颈动脉斑块灰阶中位数、斑块总体积及其比值Q与缺血性脑梗死的相关性研究

目的应用三维超声测量颈动脉斑块的灰阶中位数(GSM)和斑块总体积(TPV),分析GSM、TPV及二者比值(Q)与缺血性脑梗死发生的相关性。方法随机选取颈动脉斑块患者107例,根据其颅脑CT和MRI检查结果,将颈动脉斑块与脑梗死发生部位为同侧者66例判定为脑梗死组(A组),将颈动脉斑块与脑梗死发生部位为异侧者41例判定为非脑梗死组(B组)。两组患者均行三维超声检查,应用QLAB-VPQ软件获取GSM和TPV,并计算其比值Q,分析GSM、TPV及Q值与缺血性脑梗死的相关性。绘制ROC曲线比较GSM、TPV及Q值诊断缺血性脑梗死的曲线下面积和95%可信区间。结果 A、B组GSM、TPV及Q值行Wilcoxon秩和检验,差异均有统计学意义(Z=-1.644、-4.515、-4.857,P=0.032、0.043、0.000)。非条件Logistic回归分析显示,GSM的OR值为1.078(1.024~1.135),TPV的OR值为1.037(1.019~1.056),Q值的OR值为1.015(1.007~1.024)。ROC曲线显示GSM诊断缺血性脑梗死的曲线下面积为0.812,95%可信区间0.729~0.894(P=0.000);TPV诊断缺血性脑梗死的曲线下面积为0.806,95%可信区间0.729~0.891(P=0.000);Q值诊断缺血性脑梗死的曲线下面积为0.821,95%可信区间0.743~0.899(P=0.000)。结论 GSM、TPV及Q值均与缺血性脑梗死的发生具有一定相关性,Q值的诊断价值最高。     

三维超声斑块定量参数评估颈动脉斑块患者脑卒中风险的价值研究

目的 探讨三维超声斑块定量参数在评估颈动脉斑块患者脑卒中风险中的应用价值。方法 选择134例存在颈动脉斑块患者,所有患者均接受三维超声检查,并获取斑块定量参数;根据缺血性脑卒中诊断标准,将63例发生缺血性脑卒中的患者归为脑卒中组,将仅存在颈动脉斑块而未发生脑卒中的71例患者归为对照组,比较两组临床资料和三维超声斑块定量参数,分析颈动脉斑块患者缺血性脑卒中的危险因素和三维超声斑块定量参数评估脑卒中风险的价值。结果 脑卒中组患者斑块体积、斑块厚度明显高于对照组（t分别=3.02、2.83,P均<0.05）,脑卒中组患者灰阶中位数（GSM）均明显低于对照组（t=-9.23,P<0.05）。年龄、吸烟史、斑块性质、低密度脂蛋白胆固醇（LDL-C）、斑块体积、斑块厚度、GSM值是颈动脉斑块患者发生缺血性脑卒中的影响因素（OR分别=1.08、1.05、1.21、1.26、2.92、1.27、0.98,P均<0.05）;斑块体积、斑块厚度、GSM预测颈动脉斑块脑卒中风险的曲线下面积分别为0.64、0.67、0.80,GSM值的诊断价值最高。结论 三维超声斑块定量参数GSM值与颈动脉...     

三维超声灰阶中位数联合同型半胱氨酸及脂蛋白a评估缺血性脑卒中风险

目的 探讨三维超声灰阶中位数(GSM)评估颈动脉斑块易损性的价值及3D-US GSM联合同型半胱氨酸、脂蛋白a评估脑卒中风险的价值。方法 (1)选取接受颈动脉内膜剥脱术(CEA)获得病理结果的患者，3D-US计算GSM值，根据病理结果将斑块分成易损斑块组及不易损斑块组，对比分析斑块GSM值在组间差异；(2)追踪同型半胱氨酸、脂蛋白a数据；(3)通过Pearson双变量相关性分析方法，分析GSM与同型半胱氨酸、GSM与脂蛋白a的相关性；(4)GSM联合同型半胱氨酸、脂蛋白a评估脑卒中风险，计算灵敏度及特异度。结果 (1)39例患者GSM值16.20～62.33,平均值44.03±10.75,其中33例不稳定斑块组GSM值36.69±12.47,6例稳定斑块组GSM值53.44±10.39,两组比较采用独立样本t检验，P<0.01,差异有统计学意义。(2)同型半胱氨酸值(15.57±10.86)μmol/L,脂蛋白a值(316.49±107.93)mg/L。(3)GSM与同型半胱氨酸、GSM与脂蛋白a比较相关性系数，P<0.05,两者相关性均有统计学意义。(4)GSM对易损性斑...     

