两侧脑组织的CBF图和CBV图均无明显差异。闭塞组TS图、TP图两侧均显示不同程度的差异;而在重度狭窄组仅有4例(4/9)TS图、TP图显示两侧脑组织存在不同程度的差异;中度狭窄组所有病例TS图、TP图两侧脑组织均无明显差异。(2)闭塞组、重度狭窄组、中度狭窄组所有解剖部位两侧脑组织的CBF和CBV均无统计学差异(P>0.05)。(3)闭塞组:闭塞侧前分水岭区灰质及白质的TS与对侧相比有明显的统计学差异(P<0.01),闭塞侧前分水岭区白质的TP与对侧相比有统计学差异(P<0.05);闭塞侧后分水岭区灰质及白质的TS(P<0.01)、TP(P<0.05)与对侧脑组织相比均有统计学差异。(4)重度狭窄组,仅有颞叶(P<0.01)、后分水岭区白质(P<0.05)狭窄侧的TS与对侧相比有统计学差异。(5)中度狭窄组所有解剖部位两侧脑组织的TS、TP均无统计学差异(P>0.05)。(6)颞叶、基底节区、前分水岭区灰质及白质、后分水岭区灰质及白质的rCBF、rCBV均无统计学差异(P>0.05)。(7)颞叶的rTS、rTP三组间有统计学差异(P_(rTS)=0.0090,P_(rTP)=0.0104),闭塞组和中度狭窄组间的rTS、rTP具有统计学差异;基底节区的rTS、rTP三组间有明显的统计学差异(P_(rTS)=0.0281,P_(rTP)=0.0017),闭塞组和中度狭窄组间的rTS具有统计学差异,闭塞组和中度、重度狭窄组间的rTP具有统计学差异;前分水岭区灰质及白质的rTS、rTP三组间有明显的统计学差异(灰质:P_(rTS)=0.0173,P_(rTP)=0.0397;白质:P_(rTS)=0.0482,P_(rTP)=0.00321);后分水岭区灰质的rTS、rTP三组间有统计学差异(P_(rTS)=0.0203,P_(rTP)=0.0049);后分水岭区白质的rTS三组间有统计学差异(P_(rTS)=0.0015),但三组间rTP无统计学差异。
     结论:CT灌注成像能有效评价颈内动脉狭窄或闭塞患者脑灌注的改变,为临床治疗提供依据;在颈内动脉狭窄或闭塞患者中,灌注异常见于前后分水岭区,以分水岭区的白质最易受累,使用绝对及相对的TS能早期、敏感的发现灌注异常。
PartⅠAnalysis of CT characteristics for carotid artery atherosclerotic plaque by 64 rows CT angiography
     Purpose: To explore the MDCTA findings and clinical values of carotid artery atherosclerotic plaque.
     Material and Methods: All the patients with the history of known or suspected carotid artery atherosclerotic disease underwent the 64 rows CT angiography. The patients with posterior circulation symptoms and stenosis of the intracranial artery which conformed by DSA or CTA or MRA were excluded from the study. The degree of the stenosis was defined by the criteria of the North American Symptomatic Carotid Endarterectomy Trial Collaborators. We retrospectively analyzed the type and distribution of carotid plaque, distribution and morphology of the calcium, and measured the degree of stenosis on the axial source and reconstruction images. The relationship between the MDCTA findings and the clinical symptoms was also investigated.
     Results: Three hundred and seventy-seven plaques (116 patients) were included in the study, including 138 soft plaques, 115 calcified plaques, 29 mixed plaques with obvious calcium and 29 mixed plaques with obvious lipid core. The distribution of the plaque was as following: the original part of the common carotid artery 23, the common carotid artery 105, carotid bifurcation 150, the internal carotid artery 81 and the external carotid artery 18. The incidence of the mild-, moderate- and high grade stenosis and occlusion were 57.56 %, 24.67 %, 11.94% and 5.83 % respectively. There was significantly statistical difference of the plaque type between lower than 50 year and higher than 70 year(p =0.005, p <0.01). The plaque type was significantly statistical difference between the common carotid artery and the carotid bifurcation(p =0.000, p <0.01), and between the common carotid artery and the internal carotid artery(p =0.000, p <0.01).The different type of plaque were distributed in the different vascular segments and resulted in the different degree of stenosis. The incidence of the calcium at the carotid bifurcation was 84% with slight and moderate degree of stenosis. There was no significantly statistical difference among the plaque type, the degree of stenosis and vascular segments. Plaque type, the degree of stenosis and vascular segment initially were identified as potentially significant variables of symptomatology for Backward logistic regression analysis. However, only the occlusion and simply calcified plaque was accepted in the model. The occlusion was a positive and significant association with the symptomatology (p=0.023, B=1.080) and the simply calcified plaque was significantly inverse associated with the occurrence of symptoms (p= 0.006, B=-0.688).
