高血压、糖尿病和高脂血症对脑梗死患者血管内皮功能损伤的相关研究

目的探讨脑梗死危险因素与血管内皮功能的相关性。方法选取血管性假血友病因子(vWF)与可溶性血管内皮细胞蛋白C受体(sEPCR)作为脑梗死患者血管内皮功能的评价指标。将急性脑梗死患者分为多危险因素脑梗死组、单危险因素脑梗死组,并选取健康对照组,采用ELISA方法检测其血清中vWF与sEPCR含量。组间比较采用独立样本t检验。且分别将vWF、sEPCR作为因变量,高血压、糖尿病和高脂血症作为自变量行多元线性回归分析。结果多危险因素脑梗死组血浆中vWF与sEPCR含量显著高于单危险因素脑梗死组(P<0.001)。高血压、糖尿病和高脂血等脑梗死危险因素均与vWF和sEPCR存在线性回归关系。结论脑梗死危险因素越多,则血管内皮功能损伤可能越严重。     

单核细胞趋化蛋白-1和脑梗死患者颈动脉粥样硬化斑块稳定性的关系

目的探讨血浆单核细胞趋化蛋白-1(MCP-1)水平与脑梗死患者颈动脉粥样硬化斑块稳定性的关系。方法根据颈动脉彩色多普勒超声仪检查结果,将116例脑梗死患者分为无斑块组(29例)、稳定斑块组(47例)和不稳定斑块组(40例)。采用ELISA法检测脑梗死患者以及30名正常对照组血浆MCP-1水平。分析血浆MCP-1水平与脑梗死患者颈动脉粥样硬化斑块稳定性的关系。结果 (1)不稳定斑块组血浆MCP-1水平明显高于稳定斑块组(P<0.05);(2)脑梗死患者颈动脉斑块稳定性与血浆MCP-1水平呈负相关(r=-0.683,P<0.05)。结论血浆MCP-1水平的增高和颈动脉粥样硬化斑块的不稳定性密切相关。     

脑梗死患者颈动脉粥样硬化斑块稳定性与血清C反应蛋白水平的关系

目的探讨脑梗死患者颈动脉粥样硬化斑块的稳定性与血清C反应蛋白(CRP)水平的关系。方法对112例颈内动脉系统脑梗死患者进行颈动脉彩色多普勒超声检查,明确粥样硬化斑块类型,同时测定血清CRP水平。结果脑梗死患者中不稳定斑块组、稳定斑块组、无斑块组血清CRP水平比较差异有统计学意义(P<0.01)。结论血清CRP水平可反映脑梗死患者颈动脉粥样硬化斑块的稳定性。     

彩色多普勒超声检测颈动脉粥样硬化斑块在预防脑梗死中的应用

目的探讨颈动脉粥样硬化斑块与脑梗死的关系。方法对69例急性脑梗死患者(脑梗死组)及29例非脑梗死患者(对照组)分别进行颈动脉彩色多普勒超声检测,记录动脉粥样硬化斑块的数量、性质和部位。结果脑梗死组颈动脉粥样硬化斑块检出率(72%)明显高于对照组(34%)。不稳定性斑块的发生率(86%)也明显高于对照组不稳定性斑块发生率(50%)。脑梗死组颈动脉粥样硬化斑块位于颈动脉窦部最多(49%),其次是颈总动脉(31%)、颈内动脉(20%)。结论颈动脉粥样硬化斑块与脑梗死密切相关,早期发现并早期干预对于减少和推迟脑梗死发生有重要指导意义。     

