高频超声对氟伐他汀干预的动脉粥样硬化性脑梗死患者动脉斑块和血管内皮功能的评价
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摘要
背景
世界卫生组织(WHO)将脑血管病列为21世纪十大疾病之一。在我国,脑血管病患病率居第3位,其中缺血性脑血管病(脑梗死)约占80%。临床研究及病理证实,脑梗死主要分为大动脉粥样硬化性脑梗死(ATCI)、心源性栓塞性脑梗死(CCI)、小动脉闭塞性脑梗死(LCI)、其他明确病因和不明原因等5大类。ATCI的病变基础就是动脉粥样硬化,具有高发病率、高致残率、高死亡率特点。因此,早期发现动脉硬化病变,及时进行有效的一、二级预防意义重大。
尽管动脉造影、64排CT动脉成像等方法可以进行动脉病变检查,但因其有创、价格高、少数可有较严重并发症等原因不宜作为常规的早期检查方法。外周动脉粥样硬化程度在一定程度上可反映动脉粥样硬化及其严重程度,因此,对外周动脉管壁的形态及弹性功能的检测有助于预测动脉病变。
近年来,病理学证实炎症过程贯穿于动脉粥样硬化的形成、起始及发展全过程。ATCI发生的主要机制是炎症活性诱导的易损斑块破裂诱发的急性血栓形成。易损斑块的炎性标记物越来越多地应用于ATCI病情的综合评价,常用的有hs-CRP、粘附分子(ICAM-1、VCAM-1)等。血管内皮是一种动力器官,通过各种机制抑制血液凝固和白细胞粘附,保持血液的流动性。单核细胞吞噬泡沫细胞,粘附在活化的内皮上,继而侵入内皮下层,这是形成动脉粥样硬化的关键启动步骤,这种粘附作用由ICAM-1、VCAM-1等介导。
研究显示,氟伐他汀除能显著降低高密度胆固醇,还能够稳定动脉硬化斑块。
目的
本课题研究氟伐他汀对炎性易损斑块的稳定作用;并研究氟伐他汀应用前后患者动脉管壁及弹性变化,进一步验证氟伐他汀对ATCI的治疗作用。同时,利用高频超声对氟伐他汀干预的ATCI患者血管内皮功能及动脉斑块进行深入研究,来阐明超声在评价药物对血管功能中发挥着重要作用。
方法
将动脉粥样硬化性脑梗死组(ATCI)患者分为给予氟伐他汀(40mg qd po)治疗组和未给予氟伐他汀治疗组;每组34例,并与30例正常对照组进行比较。所有患者于入院次日及3个月后两次进行下述指标检测:①颈动脉超声、眼动脉超声(稳定和易损斑块数量、斑块指数、动脉内膜-中膜厚度IMT、收缩峰值速度PSV、舒张末速度EDV、阻力指数RI及搏动指数PI);②血脂(总胆固醇TC、甘油三酯TG、低密度脂蛋白胆固醇LDL-c、高密度脂蛋白胆固醇HDL-c);③可溶性细胞间黏附因子-1(sICAM-1)、可溶性血管细胞粘附因子-1(sVCAM-1)含量及mRNA和蛋白表达;④头颅CT/MRI;⑤神经功能缺损评分(NDS)。正常对照组也进行除了NDS以外的相同指标检测。所有患者在住院期间,均进行一般状况评估(血压、血糖),均给予改善循环、营养神经等治疗。
结果
1.颈动脉斑块比较:①两组ATCI患者在治疗前颈动脉斑块总数、稳定斑块或易损斑块数量差异无统计学意义(P＞0.05);经过治疗3个月,颈动脉斑块总数明显减少,稳定斑块有所增多,易损斑块明显减少,两组ATCI比较,差异有统计学意义(P＜0.01)。②两组ATCI间治疗前斑块指数和IMT比较,差异也无统计学意义(P＞0.05);经过治疗3个月,两组ATCI中斑块指数和IMT比较,差异也有统计学意义(P＜0.01)。
2.颈动脉和眼动脉超声检测的血流动力学参数变化:两组ATCI患者在治疗前PSV、EDV、RI、PI等指标差异无统计学意义(P＞0.05);治疗3个月后,PSV、EDV增快,RI、PI下降,与治疗前相比较,氟伐他汀组改变更加显著(P＜0.01或P＜0.05),ATCI两组间上述各指标差异有统计学意义(P＜0.01)。
3.血脂分析:两组ATCI患者治疗前TC、TG、LDL-c、HDL-c比较,差异无统计学意义(P＞0.05);经过治疗3个月,TC、TG、LDL-c浓度下降,HDL-c浓度升高,氟伐他汀组改变更显著,与常规治疗组相比较,差异有统计学意义(P＜0.01)。
4.sICAM-1、sVCAM-1含量及mRNA和蛋白表达:两组ATCI患者治疗前sICAM-1、sVCAM-1含量及mRNA和蛋白表达比较,差异无统计学意义(P＞0.05);经过氟伐他汀治疗3个月,这两种粘附分子含量及mRNA和蛋白表达均有所下降,与常规治疗组相比较,差异有统计学意义(P＜0.01)。大、中、小病灶ATCI患者之间sICAM-1、sVCAM-1含量有差异(P＜0.01)。
5.药物疗效的判定:两组ATCI患者在治疗前NDS无显著性差异(P＞0.05);经治疗3各月后,两组患者NDS均明显降低,与治疗前比较有统计学意义(P＜0.01),而氟伐他汀组降低的更明显,两组治疗后比较有统计学意义(P＜0.01)。
6.药物不良反应的判定:所有患者在观察期间血、尿常规、肝肾功能、济钙孜捶⑸飨员浠?P＞0.05);也未见药物过敏、消化道反应、造血系统损害等不良反应及横纹肌溶解症的发生。
结论
氟伐他汀通过稳定斑块、改善动脉硬化血管的顺应性及弹性、降低LDL-c浓度、保护血管内皮功能等机制在ATCI的治疗中起着积极作用。颈动脉和眼动脉超声检测在评价药物对血管功能及在诊断ATCI中均发挥着重要作用。
Backgrounds
Cerebral vascular diseases have been listed as one of ten most common diseases by World Health Organization (WHO) in the 21st century. In China, the prevalence of cerebrovascular disease ranks No. 3, in which ischemic cerebrovascular disease (cerebral infarction) accounts for about 80%. According to clinical and pathological examination, cerebral infarctions were divided into five categories including atherosclerotic cerebral infarction (ATCI), cardiogenic cerebral infarction (CCI), lacunar cerebral infarction (LCI), other determined etiologies and unknown reasons of cerebral infarction. Pathological basis of ATCI, which is characterized by high morbidity, high disability and high mortality, is atherosclerosis. Therefore, it's very important to early detect atherosclerotic lesions, and timely and effectively prevent it in the first and second level.
Although angiography, 64-slice CT scan has been used to detect arterial diseases, those methods are not routine ones because of invasive, expensive and some severe complications. Peripheral arterial atherosclerosis can reflect the atherosclerosis and its severity to some extent, therefore, vessel wall morphology and elasticity of peripheral arteries can predict arterial diseases.
In recent years, pathology has confirmed inflammation run through the formation and development of the atherosclerosis. The main mechanism of ATCI is acute thrombosis induced by vulnerable plaque rupture which is caused by inflammation. Inflammatory markers from vulnerable plaque including hs-CRP, adhesion molecules (ICAM-1, VCAM-1) etc. have been used to evaluate ATCI.
Vascular endothelial, a dynamic organ, can inhibit blood coagulation and leukocyte adhesion to maintain blood flow through various mechanisms. The key steps in the formation of atherosclerosis include monocytes engulfing foam cells, adhering to the activated endothelium and invading subendothelial layer, which of the process was mediated by ICAM-1, VCAM-1.