超声检测视神经鞘直径预测缺血性脑卒中不良事件的临床价值

目的 探讨超声检测视神经鞘直径（ONSD）预测缺血性脑卒不良事件中的临床价值。方法 选取我院收治的38例缺血性脑卒中患者，根据治疗后是否发生不良事件分为不良事件组8例和对照组30例，应用超声检测OSND,MRI获取斑块特征，包括偏心指数、斑块面积、斑块长度及强化幅度，比较两组上述指标的差异。应用Logistic回归分析缺血性脑卒中患者不良事件的危险因素。绘制受试者工作特征（ROC）曲线分析ONSD和斑块特征对缺血性脑卒中患者不良事件的预测价值。结果 不良事件组ONSD、偏心指数、斑块面积、斑块长度、强化幅度均高于对照组，差异均有统计学意义（均P<0.05）。Logistic回归分析显示，ONSD、偏心指数、斑块面积、斑块长度、强化幅度均为缺血性脑卒中患者不良事件的危险因素（均P<0.05）。ROC曲线分析显示，ONSD、偏心指数、斑块面积、斑块长度、强化幅度预测缺血性脑卒中患者不良事件的曲线下面积（AUC）分别为0.894、0842、0.708、0.746、0.738，除偏心指数外，ONSD的AUC与其余斑块特征比较差异均有统计学意义（均P<0.05）。结论 超声检测...     

超声造影评级联合血同型半胱氨酸对动脉硬化型缺血性脑卒中发生的相关研究

目的探讨颈动脉斑块超声造影评级和血同型半胱氨酸(Hcy)与动脉硬化型缺血性脑卒中的相关性。方法选择2013年10月至2014年7月宁波市第二医院神经内科患者159例,根据中国缺血性脑卒中诊断标准及改良TOAST分型,选择其中动脉硬化型缺血性脑卒中及非缺血性脑卒中患者,分别进入A组和B组,其中A组72例,B组76例。所有患者均进行颈动脉斑块超声造影评级和血Hcy检测,分别采用Spearman相关性检验和Pearson相关性检验分析颈动脉斑块超声造影评级、血Hcy水平与动脉硬化型缺血性脑卒中发生的相关性。结果 (1)A、B组斑块厚度和斑块类型之间比较,差异无统计学意义(F=0.865、0.827,P值均0.05),超声造影评级之间比较,差异具有统计学意义(Z=192.350,P0.01),以超声造影评级≥3级作为预测发生动脉硬化型缺血性脑卒中的诊断标准,则其敏感度和特异度分别为94.44%、94.74%;(2)A、B组患者间血Hcy水平比较,差异具有统计学意义(t=152.383,P0.01),ROC曲线下面积为0.978,以血Hcy≥13.50μmol/L作为诊断标准,预测动脉硬化型缺血性脑卒中发生的敏感度、特异度分别为97.21%、90.80%;(3)以颈动脉斑块超声造影评级≥3级或血Hcy≥13.50μmol/L作为诊断标准预测颈动脉粥样硬化性缺血性脑卒中发生的敏感度、特异度分别为98.71%、96.45%;(4)颈动脉斑块超声造影评级、血Hcy水平与颈动脉粥样硬化性缺血性脑卒中之间存在高度线性正相关(r=0.865、0.827,P值均0.01)。结论颈动脉斑块超声造影评级和血同型半胱氨酸可作为动脉硬化型缺血性脑卒中的重要检查手段,为临床二级预防提供重要信息。     