脑梗死患者血清超敏C反应蛋白D-二聚体含量及颈动脉粥样硬化斑块的测定及分析

目的探讨颈内动脉系统急性脑梗死患者血清超敏C反应蛋白(hs-CRP)、D-二聚体(D-Dimer)含量及颈动脉粥样硬化斑块的变化及意义。方法测定85例首次颈内动脉系统急性脑梗死患者血清hs-CRP和血浆D-Dimer含量,并与正常对照组进行比较;颈动脉彩超测定颈动脉粥样硬化斑块情况。分析血清hs-CRP、血浆D-Dimer含量、颈动脉粥样硬化斑块情况与神经功能缺损程度评分的关系。结果脑梗死组血清hs-CRP和血浆D-Dimer含量、不稳定斑块率明显高于正常对照组(均P0.05),脑梗死中重度组明显高于轻度组(均P0.05),伴不稳定斑块患者血清hs-CRP和血浆D-Dimer含量明显高于不伴不稳定斑块患者(P0.05)。脑梗死组hs-CRP和D-Dimer含量与NIHSS评分呈正相关(r=0.57和0.38,均P0.05)。结论急性脑梗死患者血清hs-CRP及D-Dimer含量及不稳定斑块率明显增高,观察其情况对于预测脑梗死的发生和病情轻重具有重要意义。     

颈动脉粥样硬化斑块与脑梗死关系的临床观察

目的探讨颈动脉粥样硬化斑块与脑梗死的相关性。方法选取100例脑梗死患者进行颈动脉B超检查,明确有无颈动脉粥样硬化斑块,随机抽取体格检查者50例作为对照组,分析斑块与脑梗死发生的相关性。结果脑梗死组颈动脉粥样硬化斑块发生率79%,对照组16%,2组差异有统计学意义(P<0.01)。结论颈动脉粥样硬化斑块的形成与脑梗死密切相关。     

脑梗死患者颈动脉斑块稳定性及其相关因素分析

目的探讨脑梗死患者颈动脉粥样硬化斑块稳定性及其有关危险因素。方法对139例脑梗死患者行颈部血管超声和血液检查;根据颈部血管超声分为斑块稳定组和不稳定组,比较2组间颈动脉粥样硬化斑块的稳定性及危险因素的差异。结果脑梗死患者颈动脉粥样硬化斑块发生率85.61%,不稳定组血清总胆固醇（CHOL）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、同型半胱氨酸（HCY）、纤维蛋白原（FIB）水平及性别、糖尿病史、吸烟患者比例与稳定组相比差异有统计学意义（P〈0.05）。结论颈动脉粥样硬化斑块与脑梗死密切相关,高水平的CHOL、TG、HCY、FIB,低水平的HDL-C及糖尿病史、吸烟史促使颈动脉粥样硬化斑块演变为不稳定斑块,故积极控制上述危险因素对预防脑梗死发生有重要意义。     

血清可溶性CD40配体与急性脑梗死患者颈动脉斑块的关系

目的 探讨血清可溶性CD40配体（sCD40L）水平与急性脑梗死患者颈动脉粥样硬化斑块的关系。方法 选取2018年5月至2019年5月在中国医科大学附属盛京医院神经内科住院的急性脑梗死患者108例。根据颈部动脉超声结果分为无斑块组和斑块组,斑块组根据斑块性质进一步分为稳定斑块组和不稳定斑块组。应用酶联免疫吸附法（ELISA）测定血清sCD40L水平;分析血清sCD40L水平与颈动脉粥样硬化斑块的关系。结果 颈动脉斑块组患者高血压（P=0.026）、空腹血糖（P=0.045）、三酰甘油（P=0.027）、低密度脂蛋白胆固醇（LDL-c）（P=0.005）和sCD40L水平（P<0.001）均高于无斑块组。高血压（OR=2.598,P=0.028）、LDL-C（OR=4.247,P=0.006）和sCD40L水平（OR=1.079,P=0.009）是急性脑梗死患者存在颈动脉粥样硬化斑块的危险因素。颈动脉不稳定斑块组患者高血压（P=0.031）、白细胞计数（P=0.002）、低密度脂蛋白胆固醇（P=0.003）和sCD40L水平（P<0.001）均高于稳定斑块组。不稳定颈动脉斑块组患者,高血压（OR=2.918,P=0.033）和sCD40L水平（OR=2.712,P<0.001）是急性脑梗死患者颈动脉斑块不稳定性的危险因素。结论 急性脑梗死患者血清sCD40L水平的升高与颈动脉粥样硬化斑块的发生和发展相关,亦与颈动脉斑块的不稳定性相关。     

