颈动脉斑块内新生血管显影程度及血浆Lp-PLA2在急性脑梗死的临床诊断价值

发布时间：2019-04-27 17:54

【摘要】：研究背景脑血管病变在全球的发病率和死亡率较高[1],尤其是其高的致残率和致死率给人类及社会带来极大的危害。急性脑梗死又称缺血性脑梗死,是临床常见病、多发病,大量研究表明其主要的病理学基础是动脉粥样硬化(Atherosc1erosis,AS)[2],动脉粥样硬化性脑梗死占缺血性脑梗死患病率的74%[3]。颈动脉硬化是全身动脉硬化的局部表现。斑块内出血、斑块破裂、血栓形成、动脉瘤形成等是颈动脉斑块继发性改变。颈动脉作为脑血循环的上游血管,其内不稳定斑块的破裂、脱落造成的动脉到动脉栓塞是缺血性脑梗死的独立危险因素[4]。血浆脂蛋白相关磷脂酶 A2(Lipoprotein-associated Phospholipase A2,Lp-PLA2)作为一种新的炎症反应标志物,受到越来越多的重视。近年来的研究认为AS是由血管的慢性炎症反应引起,Lp-PLA2参与到AS的发生发展中。颈动脉斑块内新生血管是斑块不稳定性的重要因素,有研究表明其与血管的慢性炎症有关。超声造影已经成为超声检查的一项重要的辅助技术,可以清楚显示颈动脉管腔外膜滋养血管和斑块内新生血管。既然斑块内新生血管与Lp-PLA2均与血管慢性炎症有关,两者之间又有什么联系?两者在急性缺血性脑梗死(Acute cerebral infarction,ACI)的发生中又发挥怎样的作用呢?本项研究即通过超声造影检查,半定量分析斑块内新生血管的显影情况,从新生血管角度分析讨论颈动脉斑块稳定性、血浆Lp-PLA2水平与ACI间的关系。研究目的探讨颈动脉斑块内新生血管显影程度与血浆Lp-PLA2水平在ACI的临床诊断价值及两者间的关系。方法1研究对象本项研究对象分为两组:ACI组与非ACI组。ACI组为2015年7月至2016年9月在我院神经内科住院的急性前循环脑梗死患者44例,非ACI组为同期查体中心体检有不稳定斑块者41例。2颈动脉常规超声及超声造影检查采用VividE9超声诊断仪,9L探头行颈动脉常规超声及超声造影检查。连续扫查颈动脉,选取目标斑块。选用意大利Bracco公司的声诺维(SonoVue)造影剂,经肘正中静脉注入。观察超声造影图像并储存,留后分析。依据文献数据将斑块内新生血管显影分级:斑块内无增强的新生血管信号(Ⅰ级);斑块内及周边新生血管信号呈点状分布(Ⅱ级);斑块内新生血管信号呈散在点状及线状分布(Ⅲ级);斑块内新生血管呈弥漫点状或多条线状分布(Ⅳ级)。3血浆Lp-PLA2测定ACI组与非ACI组均清晨空腹于肘部静脉采血4 mL,枸橼酸钠抗凝,混匀后,于标本采集30 min内,在2～8℃环境下离心15min(3000 r/min),后分离血浆,置-20℃C以下保存备用。按照说明书采用双抗体夹心免疫层析法检测血浆Lp-PLA2。结果1 ACI组与非ACI组颈动脉斑块内新生血管显影分级比较:ACI组Ⅰ级显影斑块为3例,占6.82%;Ⅱ级显影斑块为8例,占18.18%;Ⅲ级显影斑块为23例,占52.27%;Ⅳ级显影斑块为10例,占22.73%。非ACI组Ⅰ级显影斑块为19例,占46.34%;Ⅱ级显影斑块为15例,占36.59%;Ⅲ级显影斑块为5例,占12.20%;Ⅳ级显影斑块为2例,占4.88%。颈动脉斑块内新生血管分级明显高于非ACI组,两组差异有统计学意义(Z=-5.29,P=0.00)。ACI组内新生血管分级多为Ⅲ、Ⅳ级,所占比例为75.0%,非ACI组分级多为Ⅰ、Ⅱ级所占比例为82.9%,以大于等于Ⅲ级区分ACI与非ACI的敏感性为75%,特异性为82.9%。更进一步,ACI组新生血管显影分级以Ⅲ、Ⅳ级为主,且中位等级为Ⅲ级;非ACI组则以Ⅰ、Ⅱ级为主,中位等级为Ⅱ级。2 ACI组与非ACI组血浆Lp-PLA2水平比较:ACI组血浆Lp-PLA2 水平为247.37 ±58.30μg/L,非 ACI 组血浆 Lp-PLA2 水平为 156.88 ±66.78μg/L,ACI 组明显高于非ACI组,差异有统计学意义(t= 6.64,P= 0.00)。血浆Lp-PLA2对ACI的诊断效能分析采用ROC曲线分析,以约登指数最大确定最佳临界值,其截断值为199.76 μg/L,灵敏度为84.10%,特异性为68.30%,曲线下面积为0.84,诊断的准确度为84.10%。3斑块内新生血管显影分级与血浆Lp-PLA2水平之间呈显著的正相关(rs =0.60,P0.01),即斑块内新生血管显影分级越高的患者,其血浆Lp-PLA2水平越高。结论1 ACI组颈动脉斑块内新生血管的显影分级与血浆Lp-PLA2水平均高于非ACI组,推测两者可能是ACI的危险因素。2斑块内新生血管的显影分级与血浆Lp-PLA2水平呈正相关。
[Abstract]:In this paper, the incidence and mortality of cerebrovascular disease in the world are high[1], especially the high disability rate and the high mortality rate, which bring great harm to the human and the society. Acute cerebral infarction, also known as ischemic cerebral infarction, is a common and frequently occurring disease. The main pathological basis is atherosclerosis (AS)[2], and the atherosclerotic cerebral infarction accounts for 74% of the prevalence of ischemic cerebral infarction[3]. Carotid arteriosclerosis is a local manifestation of whole body arteriosclerosis. Plaque hemorrhage, plaque rupture, thrombosis, aneurysm formation, and the like are secondary changes in carotid plaque. As the upstream blood