     Conclusion: MDCTA can accurately assess the characteristics of carotid plaque and measure the degree of stenosis. Our findings may have clinical value for the risk stratification of carotid atherosclerosis disease and could be used to predict the occurrence of symptom and the degree of stenosis.
     PartⅡThe clinical value of carotid artery plaque calcification analyzed by 64 rows CT angiography
     Purpose: To explore the relationship between the calcification of carotid artery plaque and the clinical symptoms.
     Material and Methods: All the patients underwent the 64 rows CT angiography. The degree of the stenosis was defined by the criteria of the North American Symptomatic Carotid Endarterectomy Trial Collaborators. We retrospectively analyzed the distribution of calcified plaque in the different age groups and different vascular segments, the degree of stenosis caused by calcification, distribution and morphology of intraplaque calcium. The relationship between the carotid calcification and the clinical symptoms was also investigated.
     Results: One hundred and sixteen patients with 377 plaques were included in the study, including 115 calcified plaques, 29 mixed plaques with obvious calcium and 95 soft plaques accompanied by calcification. The incidence of carotid plaque calcification was 63.40%.There was significant difference between the incidence of plaque calcification and different age groups and it was obvious that the prevalence is age dependent. The distributions of the calcification in different vascular segments were as following: the original part of the common carotid artery 60.87%, the common carotid artery 27.62%, carotid bifurcation 84%, the internal carotid artery 69.14% and the external carotid artery 77.78% respectively. The incidence of the calcium at the carotid bifurcation was higher than the other vascular segments. The incidence of calcification in the mild, moderate and severe degree of stenosis and occlusion were 46.51 %, 33.33 %, 26.67% and 0.00% respectively. However, there was significant difference of the incidence of calcification between the mild and severe degree of stenosis. There was no significant difference between distribution of calcification intraplaque in the symptomatic and asymptomatic group. Calcified plaque was negatively associated with symptomatology in backward logistic regression analysis (p<0.05).
     Conclusion: CT-angiography permits the reliable quantification and characterization of carotid calcium and may help noninvasively risk stratify patients with symptomatic and asymptomatic stenosis.
     PartⅢCombination of Agatston Calcium Score and Neuro DSA: quantification and characterization of carotid calcium
     Purpose: First, to quantify and qualities carotid calcification by MDCTA and Agatston calcium scores and determines whether the Agatston calcium scores and MDCTA appropriately evaluate calcified atherosclerotic burden and might be applied as a useful decision-making tool for treatment and, second to determine the relationship of carotid s calcium cores with luminal stenosis and ischemic symptoms.
     Materials and Methods: A total of 136 carotid arteries were examined with MDCT angiography (67.6±10.2 years; age ranges from 37-86 year; 1 woman, 57 men). Pre-contrast data was transferred to coronary calcium score software and calcium scores were determined according to the method described by Agatston et al. Post-contrast data was transferred to NuroDSA and vessel analysis software for stenosis analysis by North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria.
     Results: Symptomatic patients had higher total calcium volume, total equiv mass and total calcium score than asymptomatic patients, but this difference did not reach statistical significance with or without age and stenosis taken into account. According to the stenotic degree of ipilateral ICA, there was a significant difference among the three stenotic subgroups of total calcium volume, total equiv mass and total calcium score. Pair-wise comparisons indicated there was a significant difference between high-grade and mild-grade stenotic vessels (p<0.001), moderate- grade and mild-grade stenotic vessels (p< 0.001) without interaction with patient age. There was a statistically significant difference among the three age groups (p<0.01) and a significant difference between group two and three (p<0.001). Multiple logistic regressions indicated there was a significant association between symptomatology and luminal stenosis of ipsilateral internal carotid artery in the model(B=0.568, P=0.010). Pearsonχ~2 test showed a mild but significant correlation between stenotic grade of carotid bifurcation and ipsilateral ICA and total calcium volume (r_(bifurcation) = 0.322 and r_(ICA) = 0.418 respectively, p < 0.01). There were 217 calcifications in asymptomatic group and 120 calcifications in symptomatic group. However, there was no significant difference for all the individual calcium property between symptomatic and asymptomatic patients. There was no difference in intra-plaque Ca distribution patterns between symptomatic and asymptomatic patients (p >0.05).
     Conclusions: Carotid calcium scores is likely to emerge as the noninvasive investigation of choice to accurately assess the severity of carotid atherosclerosis and provide valuable insights into plaque characterization and stability especially for the calcified plaque in view of its ability. More important, Carotid calcium scores is a potential independent risk marker for TIA and stroke that could be used to stratify patients on the basis of risk and to monitor the effects of therapy.
     PartⅣCT Perfusion Study of Cerebral Hemodynamics in Patients with unilateral stenosis (> 50%) or occlusion of the ICA
     Purpose: first, to investigate hemodynamic changes in different cerebral anatomic areas in patients with unilateral stenosis (>50%) or occlusion of the internal carotid artery (ICA) using CT Perfusion (CTP) imaging and, second to evaluate its potential value in identifying higher risk patients for TIAs or strokes.