颈动脉粥样硬化斑块与急性脑梗死患者血脂、血压关系的探讨

目的探讨急性脑梗死患者血脂浓度、血压与颈动脉粥样硬化斑块的关系。方法应用彩色多普勒超声检查急性脑梗死患者的颈动脉内膜-中膜厚度、斑块数和性状，同时检测血压。查血脂；121例急性脑梗死患者根据有无高血压分为脑梗死组47例、高血压并发脑梗死组74例，年龄相匹配的正常对照组35例。各项数据用SPSS10．0软件统计分析。结果脑梗死合并高血压组颈动脉粥样硬化斑块发生率最高（69．7％），且以软斑及混合斑为主，脑梗死组次之（59．6％），正常组最低（20％）。有颈动脉粥样硬化斑块与无颈动脉粥样硬化斑块相比．血清LDL—C水平明显升高。结论颈动脉粥样硬化斑决是脑梗死的重要危险因素，高血压及高LDL—C血症是颈动脉粥样硬化的危险因素．     

血清TGF-β1和VEGF与脑梗死患者颈动脉粥样斑块易损性的相关性

目的探讨血管内皮细胞生长因子(VEGF)和转化生长因子-β1(TGF-β1)与脑梗死患者颈动脉粥样硬化斑块易损性的关系。方法收集96例急性期动脉粥样硬化性脑梗死患者和30名健康对照者。采取酶联免疫法检测血清VEGF和TGF-β1水平;采用彩色多普勒超声对脑梗死患者的颈动脉粥样硬化情况进行评估,并将脑梗死患者分为伴易损性颈动脉斑块组、伴稳定性颈动脉斑块组和无颈动脉粥样硬化组,分析血清VEGF和TGF-β1水平与脑梗死患者颈动脉粥样硬化易损斑块的相关性。结果脑梗死患者血清VEGF水平明显高于对照组,而TGF-β1水平明显低于对照组(P0.01);伴易损性颈动脉斑块的脑梗死患者血清VEGF水平明显高于伴稳定性颈动脉斑块的脑梗死患者(P0.01),而TGF-β1水平明显低于伴稳定性颈动脉斑块的脑梗死患者(P0.01);VEGF水平与颈动脉斑块易损性呈正相关(r=0.493,P0.01),而TGF-β1水平与颈动脉斑块易损性呈负相关(r=-0.524,P0.01)。结论 VEGF和TGF-β1在脑梗死的发病和脑缺血损伤中可能起重要的作用,TGF-β1高表达和脑梗死患者颈动脉粥样硬化斑块稳定性之间存在密切联系,TGF-β1具有稳定颈动脉粥样硬化斑块的作用。     

颈动脉粥样硬化斑块的稳定性与缺血性脑血管疾病危险因素的相关研究

目的探讨颈动脉粥样硬化斑块稳定性与缺血性脑血管病危险因素的相关性。方法选取2010年10月-2010年12月在广州军区武汉总医院住院的缺血性脑血管病患者203例为研究对象,应用颈动脉彩色多普勒超声技术检查颈动脉粥样硬化斑块的大小、数目及性质,并评估研究对象脑梗死危险因素,行Logistic回归分析。结果脑梗死危险因素包括性别、年龄、吸烟、高血压、糖尿病、冠心病与高血压性心脏病、低密度脂蛋白、脂蛋白(a)、纤维蛋白原、超敏C反应蛋白及高同型半胱氨酸,均与颈动脉粥样硬化不稳定斑块的形成相关(P<0.05)。并且年龄、糖尿病、冠心病与高血压性心脏病、低密度脂蛋白、纤维蛋白原、同型半胱氨酸等脑梗死危险因素可纳入Logistic回归方程,为颈动脉粥样硬化不稳定斑块形成的独立危险因素。结论年龄、糖尿病、冠心病与高血压性心脏病、低密度脂蛋白、纤维蛋白原、高同型半胱氨酸等缺血性脑血管疾病危险因素是导致颈动脉粥样硬化不稳定斑块形成的独立危险因素。     