Studies have shown that fluvastatin significantly reduce level of high-density cholesterol and stabilize the atherosclerotic plaque.
Objectives
To determine the effect of fluvastatin on stabilizing inflammatory vulnerable plaques through inhibiting ICAM-1, VCAM-1 before and after having been treated by fluvastatin in the patients with ATCI. Meanwhile, endothelial function and arterial plaque were studied by high frequency ultrasound in the patients with ATCI before and after having been treated by fluvastatin to clarify high-frequency ultrasound in evaluating on carotid and ophthalmic artery plaques from the patients with ATCI intervened by fluvastatin.
Methods
Sixty-eight patients with ATCI were divided into two groups, conventional treatment group and fluvastatin treatment group, and 30 healthy men were chosen as controls.
The following indexes were detected twice in all patients when they were 2nd day in the hospital and after 3 months.①Carotid artery ultrasound, ophthalmic artery ultrasound (the number of stable and vulnerable plaque; plaque index; arterial intima - media thickness, IMT; systolic peak velocity, PSV; end diastolic velocity, EDV; resistance index, RI and pulsatility index, PI)②Lipids (total cholesterol, TC; triglyceride, TG; low density lipoprotein cholesterol, LDL-c; high-density lipoprotein cholesterol, HDL-c)③Content, mRNA and protein expression of soluble intercellular adhesion molecule -1 (sICAM-1), soluble vascular cell adhesion molecule -1 (sVCAM-1);④Head CT / MRI;⑤Neurological deficit score (NDS). In addition, the normal control group were also detected the same indexes except for NDS. General conditions (blood pressure, blood sugar) were assessed in all of patients with ATCI when they were in the hospital, and some of drugs improving circulation, nervous protection were given in all of patients with ATCI.
Results
1. Comparison of carotid artery plaque:①Number of total, stable and unstable carotid artery plaques were no difference between two groups of ATCI before treatment (P>0.05). Number of total and unstable carotid artery plaques decreased, number of stable plaques increased, there were significant differences in above index between two groups of ATCI after 3 month treatment (P<0.01).②Plaque index and IMT were no difference between two groups of ATCI before treatment (P> 0.05). There were significant differences in plaque and IMT between two groups of ATCI after 3 month treatment (P<0.01).
2. Hemodynamic parameters in carotid artery and ophthalmic artery by ultrasonic exam: There were no significant difference in PSV, EDV, RI and PI between two groups of ATCI before treatment (P>0.05). But PSV and EDV increased, RI and PI decreased in the patients with ATCI after treatment, especially in the patients intervened by fluvastatin, there were significant differences in above index between two groups of ATCI (P<0.01).
3. Lipids: There were no significant difference in TC, TG, HDL-c and LDL-c between two groups of ATCI before treatment (P>0.05). Concentrations of TC, TG and LDL-c decreased, and concentration of HDL-c increased in the patients with ATCI after treatment, especially in the patients intervened by fluvastatin, there were significant differences in above index between two groups of ATCI (P<0.0l).
4. Contents, mRNA and protein expressions of sICAM-1 and sVCAM-1: There were no significant difference in all of indexes between two groups of ATCI before treatment (P>0.05). Contents, mRNA and protein expressions of sICAM-1 and sVCAM-1 decreased after treatment, especially in the patients intervened by fluvastatin, there were significant differences between two groups of ATCI (P<0.01). Among large, medium and small lesions in the patients with ATCI treated by fluvastatin, sICAM-1 and sVCAM-1 levels were significantly different (P<0.01).
5. Drug efficacy: There were no significant difference in NDS between two groups of ATCI before treatment (P>0.05). NDS decreased after treatment, especially in the patients intervened by fluvastatin, there were significant differences between two groups of ATCI (P<0.01).
6. Drug adverse reactions: All the patients in the observation period had no significant changes in blood, urine, liver and kidney function and muscle enzymes (P > 0.05); no patient has drug allergy, gastrointestinal reactions, coagulation mechanism damage and other adverse reactions, neither has rhabdomyolysis.
Conclusions
Fluvastatin plays an active role in the treatment of ATCI through stabilizing the plaque, improving compliance and flexibility of atherosclerotic blood vessels, reducing concentration of LDL-c and protecting function of vascular endothelial. Carotid artery and ophthalmic artery ultrasonography play an important role in both the evaluation of drugs on vascular function and the diagnosis of ATCI.
世界卫生组织(WHO)将脑血管病列为21世纪十大疾病之一。在我国,脑血管病患病率居第3位,其中缺血性脑血管病(脑梗死)约占80%。临床研究及病理证实,脑梗死主要分为大动脉粥样硬化性脑梗死(ATCI)、心源性栓塞性脑梗死(CCI)、小动脉闭塞性脑梗死(LCI)、其他明确病因和不明原因等5大类。ATCI的病变基础就是动脉粥样硬化,具有高发病率、高致残率、高死亡率特点。因此,早期发现动脉硬化病变,及时进行有效的一、二级预防意义重大。
尽管动脉造影、64排CT动脉成像等方法可以进行动脉病变检查,但因其有创、价格高、少数可有较严重并发症等原因不宜作为常规的早期检查方法。外周动脉粥样硬化程度在一定程度上可反映动脉粥样硬化及其严重程度,因此,对外周动脉管壁的形态及弹性功能的检测有助于预测动脉病变。
近年来,病理学证实炎症过程贯穿于动脉粥样硬化的形成、起始及发展全过程。ATCI发生的主要机制是炎症活性诱导的易损斑块破裂诱发的急性血栓形成。易损斑块的炎性标记物越来越多地应用于ATCI病情的综合评价,常用的有hs-CRP、粘附分子(ICAM-1、VCAM-1)等。血管内皮是一种动力器官,通过各种机制抑制血液凝固和白细胞粘附,保持血液的流动性。单核细胞吞噬泡沫细胞,粘附在活化的内皮上,继而侵入内皮下层,这是形成动脉粥样硬化的关键启动步骤,这种粘附作用由ICAM-1、VCAM-1等介导。
研究显示,氟伐他汀除能显著降低高密度胆固醇,还能够稳定动脉硬化斑块。
目的
本课题研究氟伐他汀对炎性易损斑块的稳定作用;并研究氟伐他汀应用前后患者动脉管壁及弹性变化,进一步验证氟伐他汀对ATCI的治疗作用。同时,利用高频超声对氟伐他汀干预的ATCI患者血管内皮功能及动脉斑块进行深入研究,来阐明超声在评价药物对血管功能中发挥着重要作用。
方法
将动脉粥样硬化性脑梗死组(ATCI)患者分为给予氟伐他汀(40mg qd po)治疗组和未给予氟伐他汀治疗组;每组34例,并与30例正常对照组进行比较。所有患者于入院次日及3个月后两次进行下述指标检测:①颈动脉超声、眼动脉超声(稳定和易损斑块数量、斑块指数、动脉内膜-中膜厚度IMT、收缩峰值速度PSV、舒张末速度EDV、阻力指数RI及搏动指数PI);②血脂(总胆固醇TC、甘油三酯TG、低密度脂蛋白胆固醇LDL-c、高密度脂蛋白胆固醇HDL-c);③可溶性细胞间黏附因子-1(sICAM-1)、可溶性血管细胞粘附因子-1(sVCAM-1)含量及mRNA和蛋白表达;④头颅CT/MRI;⑤神经功能缺损评分(NDS)。正常对照组也进行除了NDS以外的相同指标检测。所有患者在住院期间,均进行一般状况评估(血压、血糖),均给予改善循环、营养神经等治疗。
结果
1.颈动脉斑块比较:①两组ATCI患者在治疗前颈动脉斑块总数、稳定斑块或易损斑块数量差异无统计学意义(P＞0.05);经过治疗3个月,颈动脉斑块总数明显减少,稳定斑块有所增多,易损斑块明显减少,两组ATCI比较,差异有统计学意义(P＜0.01)。②两组ATCI间治疗前斑块指数和IMT比较,差异也无统计学意义(P＞0.05);经过治疗3个月,两组ATCI中斑块指数和IMT比较,差异也有统计学意义(P＜0.01)。
2.颈动脉和眼动脉超声检测的血流动力学参数变化:两组ATCI患者在治疗前PSV、EDV、RI、PI等指标差异无统计学意义(P＞0.05);治疗3个月后,PSV、EDV增快,RI、PI下降,与治疗前相比较,氟伐他汀组改变更加显著(P＜0.01或P＜0.05),ATCI两组间上述各指标差异有统计学意义(P＜0.01)。