     Material and Methods: Twenty-five patients (21 men, 4 women; mean age, 56.72±11.07years) with unilateral internal carotid artery stenosis (>50%) or occlusion underwent 64-detector perfusion CT. Exclusion criteria were intracranial artery stenosis with DSA or CTA or MRA. Stenosis was graded in accordance to the NASCET criteria and patients were divided into three groups: patients with a unilateral ICA occlusion, patients with high-grade (70%~99%) and patients with moderate-grade (50% ~ 69%). We manually drew the ROIs of eight different anatomic regions to outline various cerebral flow territories on bilateral hemisphere. Cerebral blood volume (CBV), cerebral blood flow (CBF) , time to start (TS) and time to peak ( TP) were calculated, and relative values based on the comparison between stenotic and contrlateral hemispheres—specifically, rCBV, rCBF, rTS and rTP were derived. The absolute and relative perfusion values analyses were performed for the group as a whole by using the Student's t-test and Mann-Whitney test; and after subdividing patients into three groups according to the degree of stenosisof ICA by using the One-way ANOVA and Kruskal-Wallis test.
     Result: (1) All the patients in occlusion group and 4 patients in high-grade group had abnormal perfusion characterized by TS or TP color perfusion maps. (2) Among the absolute perfusion values, the TS of the occlusive hemisphere in gray matter and white matter of the anterior and posterior washeld regions had significantly statistical significance compared to contraside (P_(TS)<0.01). But the TP of the occlusive hemisphere only in the white matter of the anterior washeld region and the gray matter and white matter of the anterior and posterior washeld regions had significantly statistical significance compared to contraside (P_(TP) <0.05). (3) In high-grade stenotic group, the TS of stenotic side only in temporal lobe (P_(TS)<0.01) and in the white matter of the posterior washeld region (P_(TS)<0.05) were significantly increased compared to contraside. (4) Among the relative values, there were significantly statistical significance in rTS and rTP of temporal lobe(P_(rTS)=0.0090, P_(_(rTP))=0.0104), basal ganglia region (P_(rTS)=0.0281, P_(rTP)=0.0017), the gray matter and white matter of the anterior washeld regions (GM: P_(rTS)=0.0173, P_(rTP)=0.0397; WM: P_(rTS)=0.0482, P_(rTP)=0.0032) and the gray matter of posterior washeld region (P_(rTS)=0.0203, P_(rTP)=0.0049) had significantly statistical significance among three groups. However, only the rTS in the white matter of posterior washeld region had significantly statistical significance among three groups (P_(rTS)=0.0015).
     Conclusion: CT Perfusion may provide valuable information of the cerebral hemodynamic status in patients with unilateral internal carotid artery stenosis (>50%) or occlusion. Abnormal cerebral perfusion is often present in anterior and posterior washeld regions, predominantly in the white matter region. Absolute and relative TS are the most sensitive parameters to detect the changes in cerebral perfusion.
引文
[1] De Monti M, Ghilardi G, Caverni L, et al. Multidetector Helical Angio CT Oblique Reconstructions Orthogonal to Internal Carotid Artery for Preoperative Evaluation of Stenosis: a Perspective Studyof Comparison with US Color Doppler, Digital Subtraction Angiography and Intraoperative Data. [J] Minerva Cardioangiol, 2003, 51 (4):373-385.
    [2] Porsche C, Walker L, Mendelow AD, et al. Assessment of Vessel Wall Thickness in Carotid Atherosclerosis Using Spiral CT Angiography [J] Eur J Vasc Endovasc Surg, 2002, 23 (5):437-440.
    [3] Randoux B, Marro B, Koskas F, et al. Carotid artery stenosis: prospective comparison of CT, three - dimensional Gadolinium -enhanced MR, and conventional angiography. Radiology, 2001, 220:179-185.
    [4] Fayad ZA, Fuster V, Nikolaou K, et al. Computed tomography and magnetic resonance imaging for noninvasive coronary angiography and plaque imaging: current and potential future concepts . Circulation, 2002, 16; 2026-2034.
    [5] Clarke SE, BeletskyV, Hammond RR, et al. Validation of Automatically Classified Magnetic Resonance Images for Carotid Plaque Compositional Analysis. Stroke 2006; 37:93-97.
    [6] North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endartrectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med, 1991, 325: 445-453.
    [7] Bartlett E S, Walters T D, Symons S P, et al. Quantification of Carotid Stenosis on CT Angiography. AJNR 2006, 27:13-19.
    [8] Fox AJ, Eliasziw M, Rothwell PM, et al, for the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST) Groups. Identification, prognosis, and management of patients with carotid artery near occlusion. AJNR 2005; 26:2086-94.
    [9] Burke AP, Weber D, Kolodgie F, et al. Pathophysiology of calcium deposition in coronary arteries. Herz 2001; 26:239-244.