vessel of the cerebral blood circulation, the carotid artery is the independent risk factor of ischemic cerebral infarction[4]. The plasma lipoprotein-related phospholipase A2 (Lp-PLA2), as a new marker of inflammation, was given more and more attention. In recent years, it is considered that AS is caused by chronic inflammatory reaction of blood vessel, and Lp-PLA2 is involved in the development of AS. Neovascularization in the carotid plaque is an important factor in the instability of the plaque, and it has been shown that it is related to the chronic inflammation of the blood vessel. The ultrasound contrast has become an important auxiliary technique for ultrasonic examination, and it is clear that the adventitia of the carotid artery and the new blood vessels in the plaque can be displayed. Since the new blood vessels in the plaque and the Lp-PLA2 are all related to the chronic inflammation of the blood vessel, what is the connection between them? What is the effect of both in the occurrence of acute ischemic cerebral infarction (ACI)? The relationship between the carotid plaque stability, plasma Lp-PLA2 level and ACI was discussed from the angle of the new blood vessel by means of the ultrasound contrast examination and the semi-quantitative analysis of the development of the new blood vessels in the plaque. Objective To study the relationship between the degree of blood vessel development and the plasma Lp-PLA2 level in the carotid plaque in the clinical diagnosis of ACI. Method 1 The object of this study was divided into two groups: ACI group and non-ACI group. The ACI group was 44 cases of acute pre-circulating cerebral infarction in the Department of Neurology of our hospital from July 2015 to September 2016, In the non-ACI group, there were 41 cases of unstable plaque in the physical examination of the same period. The carotid artery was scanned continuously and the target plaque was selected. The sonoVue contrast agent was selected from Bracco, Italy, and injected through the median of the elbow. The ultrasound contrast image was observed and stored and analyzed. According to the literature data, the new blood vessel in the plaque was developed and classified: there was no enhanced new blood vessel signal in the plaque (stage I), and the signal of the new blood vessel in the plaque was distributed in point (level II), and the new blood vessel signal in the plaque was scattered in the point and the linear distribution (stage III); The plasma Lp-PLA2 (plasma Lp-PLA2) was collected in the early morning of the non-ACI group at the elbow vein for 4 mL, and the sodium gluconate was anticoagulated. After the mixture was mixed, the samples were centrifuged at 2-8 鈩，

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