3.血脂分析:两组ATCI患者治疗前TC、TG、LDL-c、HDL-c比较,差异无统计学意义(P＞0.05);经过治疗3个月,TC、TG、LDL-c浓度下降,HDL-c浓度升高,氟伐他汀组改变更显著,与常规治疗组相比较,差异有统计学意义(P＜0.01)。
4.sICAM-1、sVCAM-1含量及mRNA和蛋白表达:两组ATCI患者治疗前sICAM-1、sVCAM-1含量及mRNA和蛋白表达比较,差异无统计学意义(P＞0.05);经过氟伐他汀治疗3个月,这两种粘附分子含量及mRNA和蛋白表达均有所下降,与常规治疗组相比较,差异有统计学意义(P＜0.01)。大、中、小病灶ATCI患者之间sICAM-1、sVCAM-1含量有差异(P＜0.01)。
5.药物疗效的判定:两组ATCI患者在治疗前NDS无显著性差异(P＞0.05);经治疗3各月后,两组患者NDS均明显降低,与治疗前比较有统计学意义(P＜0.01),而氟伐他汀组降低的更明显,两组治疗后比较有统计学意义(P＜0.01)。
6.药物不良反应的判定:所有患者在观察期间血、尿常规、肝肾功能、济钙孜捶⑸飨员浠?P＞0.05);也未见药物过敏、消化道反应、造血系统损害等不良反应及横纹肌溶解症的发生。
结论
氟伐他汀通过稳定斑块、改善动脉硬化血管的顺应性及弹性、降低LDL-c浓度、保护血管内皮功能等机制在ATCI的治疗中起着积极作用。颈动脉和眼动脉超声检测在评价药物对血管功能及在诊断ATCI中均发挥着重要作用。
Backgrounds
Cerebral vascular diseases have been listed as one of ten most common diseases by World Health Organization (WHO) in the 21st century. In China, the prevalence of cerebrovascular disease ranks No. 3, in which ischemic cerebrovascular disease (cerebral infarction) accounts for about 80%. According to clinical and pathological examination, cerebral infarctions were divided into five categories including atherosclerotic cerebral infarction (ATCI), cardiogenic cerebral infarction (CCI), lacunar cerebral infarction (LCI), other determined etiologies and unknown reasons of cerebral infarction. Pathological basis of ATCI, which is characterized by high morbidity, high disability and high mortality, is atherosclerosis. Therefore, it's very important to early detect atherosclerotic lesions, and timely and effectively prevent it in the first and second level.
Although angiography, 64-slice CT scan has been used to detect arterial diseases, those methods are not routine ones because of invasive, expensive and some severe complications. Peripheral arterial atherosclerosis can reflect the atherosclerosis and its severity to some extent, therefore, vessel wall morphology and elasticity of peripheral arteries can predict arterial diseases.
In recent years, pathology has confirmed inflammation run through the formation and development of the atherosclerosis. The main mechanism of ATCI is acute thrombosis induced by vulnerable plaque rupture which is caused by inflammation. Inflammatory markers from vulnerable plaque including hs-CRP, adhesion molecules (ICAM-1, VCAM-1) etc. have been used to evaluate ATCI.
Vascular endothelial, a dynamic organ, can inhibit blood coagulation and leukocyte adhesion to maintain blood flow through various mechanisms. The key steps in the formation of atherosclerosis include monocytes engulfing foam cells, adhering to the activated endothelium and invading subendothelial layer, which of the process was mediated by ICAM-1, VCAM-1.
Studies have shown that fluvastatin significantly reduce level of high-density cholesterol and stabilize the atherosclerotic plaque.
Objectives
To determine the effect of fluvastatin on stabilizing inflammatory vulnerable plaques through inhibiting ICAM-1, VCAM-1 before and after having been treated by fluvastatin in the patients with ATCI. Meanwhile, endothelial function and arterial plaque were studied by high frequency ultrasound in the patients with ATCI before and after having been treated by fluvastatin to clarify high-frequency ultrasound in evaluating on carotid and ophthalmic artery plaques from the patients with ATCI intervened by fluvastatin.
Methods
Sixty-eight patients with ATCI were divided into two groups, conventional treatment group and fluvastatin treatment group, and 30 healthy men were chosen as controls.
The following indexes were detected twice in all patients when they were 2nd day in the hospital and after 3 months.①Carotid artery ultrasound, ophthalmic artery ultrasound (the number of stable and vulnerable plaque; plaque index; arterial intima - media thickness, IMT; systolic peak velocity, PSV; end diastolic velocity, EDV; resistance index, RI and pulsatility index, PI)②Lipids (total cholesterol, TC; triglyceride, TG; low density lipoprotein cholesterol, LDL-c; high-density lipoprotein cholesterol, HDL-c)③Content, mRNA and protein expression of soluble intercellular adhesion molecule -1 (sICAM-1), soluble vascular cell adhesion molecule -1 (sVCAM-1);④Head CT / MRI;⑤Neurological deficit score (NDS). In addition, the normal control group were also detected the same indexes except for NDS. General conditions (blood pressure, blood sugar) were assessed in all of patients with ATCI when they were in the hospital, and some of drugs improving circulation, nervous protection were given in all of patients with ATCI.
Results
1. Comparison of carotid artery plaque:①Number of total, stable and unstable carotid artery plaques were no difference between two groups of ATCI before treatment (P>0.05). Number of total and unstable carotid artery plaques decreased, number of stable plaques increased, there were significant differences in above index between two groups of ATCI after 3 month treatment (P<0.01).②Plaque index and IMT were no difference between two groups of ATCI before treatment (P> 0.05). There were significant differences in plaque and IMT between two groups of ATCI after 3 month treatment (P<0.01).
2. Hemodynamic parameters in carotid artery and ophthalmic artery by ultrasonic exam: There were no significant difference in PSV, EDV, RI and PI between two groups of ATCI before treatment (P>0.05). But PSV and EDV increased, RI and PI decreased in the patients with ATCI after treatment, especially in the patients intervened by fluvastatin, there were significant differences in above index between two groups of ATCI (P<0.01).
3. Lipids: There were no significant difference in TC, TG, HDL-c and LDL-c between two groups of ATCI before treatment (P>0.05). Concentrations of TC, TG and LDL-c decreased, and concentration of HDL-c increased in the patients with ATCI after treatment, especially in the patients intervened by fluvastatin, there were significant differences in above index between two groups of ATCI (P<0.0l).
4. Contents, mRNA and protein expressions of sICAM-1 and sVCAM-1: There were no significant difference in all of indexes between two groups of ATCI before treatment (P>0.05). Contents, mRNA and protein expressions of sICAM-1 and sVCAM-1 decreased after treatment, especially in the patients intervened by fluvastatin, there were significant differences between two groups of ATCI (P<0.01). Among large, medium and small lesions in the patients with ATCI treated by fluvastatin, sICAM-1 and sVCAM-1 levels were significantly different (P<0.01).