    [10] Wakhloo AK, Lieber BB, Seong J, et al. Hemodynamics of Carotid Artery Atherosclerotic Occlusive Disease. J Vasc Interv Radiol 2004; 15: 111-121.
    [11] Stone PH, Coskun AU, Kinlay S, et al. Effect of endothelial shear stress on the progression of coronary artery disease, vascular remodeling, and in-stent restenosis in humans. In vivo 6-month follow-up study. Circulation 2003; 108:438-444.
    [12] Slager C J, Wentzel, J J; Gijsen, F JH, et al. The role of shear stress in the destabilization of vulnerable plaques and related therapeutic implications. Nat Clin Pract Cardiovasc Med 2005, 2(9):456-464.
    [13] Nandalur KR, Baskurt E, Hagspiel KD, et al. Calcified carotid atherosclerotic plaque is associated less with ischemic symptoms than is non-calcified plaque on MDCT. AJR 2005; 184:295-298.
    [14] Huang H, Virmani R, Younis H, et al. The impact of calcification on the biomechanical stability of atherosclerotic plaques. Circulation 2001; 103:1051-1056.
    [15] Shaalan WE, Cheng H, Gewertz B, et al. Degree of carotid plaque calcification in relation to symptomatic outcome and plaque inflammation. J Vasc Surg 2004; 40:262-269.
    [16] Abedin M, Tintut Y, Demer LL. Vascular calcification mechanisms and clinical ramifications. Arterioscler Thromb Vasc Biol 2004; 24: 1161-1170.
    [17] Aikawa E, Nahrendorf M, Figueiredo JL, et al. Osteogenesis Associates With Inflammation in Early-Stage Atherosclerosis Evaluated by Molecular Imaging In Vivo. Circulation 2007; 116: 2841-2850.
    [18] Anand, DV. Multislice computed tomography evaluation of cardiac syndrome X patients. J Nucl Cardiol 2008;15:615-616.
    [19] Nandalur KR, Baskurt E, Hagspiel KD, et al. Carotid artery calcification on CT may independently predict stroke risk. AJR 2006; 186:547-552.
    [20] Hoffman U, Kait DC, Handwerker J, et al. Vascular calcification in ex vivo carotid specimens: precision and accuracy of measurements with multi-detector row CT. Radiology 2003; 229:375-381.
    [21] Miralles M, Merino J, Busto M, et al. Quantification and Characterization of Carotid Calcium with Multi-detector CT-angiography. Eur J Vasc Endovasc Surg. 2006,32:561-567.
    [22] O'Rourke R A, Brundage B H, Froelicher V F, et al. American College of Cardiology/American Heart Association expert consensus document on electron-beam computed tomography for the diagnosis and prognosis of coronary artery disease. J Am Coll Cardiol 2000; 36:326-340.
    [23] Sangiori G, Rumberger J, Severson A, et al. Arterial calcification and not lumen stenosis is correlated with atherosclerotic plaque burden in humans: a histologic study of 723 coronary artery segments using nondecalcifying methodology. J Am Coll Cardiol 1998; 31:126-133.
    [24] Alexander M, Sean O C, Mehmet T, et al. Carotid bifurcation calcium and correlation with percent stenosis of the internal carotid artery on CT angiography. Neuroradiology 2005; 47: 1-9.
    [25] Niwa Y, Katano H, Yamada K, et al. Calcification in carotid atheromatous plaque: delineation by 3D-CT angiography, compared with pathological findings. Neurol Res 2004; 26: 778-784.
    [26] Nandalur KR, Hardie AD, Raghavan P, et al. Composition of the Stable Carotid Plaque: Insights From a Multidetector Computed Tomography Study of Plaque Volume. Stroke 2007;38:935-940.
    [27] Endarterectomy for Asymptomatic Carotid Artery Stenosis: Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. AMA 1995;273:1421-1428.
    [28] Randomised trial of endarterectomy for recently symptomatic carotid stenosis: Final results of the MRC European Carotid Surgery Trial (ECST). Lancet1998; 351:1379-1387.
    [29] Choi HM, Hobson RW, Goldstein J, et al. Technical challenges in a program of carotid artery stenting. J VascSurg 2004; 40: 746-751.
    [30] Shaw LJ, Raggi P, Schisterman E, et al. Prognostic value of cardiac risk factors and coronary artery calcium screening for all-cause mortality. Radiology 2003; 228:826-833.
    [31] Kondos GT, Hoff JA, Sevrukov A, et al. Electronbeam tomography coronary artery calcium and cardiac events: a 37-month follow-up of 5635 initially asymptomatic low- to intermediate-risk adults. Circulation 2003; 107:2571-2576.
    [32] Denzel C, Lell M, Maak M, et al. Carotid artery calcium: accuracy of a calcium score by computed tomography-an in vitro study with comparison to sonography and histology. Eur J Vasc Endovasc Surg 2004;28:214-220.