高血压病与颈动脉粥样硬化斑块的关系

目的：采用颈动脉彩色多普勒超声观察高血压患者颈动脉粥样硬化的变化,探讨颈动脉粥样硬化斑块与高血压病的关系。方法：超声检测１４２例高血压患者的双侧颈动脉,高血压病可分为如下三组：①单纯高血压组（ＥＨ）;②高血压伴心肌梗塞组（ＥＨＭ）;③高血压伴缺血性脑卒中组（ＥＨＳ）。检测结果并与５１名健康者作对比。结果：高血压病患者的斑块检出率、斑块面积、斑块指数和斑块积分均明显高于对照组,以伴心肌梗塞和缺血性脑     

颈动脉斑块与缺血性脑血管病的相关性

目的应用超声方法检测颈动脉斑块情况,探讨颈动脉斑块与缺血性脑血管病的相关性,评价超声检测颈动脉斑块对缺血性脑血管病的预测价值及其性质意义。方法对115例颈内动脉粥样硬化缺血性脑血管病患者,进行颈动脉斑块情况的超声检查,并对各组病例颈动脉斑块的情况进行比较,进行统计学分析,探讨颈动脉斑块与缺血性脑血管病的相关性。结果超声检查颈动脉粥样硬化斑块检出率为81.7%（94例）,颈动脉中重度狭窄发生率为7.8%（9例）,缺血侧颈动脉斑块发生率67.7%（其中软斑发生率33.1%）高于非缺侧48.5%（其中软斑发生率20.4%）,两组比较差异有统计学意义（P〈0.05）。斑块组发生高血压病的比例85.1%明显高于无斑块组的57.1%（P〈0.05）。结论高血压病在斑块发生、发展中起重要作用,缺血性脑血管病患者,颈动脉粥样硬化以斑块居多,不稳定的软斑及溃疡斑为重要危险因素。多因素分析表明,年龄、甘油三酯、总胆固醇和低密度脂蛋白影响颈动脉斑块形成,而性别、烟酒史可能会影响斑块的稳定性。     

急性缺血性脑卒中患者血浆Lp-PLA2水平与颈动脉硬化斑块稳定性及神经功能缺损程度的关系

目的探讨血浆脂蛋白相关磷脂酶A2（Lp—PLA2）水平与急性缺血性脑卒中患者颈动脉粥样硬化斑块稳定性及神经功能缺损程度的关系。方法将106例急性缺血性脑卒中患者根据颈动脉彩超检查分为不稳定斑块组（44例）、稳定型斑块组（38例）和无斑块组（24例）,以40名健康体检者作为正常对照组,采用酶联免疫吸附试验（ELISA）测定血浆Lp—PLA2水平。所有患者按美国国立卫生研究所中风量表（NIHSS评分）进行神经功能缺损程度评估。结果急性缺血性脑卒中患者Lp—PLA2水平明显高于正常对照组（Z=-6．995,P〈0．05）;无斑块组、稳定型斑块组和不稳定斑块组Lp—PLA2水平依次升高,且无斑块组与有斑块组比较差异有统计学意义（Z=-5．670,P〈0．05）,稳定型斑块组和不稳定斑块组比较差异有统计学意义（Z=-6．185,P〈0．05）。受试者工作特征（ROC）曲线显示Lp—PLA2评估急性缺血性脑卒中患者斑块稳定性的最佳截断值为137．00μg/L,灵敏度为81．8％,特异性为95．1％。神经功能缺损程度随Lp．PLA2水平的增加呈递增趋势,差异有统计学意义（x^2=74．233,P〈0．05）。血浆Lp—PLA2水平与NIHSS评分呈明显正相关（0=0．861,P〈0．05）。结论急性缺血性脑卒中患者Lp—PLA2水平与颈动脉粥样硬化斑块稳定性和神经功能缺损程度有关,血浆Lp—PLA2水平可预测斑块稳定性,同时对急性缺血性脑卒中患者的病情监测有重要价值。     