5. Drug efficacy: There were no significant difference in NDS between two groups of ATCI before treatment (P>0.05). NDS decreased after treatment, especially in the patients intervened by fluvastatin, there were significant differences between two groups of ATCI (P<0.01).
6. Drug adverse reactions: All the patients in the observation period had no significant changes in blood, urine, liver and kidney function and muscle enzymes (P > 0.05); no patient has drug allergy, gastrointestinal reactions, coagulation mechanism damage and other adverse reactions, neither has rhabdomyolysis.
Conclusions
Fluvastatin plays an active role in the treatment of ATCI through stabilizing the plaque, improving compliance and flexibility of atherosclerotic blood vessels, reducing concentration of LDL-c and protecting function of vascular endothelial. Carotid artery and ophthalmic artery ultrasonography play an important role in both the evaluation of drugs on vascular function and the diagnosis of ATCI.
引文
1.贾建平,崔丽英,王伟.神经病学[M].北京:人民卫生出版社,2008:176.
2.李睿坤,李继锋,周晓莹,等.大蒜素对动脉粥样硬化小鼠血脂代谢的影响[J].中华临床医师杂志,2007,1(1):26-33.
3.Liebeskind DS.Aortic occlusion for cerebral ischemia:from theory to practice[J].Curr Cardiol Rep,2008,10(1):31-36.
4.林玲,罗燕,彭玉兰,等.彩色多普勒超声对脑梗死患者颈动脉病变的研究[J].中华老年心脑血管病杂志,2005,7(3):175-177.
5.Nanchen D,Chiolero A,Cornuz J,et al.Cardiovascular risk estimation and eligibility for statins in primary prevention comparing different strategies[J].Am J Cardiol,2009,103(8):1089-1095.
6.刘成华,肖兴花,杨树国,等.氟伐他汀对冠心病患者血脂及细胞黏附分子表达的影响[J].山东医药,2007,47(2):55-56.
7.钟伟济.氟伐他汀对不稳定性心绞痛患者血清细胞因子水平影响的研究[J].中山大学学报(医学科学版),2006,27(35):99-101.
8.Johnsen SH,Mathiesen EB.Carotid plaque compared with intima-media thickness as a predictor of coronary and cerebrovascular disease[J].Curr Cardiol Rep,2009,11(1):21-27.
9.简文豪,万小莉,王红,等.颅脑与外周血管超声诊断学[M].北京:科学技术文献出版社,2006:92.
10.Grohbee DE,Bots ML.Carotid-artery intima-media thickness as an indicator of generalized atherosclerosis[J].J Intern Med,1994,236(5):567-573.
11.中华神经科学会.各类脑血管疾病诊断要点[J].中华神经科杂志,1995,29(6):378-380.
12.Crouse JR,Happold GH,Kahl FR,et al.Evaluation of scoring system for extracranial carotid athrosclerosis extent with B-mode ultrasound[J].Stroke,1996,17(2):270.
13.Pullicino R Small deep infarcts diagnosed on computed tomography[J].Neurology,1980,30(10):1890-1896.
14.Petty GW,Brown RD JT,Whisnant IP,et al.Survival and recurrence after flint cerebral infarction:a population-based study in Rochester,Minnesota,1975through 1989[J].Neurology,1998,50:208-216.
15.黄静,陈越平.颈动脉粥样硬化患者斑块稳定性与血脂水平的相关性研究[J].西南军医,2008,10(4):15-16.
16.Ross R.Atherosclerosis-an inflammatory disease[J].N Engl J Med,1999,340(2):115.
17.Libby P,Ridker PM,Hansson GK,et al.Inflammation in atherosclerosis:from pathophysiology to practice[J].J Am Coll Cardiol,2009,54(23):2129-2138.
18.Nageh MF,Sandberg ET,Marotti KR,et al.Deficiency of inflammatory cell adhesion molecules protects against atherosclerosis in mice[J].Arterioscler Thromb Vasc Biol,1997,17:1517-1520.
19.Rothlein K,Dustin ML,Marlin SD,et al.A human intercellular adhesion molecule:(ICAM-1) distinct from LFA-1[J].Immunol,1986,137:1270-1274.
20.Lawson C,Wolf S.ICAM-1 signaling in endothelial cells[J].Pharmacol Rep,2009,61(1):22-32.
21.Muller WA.Mechanisms of transendothelial migration of leukocytes[J].Circ Res,2009,105(3):223-230.
22.Galkina E,Ley K.Leukocyte influx in atherosclerosis[J].Curr Drug Targets,2007,8(12):1239-1248.
23.Balciunas M,Bagdonaite L,Samalavicius R,et al.Markers of endothelial dysfunction after cardiac surgery:soluble forms of vascular-1 and intercellular-1adhesion molecules[J].Medicina,2009,45(6):434-439.
24.Boldt J,Kumle B,Papsdorf M,et al.Are circulating adhesion molecule specifically changed in cardiac surgical patient[J]?Ann Thoracic Surgery,1998,65:608.
25.Blankenberg S,Barbaux S,Tiret L.Adhesion molecules and atheroschresis[J].Atherosclerosis,2003,170:191-203.
26.Osbom L,Hsssion C,Tizard B,et al.Direct expression cloning of vascular cell adhesion molecule-1,a cytokine endothelial protein that binds to lymphocyes[J].Cell,1989,59:1023.
27.Frenette PS,Wanger DD.Adhesion molecules-part Ⅰ[J].N Engl J Med,1996,334:1526.
28.Iademarco MF,Barks JF,Dean DC,et al.Regulation of vascular cell adhesion molecule-1 expression by IL- 4 and TNF-alpha in cultured endothelial cells[J].J Clin Incest,1995,95:264.
29.Hyduk S J,Cybulsky MI Role of alpha4betal integrins in chemokine-induced monocyte arrest under conditions of shear stress[J].Microcirculation,2009,16(1):17-30.
30.Vemuganti R,Dempsey RJ,Bowen KY.Inhibition of intercellular adhesion molecule-1 protein expression by antisense oligonucleotides is neuroprotective after transient middle cerebra1 artery occlusion in rat[J].Stroke,2004,35:179-184.
31.Sanchez-Moreno C,Dashe JF,Scott T,et al.Decreased levels of plasma vitamin C and increased concentrations of inflammatory and oxidative stress markers after stroke[J].Stroke,2004,35:163-168.
32.Shyu KG,Chang H,Lin CC.Serum levels of ICAM-1 and E-selectin in patients with acute ischemic stroke[J].J Neurol,1997,244(2):90-93.
33.张丽慧,魏尔清.ICAM-1、VCAM-1在脑缺血损伤炎症机制中的作用及调控[J].中国药理学通报,2005,21(11):1281-1285.
34.Ginter E,Simko V.Statins:the drugs for the 21st century[J]? Bratisl Lek Listy,2009,110(10):664-668.
35.Nanchen D,Chiolero A,Cornuz J,et al.Cardiovascular risk estimation and eligibility for statins in primary prevention comparing different strategies[J].Am J Cardiol,2009,103(8):1089-1095.
36.Reiss AB,Wirkowski E.Statins in neurological disorders:mechanisms and therapeutic value.Scientific World Journal,2009,9:1242-1259.Paciaroni M,Bogousslavsky J.Statins and stroke prevention[J].Expert Rev Cardiovasc Ther,2009,7(10):1231-1243.
37.Pepine CJ.Residual risk for secondary ischemic events in patients with atherothrombotic disease:opportunity for future improvements in patient care[J].Ann Med,2010,42(1):19-35.