    [33] Agatston A, Janowiz WR, Hildner FJ, et al. Quantification of coronary artery calcium using ultrafastcomputed tomography. J Am Coll Cardiol. 1990;15:827-832.
    [34] Rothwell PM, Eliasziw M, Gutnikov SA, et al., Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis. Lancet 2003; 361:107-116.
    [35] Halliday A, Mansfield A, Marro J, et al. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet 2004; 363:1491-1502.
    [36] JS Yadav, MH Wholey and RE Kuntz et al., Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351:1493-1501.
    [37] Coward LJ, Featherstone RL, Brown MM, et al. Safety and efficacy of endovascular treatment of carotid artery stenosis compared with carotid endarterectomy: a Cochrane systematic review of the randomized evidence. Stroke 2005; 36: 905-911.
    [38] de Weert TT, Ouhlous M, Zondervan P, et al. In vitro characterization of atherosclerotic carotid plaque with multidetector computed tomography and histopathological correlation. Eur Radiol 2005; 15:1906-1914.
    [39] de Weert, TT, Ouhlous M, Meijering E, et al. In vivo characterization and quantification of atherosclerotic carotid plaque components with multidetector computed tomography and histopathological correlation. Arterioscler Thromb Vasc Biol 2006; 26:2366-2372.
    [40] Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. Circulation 2003; 108:1664-1672.
    [41] Polak JF, Shemanski L, O'Leary DH, et al. Hypoechoic plaque at US of the carotid artery: an independent risk factor for incident stroke in adults aged 65 years or older. Radiology 1998;208: 649-654.
    [42] Culebras A, Otero C, Toledo JR, et al. Computed tomographic study of cervical carotid calcification. Stroke 1989;20:1472-1476.
    [43] Tannenbaum S, Kondos G, Veselik K, et al. Detection of calcific deposits in coronary arteries by ultrafast computed tomography. J Am Coll Cardiol 1989;15:827-832.
    [44] Adams GJ, Simoni DM, Bordelon CB Jr, et al. Bilateral symmetry of human carotid artery atherosclerosis. Stroke 2002;33:2575-2580.
    [45] Saam T, Cai J, Ma L, et al. Comparison of Symptomatic and Asymptomatic Atherosclerotic Carotid Plaque Features with in Vivo MR Imaging. Radiology 2006;240: 464-472.
    [46] Hoff JA, Chomka EV, Krainik AJ, et al. Age and gender distributions of coronary artery calcium detected by electron beam tomography in 35,246 adults. Am J Cardiol 2001;87:1335-1339.
    [47] Raggi P, Callister TQ, Cooil B, et al. Identification of patients at increased risk of first unheralded acute myocardial infarction by electron-beam computed tomography. Circulation 2000;101:850-855.
    [48] Wong ND, Budoff MJ, Pio J, et al. Coronary calcium and cardiovascular event risk: evaluation by age- and sex-specific quartiles. Am Heart J 2002; 143:456-459.
    [49] Newman A, Naydeck B, Sutton-Tyrell K, et al. Coronary artery calcification in older adults with minimal clinical or subclinical cardiovascular disease. J Am Geriatr Soc 2000;48:256-263.
    [50] Rumberger JA, Kaufman L: A Rosetta stone for coronary calcium risk stratification: Agatston, volume, and mass scores in 11490 individuals. AJR Am J Roentgenol 2003; 181: 743-748.
    [51] McKinney AM, Casey SO, Teksam M et al. Carotid bifurcation calcium and correlation with percent stenosis of the internal carotid artery on CT angiography. Neuroradiology 2005, 47: 1-9.
    [52] Hiroyuki Katano, Kazuo Yamada, et al. Analysis of Calcium in Carotid Plaques With Agatston Scores for Appropriate Selection of Surgical Intervention. Stroke 2007; 38:3040-3044.
    [53] Tsutsumia M, Aikawaa H, Onizuka M, et al. Carotid Artery Stenting for Calcified Lesions. AJNR 2008;29:1590-1593.
    [54] Li Z Y, Howarth S, Tjun T, et al. Does Calcium Deposition Play a Role in the Stability of Atheroma? Location May Be the Key. Cerebrovasc Dis 2007;24:452-459.
    [55] Fischbach R, Maintz D, et al. Coronary Calcium Scoring With Multidetector-Row CT Rationale and Scoring Techniques. Contemporary Cardiology: CT of the Heart: Principles and Applications.
    [56] Sabetai MM, Tegos TJ, Nicolaides AN, et al. Hemispheric symptoms and carotid plaque echomorphology. J Vasc Surg 2000;31:39-49.
    [57] Mathiesen EB, Bonaa KH, Joakimsen O, et al. Echolucent plaques are associated with high risk of ischemic cerebrovascular events in carotid stenosis: the Tromso study. Circulation 2001; 103: 2171-2175.