老年2型糖尿病并发缺血性脑卒中与颈动脉内膜中层厚度及视网膜病变的相关性研究

【目的】探讨老年2型糖尿病（T2DM）并发缺血性脑卒中与颈动脉狭窄及视网膜病变程度的相关性。【方法】老年T2DM 患者161例,并发脑卒中58例（脑卒中组）,非脑卒中103例（非脑卒中组）。超声检测两组患者颈动脉内膜中层厚度（IMT）,并行眼底检查。【结果】两组患者颈动脉粥样硬化斑块发生部位多见于颈总动脉近分叉处,脑卒中组颈动脉不稳定性斑块的检出率、颈动脉 IMT值显著高于非脑卒中组（P＜0．05）,且脑卒中组单纯型糖尿病视网膜病变（NPDR）及增殖型糖尿病视网膜病变（PDR）患者 IMT值、颈动脉不稳定斑块数检出率均显著高于非脑卒中组（P＜0．05）;相关性分析显示 IMT与眼底病变程度显著相关（r＝0．5509,P ＜0．05）。【结论】颈动脉 IMT和视网膜病变程度与老年T2DM并发缺血性脑卒中存在相关性。     

缺血性脑卒中患者颈动脉粥样斑块发生与踝肱指数相关性研究

目的：探讨缺血性脑卒中患者颈动脉粥样斑块发生与踝肱指数的相关性。方法对236例缺血性脑卒中患者（观察组）和260名健康人（对照组）应用彩色多普勒超声检测颈部血管内中膜厚度及斑块形成情况,使用多普勒超声仪测量踝肱指数,并分析踝肱指数与颈动脉粥样硬化的程度和稳定性的相关性。结果236例观察组患者中,检出颈动脉粥样硬化斑块183例（77．5％）,对照组为60例（23．1％）,缺血性脑卒中颈动脉粥样硬化斑块发生率明显高于对照组（P ＜0．01）。观察组22例踝肱指数异常,发生率为9．3％;对照组有 6例踝肱指数异常,发生率为2．3％,2组比较差异有统计学意义（P ＜0．01）。缺血性脑卒中患者颈动脉内膜增厚组踝肱指数明显低于正常组,颈动脉内膜斑块形成组患者的踝肱指数明显低于增厚组（P ＜0．05）,颈动脉内膜不稳定斑块组踝肱指数明显低于稳定斑块组（P ＜0．05）。Logistic 回归分析显示颈动脉粥样硬化斑块、踝肱指数与缺血性脑卒中明显相关（OR 分别为1．118、0．054,P 均＜0．05）。结论颈动脉粥样硬化与缺血性脑卒中有关,踝肱指数可作为预测缺血性脑卒中发生的指标之一。     

Exploration of the atherosclerotic plaque

During the past 3 decades we have achieved a better understanding of the atherosclerotic process. It has been described as a series of changes in the intima of arteries consisting of the focal accumulation of lipids, complex carbohydrates, blood and blood products, fibrous tissues, and calcium that are also associated with changes in the media. The process begins with a vascular injury that is complicated by the deposition of cholesterol esters and cholesterol. It is followed by the accumulation of lipid ladened monocytes as well as the initiation of immune mechanisms. The proliferation of smooth muscle cells into the lesion assures its permanence by the synthesis of fibrous tissue. Platelet aggregation, thrombosis and hemorrhage are all key components of plaque progression, that ultimately are associated with vascular occlusion and focal vascular spasm. Calcium plays an important role in the development of hard, ulcerated lesions. Atherosclerotic risk factors are believed to accelerate the progression of atherosclerotic plaques and the control of these risk factors may retard their proliferation and progression.     