38.Cobble M,Bale B.Carotid intima-media thickness:knowledge and application to everyday practice[J].Postgrad Med,2010,122(1):10-18.
39.Coll B,Feinstein SB.Carotid intima-media thickness measurements:techniques and clinical relevance[J].Curr Atheroscler Rep,2008,10(5):444-450.
40.周 燕,毛 维,宣吉晴,等.颈动脉彩超检查对脑梗死患者的意义探讨[J].滨州医学院学报,2008,31(2):139-140.
41.Cho YP,Kwon TW,Kim GE.Sonographie appearance of a free floating atheromatous plaque in a patient with acute stroke[J].Clin Ultrasound,2002,30(5):317-321.
42.周传伟,程蕴琳,张洪慧,等.中老年TIA患者颈动脉粥样斑块防治策略分析[J].江苏医药,2008,34(2):185-186.
43.贾 伟,陈光辉.颈动脉粥样硬化易损性斑块的检测方法[J].国际脑血管病杂志,2006;14(2):132-136.
44.李子平,叶秀荣,赵红地,等.彩色多普勒超声检测老年人眼动脉和视网膜中央动膜血流[J].中华超声影像杂志,1999,8(1):31-32.
45.Tsubakimori S,Fukuda M.Color Doppler Imaging of the orbital vessels[J].Rinsho Byori,2007,55(2):170-178.
46.张屹辉,任卫东,唐 力.颈动脉狭窄致兔脑缺血时的眼动脉血流动力学改变[J].中华超声影像学杂志,2002,11(5):300-303.
47.Allan PL,Mowbrag PI,Lee A J,et al.Relationship between carotid intima media thickness and symptomatic and asymptomatic peripheral arterial disease[J].Stroke,1997,28(2):348-353.
48.Grobbee DE,Bots ML.Carotid artery intima-media thickness as an indicator of generalized atherosclerosis[J].J Intern Med,1994,236(5):567-573.
49.Zenteno-Castellanos MA,Santos-Franco JA,et al.Endovascular management of carotid atherosclerosis.Section Ⅰ:basic considerations and diagnostic elements[J].Gac Med Mex,2009,145(5):407-414.
50.GoUedge J,Greenbalgh RM,Davies AH.The symptomatic carotid plaque[J].Stroke,2000,31:774-781.
51.DeGraba TJ,Siren AL,Penix L,et al.Increased endothelial expression of intereellular adh esion molecule-1 in symptomatic versus asymptomatic human carotid atheroselerotic plaque[J].Stroke,1998,29:1405-1410.
52.Mocco J,Choudhri TF,Mack WJ,et al.Elevation of soluble intercellular adhesion molecule-1 levels in symptomatic and asymptomatic carotid atherosclerosis[J].Neurosurgery,2001,48:718-721.
53.Fazio S,Linton MF.The inflamed plaque:cytokine production and cellular cholesterol balance in the vessel wall[J].Am J Cardiol,2001,88(Suppl):12E-15E.
1.Lawson C,Wolf S.ICAM-1 signaling in endothelial cells[J].Pharmacol Rep,2009,61(1):22-32.
2.Muller WA.Mechanisms of transendothelial migration of leukocytes[J].Circ Res,2009,105(3):223-230.
3.Mestas J,Ley K.Monocyte-endothelial cell interactions in the development of atherosclerosis[J].Trends Cardiovasc Med,2008,18(6):228-232.
4.Gourdin MJ,Bree B,De Kock M.The impact of ischaemia-reperfusion on the blood vessel[J].Eur J Anaesthesiol,2009,26(7):537-547.
5.Haverslag R,Pasterkamp G,Hoefer IE.Targeting adhesion molecules in cardiovascular disorders[J].Cardiovasc Hematol Disord Drug Targets,2008,8(4): 252-260.
6. Selakovic V, Raicevic R, Radenovic L. Temporal patterns of soluble adhesion molecules in cerebrospinal fluid and plasma in patients with the acute brain infraction [J]. Dis Markers, 2009, 26(2): 65-74.
7. Castillo J, Alvarez-Sabin J, Martinez-Vila E, et al. Inflammation markers and prediction of post-stroke vascular disease recurrence: the MITICO study [J]. J Neurol, 2009, 256(2): 217- 224.
8. Wadas TM. Emerging inflammatory biomarkers with acute stroke [J]. Crit Care Nurs Clin North Am, 2009, 21(4): 493-505.
9. Mousa SA. Cell adhesion molecules: potential therapeutic & diagnostic implications [J]. Mol Biotechnol, 2008, 38(1): 33-40.
10. Tuttolomondo A, Di Sciacca R, Di Raimondo D, et al. Inflammation as a therapeutic target in acute ischemic stroke treatment [J]. Curr Top Med Chem, 2009, 9(14): 1240-1260.
11. Wassmann S, Laufs U, Baumer AT, et al. HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species [J]. Hypertension, 2001, 37(6): 1450-1457.
12. Kang BY, Mehta JL. Rosuvastatin attenuates Ang II-mediated cardiomyocyte hypertrophy via inhibition of LOX-1 [J]. J Cardiovasc Pharmacol Ther, 2009, 14(4): 283-291.
13. Westerink J, Visseren FL. Fluvastatin/fenofibrate vs. simvastatin/ezetimibe in patients with metabolic syndrome: different effects on LDL-profiles [J]. Eur J Clin Invest. 2010, 40(1): 87.
14. Fujita Y, Sawamura T. Oxidized LDL receptor LOX-1 [J]. Nippon Yakurigaku Zasshi,2009, 133(5): 295-296.
15.Namazi MR. Decreasing the expression of LFA-1 and ICAM-1 as well as hindering their interaction as the major mechanism for statin-induced neutrophil dysfunction [J]. Ann Thorac Surg, 2007, 84(6): 2137-2138.
16. Schroeter MR, Humboldt T, Schafer K, et al. Rosuvastatin reduces atherosclerotic lesions and promotes progenitor cell mobilisation and recruitment in apolipoprotein E knockout mice [J]. Atherosclerosis, 2009, 205(1): 63-73.
17. Ferri N, Granata A, Pirola C, et al. Fluvastatin synergistically improves the antiproliferative effect of everolimus on rat smooth muscle cells by altering p27Kipl/cyclin E expression [J]. Mol Pharmacol, 2008, 74(1): 144-153.
18. Libby P, Okamoto Y, Rocha VZ, et al. Inflammation in atherosclerosis: transition from theory to practice [J]. Circ J, 2010, 74(2): 213-220.
19. Fujiwara T, Saito S, Osanai T, et al. Decreased plasma and cardiac matrix metalloproteinase activities in patients with coronary artery disease and treated with pravastatin [J]. Eur J Pharmacol, 2008, 594(1-3):146-151.
20. Gonzalez-Diez M, Rodriguez C, Badimon L, et al. Prostacyclin induction by high-density lipoprotein (HDL) in vascular smooth muscle cells depends on sphingosine 1-phosphate receptors: effect of simvastatin [J]. Thromb Haemost, 2008, 100(l):119-126.
21. Hu XY, Ma YH, Wang C, et al. Effects of simvastatin on cigarette smoke extract induced tissue-type plasminogen activator and plasminogen activator inhibitor-1 expression in human umbilical vein endothelial cells [J]. Chin Med J (Engl), 2009, 122(19): 2380-1385.
22. Jimenez-Conde J, Biffi A, Rahman R, et al. Hyperlipidemia and reduced white matter hyperintensity volume in patients with ischemic stroke [J]. Stroke, 2010, 41(3): 437-442.
23. Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins [J]. Lancet, 2005, 366(9493): 1267- 1278.
24. Amarenco P, Bogousslavsky J, Callahan AS, et al. Design and baseline characteristics of the stroke prevention by aggressive reduction in cholesterol levels (SPARCL) study [J]. Cerebrovasc Dis, 2003, 16(4):389-395.