    [58] Hunt JL, Fairman R, Mitchell ME, et al. Bone formation in carotid plaques: a clinicopathological study. Stroke 2002;33:1214-1219.
    [59] Takeshi Uwatoko, Kazunori Toyoda, Tooru Inoue; et al. Carotid Artery Calcification on Multislice Detector-Row Computed Tomography. Cerebrovasc Dis 2007;24:20-26.
    [60] Li ZY, Howarth S, Rikin A, et al. Trivedi et al. Stress analysis of carotid plaque rupture based on in vivo high resolution MRI. Journal of Biomechanics 2006; 39:2611-2622.
    [61]Alessio Apruzzese, Mauro Silvestrini, Roberto Floris, et al. Cerebral Hemodynamics in Asymptomatic Patients with Internal Carotid Artery Occlusion: A Dynamic Susceptibility Contrast MR and Transcranial Doppler Study. AJNR 2001; 22:1062-1067.
    [62] Mehrkens J Ma, Holtmannspoetter M, Linke R et al. Perfusion MRI before and after acetazolamide administration for assessment of cerebrovascular reserve capacity in patients with symptomatic internal carotid artery (ICA) occlusion: comparison with ~(99m)Tc-ECD SPECT. Neuroradiology 2007; 49:317-326.
    [63]North American Symptomatic Carotid Endarterectomy Trialists' Collaborative Group. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998; 339:1415-25.
    [64]European Carotid Surgery Trialists' Collaborative Group. Randomized trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet 1998;351:1379-1380.
    [65]Moftakhar R, Turk AS, Niemann DB, et al. Effects of Carotid or Vertebrobasilar Stent Placement on Cerebral Perfusion and Cognition. AJNR 2005; 26:1772-1780.
    [66]Dmasio H. A computed tomographic guide to the identification of cerebral vascular territories. Arch Neurol 1983;40:138-42.
    [67]Del Sette M, Eliasziw M , St reifler J Y, et al . Internal borderzone infarction: a marker for severe stenosis in patients with symptomatic internal carotid artery disease. For the North American Symptomatic Carotid Endarterectomy (NASCET) Group. Stroke 2000; 31 (3):631-636.
    [68]Axel L. Cerebral blood flow determination by rapid sequence computed tomography. Radiology 1980; 137: 679-686.
    [69]eters AM, Gunasekera RD, Henderson BL, et al. Noninvasive measurements of blood-flow and extraction fraction. Nucl Med Commun 1987; 8: 823-837.
    [70]Miles KA. Measurement of tissue perfusion by dynamic computed tomogramphy. BJR 1991;64:409-412.
    [71]Klotz E, Konig M. Perfusion measurements of the brain: Using dynamic CT for the quantitative assessment of cerebral ischemia in acute stroke. Eur J Radio, 1999, 30: 170-184.
    [72]Bell SD, Peters AM. Measurement of the blood-flow from 1st-pass radionuclide angiography- Influnce of bolus volume. Eur J Nucl Med 1991; 18: 885-888.
    [73]Koenig M, Klotz E, Luka B, et al. Perfusion CT of the brain: Diagnostic approach for early detection of ischemic stroke. Radio logy 1998, 209: 85-93.
    [74] Derdeyn CP, Videen TO, Yundt KD, et al. Variability of cerebral blood volume and oxygen extraction: stages of cerebral haemodynamic impairment revisited. Brain 2002; 125:595-607.
    [75] Powers WJ, Press GA, Grubb RL Jr. The effect of hemodynamically significant carotid artery disease on the hemodynamic status of the cerebral circulation. Ann Intern Med 1987; 106:27-35.
    [76] Vernieri F, Pasqualetti P, Matteis M, et al. Effect of collateral blood flow and cerebral vasomotor reactivity on the outcome of carotid artery occlusion. Stroke 2001; 32:1552-1558.
    [77] Hankey GJ, Slattery JM, Warlow CP. The prognosis of hospital-referred transient ischaemic attacks. J Neurol Neurosurg Psychiatry 1991; 54:793-802.
    [78] Barnett HJ. Hemodynamic cerebral ischemia: an appeal for systematic data gathering prior to a new EC/IC trial. Stroke 1997; 28:1857-1860.
    [79]Blaser T, Hofmann K, Buerger T, Effenberger O, Wallesch CW, Goertler M. Risk of stroke, transient ischemic attack, and vessel occlusion before endarterectomy in patients with symptomatic severe carotid stenosis. Stroke 2002; 33:1057-1062.
    [80] Caplan LR, Hennerici M. Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Arch Neurol 1998; 55:1475-1482.
    [81] Markus H, Cullinane M. Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion. Brain 2001; 124:457-467.
    [82] Latchaw RE, Yonas H, Hunter GJ, et al. Guidelines and Recommendations for Perfusion Imaging in Cerebral Ischemia: A Scientific Statement for Healthcare Professionals by the Writing Group on Perfusion Imaging, From the Council on Cardiovascular Radiology of the American Heart Association. Stroke 2003; 34:1084-1104.