Aortic plaque imaging and monitoring atherosclerotic plaque interventions

The atherosclerotic process that results in coronary artery disease (CAD) is recognized to be a generalized process that may involve the entire vasculature. The association between CAD and atherosclerotic plaques in the thoracic aorta has often been reported using transesophageal echocardiography. An autopsy study showed plaques in the abdominal aorta, but not in the thoracic aorta, to be severe in patients with cardiac events. However, studies evaluating an association between abdominal aortic plaques and CAD are scarce. Recently, magnetic resonance imaging (MRI) has become a useful tool for the noninvasive evaluation of atherosclerotic plaques in both the thoracic and abdominal aortas. Plaques in the thoracic and abdominal aortas were found to be characteristically associated with hypercholesterolemia and smoking, respectively, suggesting different susceptibilities to risk factors. Because patients have various risk factors, it seems to be preferable to evaluate atherosclerosis in multiple vascular beds than in just 1 bed. Magnetic resonance imaging can evaluate atherosclerosis in multiple vascular beds in the same examination session. Complex aortic plaques, especially in the abdominal aorta, were found to be associated with myocardial infarction and complex coronary lesions, suggesting a link between aortic and coronary plaque instability. Aortic MRI may thus be useful for identifying vulnerable patients. Moreover, MRI is a powerful tool to serially evaluate plaque progression and regression. Intensive lipid-lowering therapy can regress aortic plaques, but the susceptibility to lipid lowering and the process of plaque regression may differ between the thoracic and abdominal aortic plaques.     

超声造影成像技术评价颈动脉斑块内新生血管与斑块声学特性的关系

目的本研究应用超声造影成像技术评价颈动脉斑块内新生血管与斑块声学特性的关系。方法104例伴颈动脉粥样斑块患者行颈动脉常规及超声造影检查,通过肉眼观测及定量分析斑块造影增强情况。结果软斑造影增强比例明显高于其他类型斑块（P〈0.001）;软斑的增强强度明显高于其他类型斑块（P〈0.001）;软斑的斑块增强强度与颈动脉管腔内造影增强强度比值也高于其他类型斑块（P〈0.001）。结论研究表明软斑造影增强显著高于其他类型斑块。超声造影技术为评价斑块内新生血管特点及其与斑块声学特性的关系提供了新方法。     

Collagenases and cracks in the plaque

The core of an atheromatous plaque contains lipids, macrophages, and cellular debris, typically covered by a fibrous cap that separates the thrombogenic core from the blood. Rupture of the fibrous cap causes most fatal myocardial infarctions. Interstitial collagen confers tensile strength on the cap, as it does in skin and tendons. In 1994, Peter Libby and colleagues demonstrated overexpression of collagenolytic enzymes in atheromatous plaques and implicated MMPs in the destabilization of these lesions.The formation of plaques within the arterial intima characterizes atherosclerosis. Plaques typically consist of a lipid core covered by a fibrous cap rich in extracellular matrix, produced largely by arterial smooth muscle cells (Figure ​(Figure1A).1A). Most fatal myocardial infarctions result from a fracture in the plaque’s fibrous cap (1). The fibrous cap derives tensile strength from interstitial collagen, as do skin and sinew. Twenty years ago, my colleagues and I proposed the hypothesis that excessive collagen catabolism could weaken the fibrous cap and thus render plaques prone to rupture (2). Our laboratory, focused on inflammatory signaling in vascular biology and atherogenesis, tested whether inflammatory mediators could elicit overexpression of interstitial collagenases — enzymes that catalyze the first step in collagen catabolism (Figure ​(Figure11B). Open in a separate windowFigure 1Regulation of collagen metabolism and the thrombotic complications of atherosclerosis.(A) A cross section of an artery containing a thin-capped atheroma with low collagen content due to decreased synthesis and increased breakdown of collagen is shown. A thin and weakened fibrous cap overlies a lipid-rich core in the center of the plaque (left). A plaque in which the fibrous cap has ruptured, exposing the blood coagulation components to thrombogenic material in the lipid core, triggering thrombosis, is also shown (right). (B) Lipid-laden macrophages in atherosclerotic plaques express MMPs. Various extracellular stimuli, including reactive oxygen species, plasmin, and thrombin, contribute to enzymatic activation of these enzymes that is required for their proteolytic activity. Macrophages in human plaques overexpress the three known MMP interstitial collagenases, MMP-1, MMP-8, and MMP-13. The endogenous inhibitors of this family of enzymes, the tissue inhibitors of MMPs (TIMPs), do not change markedly between unaffected and atherosclerotic arteries. The MMP interstitial collagenases catalyze the initial proteolytic cleavage of intact triple helical fibrillar collagen.