25. Amarenco P, Bogousslavsky J, Callahan A, et al. High-dose atorvastatin after stroke or transient ischemic attack [J]. N Engl J Med, 2006, 355(6): 549-559.
26. Ovbiagele B, Saver JL.Intensive statin therapy after stroke or transient ischemic attack: a SPARCLing success [J]? Stroke, 2007, 38(3): 1110-1112.
27. Amarenco P, Goldstein LB, Sillesen H, et al. Coronary heart disease risk in patients with stroke or transient ischemic attack and no known coronary heart disease: findings from the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial [J]. Stroke, 2010, 41(3): 426-430.
28. Vergouwen MD, de Haan RJ, Vermeulen M, et al. Statin treatment and the occurrence of hemorrhagic stroke in patients with a history of cerebrovascular disease [J]. Stroke, 2008, 39(2): 497-502.
29. Nassief A, Marsh JD. Statin therapy for stroke prevention [J]. Stroke, 2008, 39(3):1042-1048.
30.Preobrazhenskii DV,Sidorenko BA,Pataraia SA,et al.Hypercholesterolemia in men and women of various age.Part Ⅱ.The problem of efficacy and safety of statins[J].Kardiologiia,2007,47(11):75-85.
31.李明珠,徐敏,奚克敏.64-SCTA、MRA、DSA诊断脑血管狭窄对比研究[J].中国医疗设备,2009,24(7):138-140.
32.高源统,罗敏.李 阳,等.脑动脉狭窄的CTA和MRA及DSA对照分析[J].放射学实践,2009,24(3):255-259.
33.王婉春.颈动脉粥样硬化的超声诊断[J].中国当代医药,2009,6:66-67.
34.王亚红,刘丽文.脑梗死患者颈动脉粥样硬化斑块的超声表现[J].临床超声医学杂志,2008,10(4):277-278.
35.Stary HC,Chandler AB,Dinsmore RE,et al.A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis.A report form the Committee on Vascular Lesions of the Council Arteriosclerosis,American Heart Association[J].Arterioscler Thormb Vasc Biol,1995,15(9):1512-1531.
36.张 玮,王世民.颈动脉粥样硬化的超声诊断及其临床意义[J].国际脑血管病杂志,2006,14(2):128-131.
37.Hollander M,Hak AE,Koudstaal PJ,et al.Comparison between measures of atherosclerosis and risk of stroke:the Rotterdam Study[J].Stroke,2003,34(10):2367-2372.
38.Tilling K,Lawlor DA,Davey Smith G,et al.The relation between components of adult height and intimal-medial thickness in middle age:the Atherosclerosis Risk in Communities Study[J].Am J Epidemiol,2006,164(2):136-142.
39.Chambless LE,Folsom AR,Clegg LX,et al.Carotid wall thickness is predictive of incident clinical stroke:the Atherosclerosis Risk in Communities(ARIC) study [J].Am J Epidemiol,2000,151(5):478-487.
40.Cupini LM,Pasqualetti P,Diomedi M,et al.Carotid artery intima-media thickness and lacunar versus nonlacunar infarcts[J].Stroke,2002,33(3):689-694.
41.Tsivgoulis G,Vemmos K,Papamichael C,et al.Common carotid artery intima-media thickness and the risk of stroke recurrence[J].Stroke,2006,37(7):1913-1916.
42.Malik RK,Landis GS,Sundick S,et al.Predicting embolic potential during carotid angioplasty and stenting:analysis of captured particulate debris,ultrasound characteristics,and prior carotid endarterectomy[J].J Vasc Surg,2010,51(2):317-322.
43.穆玉明,韩伟,吴伟春,等.颈动脉结构及血流动力学变化与缺血性脑血管病的相关性研究[J].中国医学影像技术,2003,19(11):1499-1501.
44.赵 军,魏世辉.颈动脉狭窄致眼缺血性疾病初探[J].中国实用眼科杂志,2006,24(5):521-524.
45.黄品同,林苗,田新桥,等.超声造影对脑梗死患者颈动脉软斑块内新生血管的评价[J].中华超声影像学杂志,2007,16(12):1045-1047.
46.Seabra JC,Pedro LM,e Fernandes JF,et al.A 3-D ultrasound-based framework to characterize the echo morphology of carotid plaques[J].IEEE Trans Biomed Eng,2009,56(5):1442-1453.
2.李睿坤,李继锋,周晓莹,等.大蒜素对动脉粥样硬化小鼠血脂代谢的影响[J].中华临床医师杂志,2007,1(1):26-33.
3.Liebeskind DS.Aortic occlusion for cerebral ischemia:from theory to practice[J].Curr Cardiol Rep,2008,10(1):31-36.
4.林玲,罗燕,彭玉兰,等.彩色多普勒超声对脑梗死患者颈动脉病变的研究[J].中华老年心脑血管病杂志,2005,7(3):175-177.
5.Nanchen D,Chiolero A,Cornuz J,et al.Cardiovascular risk estimation and eligibility for statins in primary prevention comparing different strategies[J].Am J Cardiol,2009,103(8):1089-1095.
6.刘成华,肖兴花,杨树国,等.氟伐他汀对冠心病患者血脂及细胞黏附分子表达的影响[J].山东医药,2007,47(2):55-56.
7.钟伟济.氟伐他汀对不稳定性心绞痛患者血清细胞因子水平影响的研究[J].中山大学学报(医学科学版),2006,27(35):99-101.
8.Johnsen SH,Mathiesen EB.Carotid plaque compared with intima-media thickness as a predictor of coronary and cerebrovascular disease[J].Curr Cardiol Rep,2009,11(1):21-27.
9.简文豪,万小莉,王红,等.颅脑与外周血管超声诊断学[M].北京:科学技术文献出版社,2006:92.
10.Grohbee DE,Bots ML.Carotid-artery intima-media thickness as an indicator of generalized atherosclerosis[J].J Intern Med,1994,236(5):567-573.
11.中华神经科学会.各类脑血管疾病诊断要点[J].中华神经科杂志,1995,29(6):378-380.
12.Crouse JR,Happold GH,Kahl FR,et al.Evaluation of scoring system for extracranial carotid athrosclerosis extent with B-mode ultrasound[J].Stroke,1996,17(2):270.
13.Pullicino R Small deep infarcts diagnosed on computed tomography[J].Neurology,1980,30(10):1890-1896.
14.Petty GW,Brown RD JT,Whisnant IP,et al.Survival and recurrence after flint cerebral infarction:a population-based study in Rochester,Minnesota,1975through 1989[J].Neurology,1998,50:208-216.
15.黄静,陈越平.颈动脉粥样硬化患者斑块稳定性与血脂水平的相关性研究[J].西南军医,2008,10(4):15-16.
16.Ross R.Atherosclerosis-an inflammatory disease[J].N Engl J Med,1999,340(2):115.
17.Libby P,Ridker PM,Hansson GK,et al.Inflammation in atherosclerosis:from pathophysiology to practice[J].J Am Coll Cardiol,2009,54(23):2129-2138.
18.Nageh MF,Sandberg ET,Marotti KR,et al.Deficiency of inflammatory cell adhesion molecules protects against atherosclerosis in mice[J].Arterioscler Thromb Vasc Biol,1997,17:1517-1520.
19.Rothlein K,Dustin ML,Marlin SD,et al.A human intercellular adhesion molecule:(ICAM-1) distinct from LFA-1[J].Immunol,1986,137:1270-1274.
20.Lawson C,Wolf S.ICAM-1 signaling in endothelial cells[J].Pharmacol Rep,2009,61(1):22-32.