    [83] Nicholls S C, Bergelin R, Strandness DE. Neurologic sequelae of unilateral carotid artery occlusion : immediate and late. J Vasc Surg 1989; 10:542-548.
    [84] Bornstein N M, Norris J W. Benign outcome of carotid occlusion. Neurology 1989; 39: 6-8.
    [85] Kluytmans M, van der Grond J, Viergever MA et al. Gray Matter and White Matter Perfusion Imaging in Patients with Severe Carotid Artery Lesion. Radiology1998; 209:675-682.
    [86] Derdeyn CP, Khosla A, Videen TO, et al. Severe hemodynamic impairment and border zone region infarction. Radiology 2001; 220:195-201.
    [87] Powers WJ. Cerebral hemodynamics in ischemic cerebrovascular disease. Ann Neurol 1991; 29:231-40.
    
    [88] Liebeskind DS. Collateral circulation. Stroke 2003;34:2279-84.
    [89|Hofmeijer J, Klijn CJ, Kappelle LJ, et al. Collateral circulation via the ophthalmic artery or leptomeningeal vessels is associated with impaired cerebral vasoreactivity in patients with symptomatic carotid artery occlusion. Cerebrovasc Dis 2002; 14:22-26.
    [90] Bokkers RPH, van Laar PJ, van de Ven KCC, et al. Arterial Spin-Labeling MR Imaging Measurements of Timing Parameters in Patients with a Carotid Artery Occlusion. AJNR 2008; 29:1698-1703.
    [91] Wintermark M; Maeder P; Verdun FR, et al. Using 80 kVp versus 120 kVp in perfusion CT measurement of regional cerebral blood flow. AJNR 2000; 21:1881-84.
    [92] Nabavi DG, Cenic A, Dool J, et al. Quantitative assessment of cerebral hemodynamics using CT: stability, accuracy, and precision studies in dogs. J Comput Assist Tomogr 1999; 23:506-15.
    [93] Fiorella D, Heiserman J, Prenger E, et al. Assessment of the reproducibility of postprocessing dynamic CT perfusion data. AJNR 2004; 25:97-107.
    [94] Waaijer A, van der Schaaf I C, Velthuis BK, et al. Reproducibility of Quantitative CT Brain Perfusion Measurements in Patients with Symptomatic Unilateral Carotid Artery Stenosis. AJNR 2007; 28:927-32.
    [95] Turk AS, Grayev A, Rowley HA, et al. Variability of clinical CT perfusion measurements in patients with carotid stenosis. Neuroradiology 2007; 49:955-961.
    [1] Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies—part I. Circulation 2003; 108:1664-1672.
    [2] Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies—part II. Circulation 2003; 108:1772-1778.
    [3] Vasily L, Yarnykh, Chun-Yuan, et al. Simultaneous outer volume and blood suppression by quadruple inversion-recovery. Magn Reson Med 2006; 55:1083-1092.
    [4] Vasily L, Yarnykh, Chun-Yuan, et al.T1-insensitive flow suppression using quadruple inversion-recovery. Magn Reson Med 2002; 48:899-905.
    [5] Kang X, Polissar NL, Han C, Lin E, Yuan C. Analysis of the measurement precision of arterial lumen and wall areas using high resolution MRI. Magn Reson Med 2000; 44:968-972.
    [6] Hatsukami TS, Ross R, Polissar NL, Yuan C. Identification of fibrous cap thickness and cap rupture in human atherosclerotic carotid plaque in-vivo with high resolution magnetic resonance imaging. Circulation 2000; 102:959-964.
    [7] Mitsumori LM, Hatsukami TS, Ferguson MS, et al. In vivo accuracy of multisequence MR imaging for identifying unstable fibrous caps in advanced human carotid plaques. J Magn Reson Imaging 2003; 17:410—420.
    [8] Yuan C, Zhang SX, Polissar NL, et al. Identification of fibrous cap rupture with magnetic resonance imaging is highly associated with recent transient ischemic attack or stroke. Circulation 2002; 105:181-185.
    [9] Kerwin W, Hooker A, Spilker M, et al. Quantitative magnetic resonance imaging analysis neovasculature volume in carotid atherosclerotic plaque. Circulation 2003; 107:851-856.
    [10] Clarke SE, Hammond RR, Mitchell JR, Rutt BK. Quantitative assessment of carotid plaque composition using multicontrast MRI and registered histology. Magn Reson Med 2003; 50:1199-1208.
    [11]Saam T, Ferguson MS, Yarnykh VL, et al. Quantitative evaluation of carotid plaque composition by in vivo MRI. Arterioscler Thromb Vasc Biol 2005; 25:234-239.
    [12] Yuan C, Kerwin WS, Ferguson MS, et al. Contrast-enhanced high resolution MRI for atherosclerotic carotid artery tissue characterization. J Magn Reson Imaging 2002; 15:62-67.