21.Muller WA.Mechanisms of transendothelial migration of leukocytes[J].Circ Res,2009,105(3):223-230.
22.Galkina E,Ley K.Leukocyte influx in atherosclerosis[J].Curr Drug Targets,2007,8(12):1239-1248.
23.Balciunas M,Bagdonaite L,Samalavicius R,et al.Markers of endothelial dysfunction after cardiac surgery:soluble forms of vascular-1 and intercellular-1adhesion molecules[J].Medicina,2009,45(6):434-439.
24.Boldt J,Kumle B,Papsdorf M,et al.Are circulating adhesion molecule specifically changed in cardiac surgical patient[J]?Ann Thoracic Surgery,1998,65:608.
25.Blankenberg S,Barbaux S,Tiret L.Adhesion molecules and atheroschresis[J].Atherosclerosis,2003,170:191-203.
26.Osbom L,Hsssion C,Tizard B,et al.Direct expression cloning of vascular cell adhesion molecule-1,a cytokine endothelial protein that binds to lymphocyes[J].Cell,1989,59:1023.
27.Frenette PS,Wanger DD.Adhesion molecules-part Ⅰ[J].N Engl J Med,1996,334:1526.
28.Iademarco MF,Barks JF,Dean DC,et al.Regulation of vascular cell adhesion molecule-1 expression by IL- 4 and TNF-alpha in cultured endothelial cells[J].J Clin Incest,1995,95:264.
29.Hyduk S J,Cybulsky MI Role of alpha4betal integrins in chemokine-induced monocyte arrest under conditions of shear stress[J].Microcirculation,2009,16(1):17-30.
30.Vemuganti R,Dempsey RJ,Bowen KY.Inhibition of intercellular adhesion molecule-1 protein expression by antisense oligonucleotides is neuroprotective after transient middle cerebra1 artery occlusion in rat[J].Stroke,2004,35:179-184.
31.Sanchez-Moreno C,Dashe JF,Scott T,et al.Decreased levels of plasma vitamin C and increased concentrations of inflammatory and oxidative stress markers after stroke[J].Stroke,2004,35:163-168.
32.Shyu KG,Chang H,Lin CC.Serum levels of ICAM-1 and E-selectin in patients with acute ischemic stroke[J].J Neurol,1997,244(2):90-93.
33.张丽慧,魏尔清.ICAM-1、VCAM-1在脑缺血损伤炎症机制中的作用及调控[J].中国药理学通报,2005,21(11):1281-1285.
34.Ginter E,Simko V.Statins:the drugs for the 21st century[J]? Bratisl Lek Listy,2009,110(10):664-668.
35.Nanchen D,Chiolero A,Cornuz J,et al.Cardiovascular risk estimation and eligibility for statins in primary prevention comparing different strategies[J].Am J Cardiol,2009,103(8):1089-1095.
36.Reiss AB,Wirkowski E.Statins in neurological disorders:mechanisms and therapeutic value.Scientific World Journal,2009,9:1242-1259.Paciaroni M,Bogousslavsky J.Statins and stroke prevention[J].Expert Rev Cardiovasc Ther,2009,7(10):1231-1243.
37.Pepine CJ.Residual risk for secondary ischemic events in patients with atherothrombotic disease:opportunity for future improvements in patient care[J].Ann Med,2010,42(1):19-35.
38.Cobble M,Bale B.Carotid intima-media thickness:knowledge and application to everyday practice[J].Postgrad Med,2010,122(1):10-18.
39.Coll B,Feinstein SB.Carotid intima-media thickness measurements:techniques and clinical relevance[J].Curr Atheroscler Rep,2008,10(5):444-450.
40.周 燕,毛 维,宣吉晴,等.颈动脉彩超检查对脑梗死患者的意义探讨[J].滨州医学院学报,2008,31(2):139-140.
41.Cho YP,Kwon TW,Kim GE.Sonographie appearance of a free floating atheromatous plaque in a patient with acute stroke[J].Clin Ultrasound,2002,30(5):317-321.
42.周传伟,程蕴琳,张洪慧,等.中老年TIA患者颈动脉粥样斑块防治策略分析[J].江苏医药,2008,34(2):185-186.
43.贾 伟,陈光辉.颈动脉粥样硬化易损性斑块的检测方法[J].国际脑血管病杂志,2006;14(2):132-136.
44.李子平,叶秀荣,赵红地,等.彩色多普勒超声检测老年人眼动脉和视网膜中央动膜血流[J].中华超声影像杂志,1999,8(1):31-32.
45.Tsubakimori S,Fukuda M.Color Doppler Imaging of the orbital vessels[J].Rinsho Byori,2007,55(2):170-178.
46.张屹辉,任卫东,唐 力.颈动脉狭窄致兔脑缺血时的眼动脉血流动力学改变[J].中华超声影像学杂志,2002,11(5):300-303.
47.Allan PL,Mowbrag PI,Lee A J,et al.Relationship between carotid intima media thickness and symptomatic and asymptomatic peripheral arterial disease[J].Stroke,1997,28(2):348-353.
48.Grobbee DE,Bots ML.Carotid artery intima-media thickness as an indicator of generalized atherosclerosis[J].J Intern Med,1994,236(5):567-573.
49.Zenteno-Castellanos MA,Santos-Franco JA,et al.Endovascular management of carotid atherosclerosis.Section Ⅰ:basic considerations and diagnostic elements[J].Gac Med Mex,2009,145(5):407-414.
50.GoUedge J,Greenbalgh RM,Davies AH.The symptomatic carotid plaque[J].Stroke,2000,31:774-781.
51.DeGraba TJ,Siren AL,Penix L,et al.Increased endothelial expression of intereellular adh esion molecule-1 in symptomatic versus asymptomatic human carotid atheroselerotic plaque[J].Stroke,1998,29:1405-1410.
52.Mocco J,Choudhri TF,Mack WJ,et al.Elevation of soluble intercellular adhesion molecule-1 levels in symptomatic and asymptomatic carotid atherosclerosis[J].Neurosurgery,2001,48:718-721.
53.Fazio S,Linton MF.The inflamed plaque:cytokine production and cellular cholesterol balance in the vessel wall[J].Am J Cardiol,2001,88(Suppl):12E-15E.
1.Lawson C,Wolf S.ICAM-1 signaling in endothelial cells[J].Pharmacol Rep,2009,61(1):22-32.
2.Muller WA.Mechanisms of transendothelial migration of leukocytes[J].Circ Res,2009,105(3):223-230.
3.Mestas J,Ley K.Monocyte-endothelial cell interactions in the development of atherosclerosis[J].Trends Cardiovasc Med,2008,18(6):228-232.
4.Gourdin MJ,Bree B,De Kock M.The impact of ischaemia-reperfusion on the blood vessel[J].Eur J Anaesthesiol,2009,26(7):537-547.
5.Haverslag R,Pasterkamp G,Hoefer IE.Targeting adhesion molecules in cardiovascular disorders[J].Cardiovasc Hematol Disord Drug Targets,2008,8(4): 252-260.
6. Selakovic V, Raicevic R, Radenovic L. Temporal patterns of soluble adhesion molecules in cerebrospinal fluid and plasma in patients with the acute brain infraction [J]. Dis Markers, 2009, 26(2): 65-74.
7. Castillo J, Alvarez-Sabin J, Martinez-Vila E, et al. Inflammation markers and prediction of post-stroke vascular disease recurrence: the MITICO study [J]. J Neurol, 2009, 256(2): 217- 224.
8. Wadas TM. Emerging inflammatory biomarkers with acute stroke [J]. Crit Care Nurs Clin North Am, 2009, 21(4): 493-505.
9. Mousa SA. Cell adhesion molecules: potential therapeutic & diagnostic implications [J]. Mol Biotechnol, 2008, 38(1): 33-40.
10. Tuttolomondo A, Di Sciacca R, Di Raimondo D, et al. Inflammation as a therapeutic target in acute ischemic stroke treatment [J]. Curr Top Med Chem, 2009, 9(14): 1240-1260.
11. Wassmann S, Laufs U, Baumer AT, et al. HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species [J]. Hypertension, 2001, 37(6): 1450-1457.
12. Kang BY, Mehta JL. Rosuvastatin attenuates Ang II-mediated cardiomyocyte hypertrophy via inhibition of LOX-1 [J]. J Cardiovasc Pharmacol Ther, 2009, 14(4): 283-291.
13. Westerink J, Visseren FL. Fluvastatin/fenofibrate vs. simvastatin/ezetimibe in patients with metabolic syndrome: different effects on LDL-profiles [J]. Eur J Clin Invest. 2010, 40(1): 87.
14. Fujita Y, Sawamura T. Oxidized LDL receptor LOX-1 [J]. Nippon Yakurigaku Zasshi,2009, 133(5): 295-296.
15.Namazi MR. Decreasing the expression of LFA-1 and ICAM-1 as well as hindering their interaction as the major mechanism for statin-induced neutrophil dysfunction [J]. Ann Thorac Surg, 2007, 84(6): 2137-2138.
16. Schroeter MR, Humboldt T, Schafer K, et al. Rosuvastatin reduces atherosclerotic lesions and promotes progenitor cell mobilisation and recruitment in apolipoprotein E knockout mice [J]. Atherosclerosis, 2009, 205(1): 63-73.
17. Ferri N, Granata A, Pirola C, et al. Fluvastatin synergistically improves the antiproliferative effect of everolimus on rat smooth muscle cells by altering p27Kipl/cyclin E expression [J]. Mol Pharmacol, 2008, 74(1): 144-153.
18. Libby P, Okamoto Y, Rocha VZ, et al. Inflammation in atherosclerosis: transition from theory to practice [J]. Circ J, 2010, 74(2): 213-220.
19. Fujiwara T, Saito S, Osanai T, et al. Decreased plasma and cardiac matrix metalloproteinase activities in patients with coronary artery disease and treated with pravastatin [J]. Eur J Pharmacol, 2008, 594(1-3):146-151.
20. Gonzalez-Diez M, Rodriguez C, Badimon L, et al. Prostacyclin induction by high-density lipoprotein (HDL) in vascular smooth muscle cells depends on sphingosine 1-phosphate receptors: effect of simvastatin [J]. Thromb Haemost, 2008, 100(l):119-126.
21. Hu XY, Ma YH, Wang C, et al. Effects of simvastatin on cigarette smoke extract induced tissue-type plasminogen activator and plasminogen activator inhibitor-1 expression in human umbilical vein endothelial cells [J]. Chin Med J (Engl), 2009, 122(19): 2380-1385.
22. Jimenez-Conde J, Biffi A, Rahman R, et al. Hyperlipidemia and reduced white matter hyperintensity volume in patients with ischemic stroke [J]. Stroke, 2010, 41(3): 437-442.
23. Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins [J]. Lancet, 2005, 366(9493): 1267- 1278.
24. Amarenco P, Bogousslavsky J, Callahan AS, et al. Design and baseline characteristics of the stroke prevention by aggressive reduction in cholesterol levels (SPARCL) study [J]. Cerebrovasc Dis, 2003, 16(4):389-395.
25. Amarenco P, Bogousslavsky J, Callahan A, et al. High-dose atorvastatin after stroke or transient ischemic attack [J]. N Engl J Med, 2006, 355(6): 549-559.
26. Ovbiagele B, Saver JL.Intensive statin therapy after stroke or transient ischemic attack: a SPARCLing success [J]? Stroke, 2007, 38(3): 1110-1112.
27. Amarenco P, Goldstein LB, Sillesen H, et al. Coronary heart disease risk in patients with stroke or transient ischemic attack and no known coronary heart disease: findings from the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial [J]. Stroke, 2010, 41(3): 426-430.
28. Vergouwen MD, de Haan RJ, Vermeulen M, et al. Statin treatment and the occurrence of hemorrhagic stroke in patients with a history of cerebrovascular disease [J]. Stroke, 2008, 39(2): 497-502.
29. Nassief A, Marsh JD. Statin therapy for stroke prevention [J]. Stroke, 2008, 39(3):1042-1048.
30.Preobrazhenskii DV,Sidorenko BA,Pataraia SA,et al.Hypercholesterolemia in men and women of various age.Part Ⅱ.The problem of efficacy and safety of statins[J].Kardiologiia,2007,47(11):75-85.
31.李明珠,徐敏,奚克敏.64-SCTA、MRA、DSA诊断脑血管狭窄对比研究[J].中国医疗设备,2009,24(7):138-140.
32.高源统,罗敏.李 阳,等.脑动脉狭窄的CTA和MRA及DSA对照分析[J].放射学实践,2009,24(3):255-259.
33.王婉春.颈动脉粥样硬化的超声诊断[J].中国当代医药,2009,6:66-67.
34.王亚红,刘丽文.脑梗死患者颈动脉粥样硬化斑块的超声表现[J].临床超声医学杂志,2008,10(4):277-278.
35.Stary HC,Chandler AB,Dinsmore RE,et al.A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis.A report form the Committee on Vascular Lesions of the Council Arteriosclerosis,American Heart Association[J].Arterioscler Thormb Vasc Biol,1995,15(9):1512-1531.
36.张 玮,王世民.颈动脉粥样硬化的超声诊断及其临床意义[J].国际脑血管病杂志,2006,14(2):128-131.
37.Hollander M,Hak AE,Koudstaal PJ,et al.Comparison between measures of atherosclerosis and risk of stroke:the Rotterdam Study[J].Stroke,2003,34(10):2367-2372.
38.Tilling K,Lawlor DA,Davey Smith G,et al.The relation between components of adult height and intimal-medial thickness in middle age:the Atherosclerosis Risk in Communities Study[J].Am J Epidemiol,2006,164(2):136-142.
39.Chambless LE,Folsom AR,Clegg LX,et al.Carotid wall thickness is predictive of incident clinical stroke:the Atherosclerosis Risk in Communities(ARIC) study [J].Am J Epidemiol,2000,151(5):478-487.
40.Cupini LM,Pasqualetti P,Diomedi M,et al.Carotid artery intima-media thickness and lacunar versus nonlacunar infarcts[J].Stroke,2002,33(3):689-694.
41.Tsivgoulis G,Vemmos K,Papamichael C,et al.Common carotid artery intima-media thickness and the risk of stroke recurrence[J].Stroke,2006,37(7):1913-1916.
42.Malik RK,Landis GS,Sundick S,et al.Predicting embolic potential during carotid angioplasty and stenting:analysis of captured particulate debris,ultrasound characteristics,and prior carotid endarterectomy[J].J Vasc Surg,2010,51(2):317-322.
43.穆玉明,韩伟,吴伟春,等.颈动脉结构及血流动力学变化与缺血性脑血管病的相关性研究[J].中国医学影像技术,2003,19(11):1499-1501.
44.赵 军,魏世辉.颈动脉狭窄致眼缺血性疾病初探[J].中国实用眼科杂志,2006,24(5):521-524.
45.黄品同,林苗,田新桥,等.超声造影对脑梗死患者颈动脉软斑块内新生血管的评价[J].中华超声影像学杂志,2007,16(12):1045-1047.
46.Seabra JC,Pedro LM,e Fernandes JF,et al.A 3-D ultrasound-based framework to characterize the echo morphology of carotid plaques[J].IEEE Trans Biomed Eng,2009,56(5):1442-1453.