    [13]Wasserman BA, Smith WI, Trout HH 3rd, et al. Carotid artery atherosclerosis: in vivo morphologic characterization with gadolinium-enhanced double-oblique MR imaging initial results. Radiology 2002; 223:566-573.
    [14]Stary HC. Natural history and histological classification of atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2000; 20: 1777-1778.
    [15]Cai JM, Ferguson MS, Polissar N, et al. Classification of human carotid atherosclerotic lesions using in vivo multi-contrast MR imaging. Circulation 2002;106:1368-1373.
    [16]Corti R, Osende JI, Fayad ZA, et al. In vivo noninvasive detection and age definition of arterial thrombus by MRI. J Am Coll Cardiol 2002; 39:1366-1373.
    [17] Moody AR, Murphy RE, Morgan PS, et al. Characterization of complicated carotid plaque with magnetic resonance direct thrombus imaging in patients with cerebral ischemia. Circulation 2003; 107: 3047-3052.
    [18] Kolodgie FD, Gold HK, Burke AP, et al. Intraplaque hemorrhage and progression of coronary atheroma. N Engl J Med 2003; 349:2316-2325.
    [19]Takaya N, Yuan C, Chu B, et al. Presence of intraplaque hemorrhage stimulates progression of carotid atherosclerotic plaques: a high-resolution magnetic resonance imaging study. Circulation 2005; 111:2768-2775.
    [20] Virmani R, Kolodgie FD, Burke AP, et al. Atherosclerotic plaque progression and vulnerability to rupture: angiogenesis as a source of intraplaque hemorrhage. Arterioscler Thromb Vasc Biol 2005; 25:2054-2061.
    [21]Norbert N, Laurent D, Philippe D, et al. The Vulnerable Carotid Artery Plaque : Current Imaging Methods and New Perspectives. Stroke 2005; 36:2764.
    [22]Kampschulte A, Ferguson MS, Kerwin WS, et al. Differentiation of intraplaque versus juxtaluminal hemorrhage/thrombus in advanced human carotid atherosclerotic lesions by in vivo magnetic resonance imaging. Circulation 2004; 110:3239-3244.
    [23]Saam T, Cai J, Ma L, et al. Comparison of symptomatic and asymptomatic atherosclerotic carotid plaque features with in vivo MR imaging. Radiology 2006; 240(2):464-472.
    [24]Tobias S, Thomas S, Norihide T, et al. The Vulnerable, or High-Risk, Atherosclerotic Plaque: Noninvasive MR Imaging for Characterization and Assessment 1.Radiology 2007; 244:64-77.
    [25]Kerwin WS, O'Brien KD, Ferguson MS, et al. Inflammation in carotid atherosclerotic plaque: a dynamic contrast-enhanced MR imaging study. Radiology 2006; 241(2):459-468.
    [26]Kerwin WS, Hooker A, Spilker M, et al. Quantitative magnetic resonance imaging analysis of neovasculature volume in carotid atherosclerotic plaque. Circulation 2003; 107:851-856.
    [27]Kooi ME, Cappendijk VC, Cleutjens KB, et al. Accumulation of ultrasmall superparamagnetic particles of iron oxide in human atherosclerotic plaques can be detected by in vivo magnetic resonance imaging. Circulation 2003;107:2453-2458.
    [28]Trivedi RA, U-King-Im JM, Graves MJ, et al. In vivo detection of macrophages in human carotid atheroma; temporal dependence of ultrasmall superparamagnetic particles of iron oxide-enhanced MRI.Stroke 2004;35: 1631-1635.
    [29]Vardan A, Michael J.L, Karen C.BS, et al. Detecting and assessing macrophages in vivo to evaluate atherosclerosis noninvasively using molecular MRI. PNAS 2007; 104:961-966.
    [30]Bjorn G, Susan Y, Angelique Y. Development of Contrast Agents Targeted to Macrophage Scavenger Receptors for MRI of Vascular Inflammation. Bioconjugate Chem 2006; 17 (2): 538 -547.
    [31]Wentzel JJ, Aguiar SH, Fayad ZA. Vascular MRI in the diagnosis and therapy of the high risk atherosclerotic plaque. J Interv Cardiol 2003; 16:129-142.
    [32]Botnar RM, Perez AS, Witte S, et al. In vivo molecular imaging of acute and subacute thrombosis using a fibrin-binding magnetic resonance imaging contrast agent. Circulation 2004; 109:2023-2029.
    [33] Winter PM, Morawski AM, Caruthers SD, et al. Molecular imaging of angiogenesis in early-stage atherosclerosis with alpha (v) beta3-integrin-targeted nanoparticles. Circulation 2003; 4:108: 2270-2274.
    [34] Lindner JR. Microbubbles in medical imaging: current applications and future directions. Nat Rev Drug Discov 2004; 3: 527-532.

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