伴有颈动脉斑块的急性前循环脑梗死患者的微栓子研究

目的 探讨颈动脉斑块、微栓子和急性前循环脑梗死的关系。方法 选择住院的急性前循环脑梗死患者65例,经颈动脉超声检查分为伴有颈动脉斑块组45例和不伴有颈动脉斑块组20例,2组均行微栓子监测。结果 伴有颈动脉斑块组与不伴有颈动脉斑块组吸烟、高血压病、糖尿病、高脂血症相比无明显差异(P>0.05); 伴有颈动脉斑块患者的微栓子阳性率为38%,不伴有颈动脉斑块患者为13%,2组相比有明显差异(P<0.05); 软斑组微栓子阳性率为45%,硬斑组微栓子阳性率为18%,2组相比有明显差异(P<0.05)。结论 急性前循环脑梗死患者多有颈动脉斑块,软斑块是微栓子的主要来源,微栓子是急性脑梗死发病的重要危险因素,对二者早期干预是防治脑卒中的重要措施之一。     

急性脑梗死患者脑血流中微栓子与颈动脉粥样硬化斑块的关系

目的 探讨急性脑梗死患者脑血流中微栓子与颈动脉粥样硬化斑块的关系.方法 67例急性脑梗死患者依据颈动脉超声检测分为颈动脉无斑块组(27例)和斑块组(40例),后者再分为不稳定斑块亚组(19例)和稳定斑块亚组(21例);对所有患者应用经颅多普勒仪进行脑血流中微栓子监测;比较各组间微栓子阳性率.结果 脑血流中微栓子阳性率颈动脉斑块组(30%)显著高于无斑块组(3.7%),不稳定斑块亚组(47%)显著高于稳定斑块亚组(14.3%)(均P<0.05).结论 颈动脉粥样硬化脑梗死患者脑血流中微栓子阳性率高;不稳定斑块更易脱落形成微栓子.     

急性脑梗死患者血清纤维蛋白原、D-二聚体与颈动脉粥样硬化斑块的相关性研究

目的 探讨急性脑梗死患者血清纤维蛋白原、D-二聚体与颈动脉粥样硬化斑块的关系. 方法 选择解放军第三医院神经内科自2009年4月至2011年4月收治的120例急性脑梗死患者(脑梗死组)、同期单纯颈动脉粥样硬化而无脑梗死患者60例(颈动脉粥样硬化组)和健康体检者80例(正常对照组)作为研究对象,采用双抗体夹心法测定血清D-二聚体含量,全自动血凝仪测定纤维蛋白原含量,颈动脉彩色多普勒超声检测患者颈动脉粥样硬化斑块和颈动脉内一中膜厚度(IMT)值. 结果 脑梗死组、颈动脉粥样硬化组及正常对照组血清纤维蛋白原、D-二聚体水平及颈动脉IMT值依次降低,差异有统计学意义(P＜0.05);进展性卒中患者血清纤维蛋白原、D-二聚体水平高于非进展性卒中患者,差异有统计学意义(P＜0.05);随着动脉粥样硬化严重程度的升高,脑梗死患者血清纤维蛋白原及D-二聚体水平逐渐升高,差异有统计学意义(P＜0.05);脑梗死患者血清纤维蛋白原、D-二聚体水平均与颈动脉粥样硬化严重程度呈正相关关系(r=0.426,P=0.006; r=0.535,P=0.001). 结论 纤维蛋白原及D-二聚体参与了急性脑梗死的发生发展,与病情进展密切相关.二者做为急时相反应物参与动脉粥样硬化的发生机制提示,相对于高凝状态,动脉粥样硬化的形成与慢性炎症反应关系更为密切.     

颅内外动脉并存粥样硬化斑块的影像学研究进展

颅内动脉和颅外颈动脉并存粥样硬化斑块(简称并存斑块)在亚洲人群中具有较高的发生率,其与缺血性卒中的发病风险具有显著的相关性。因此,早期识别并存斑块对于缺血性脑血管事件的防控具有重要意义。目前,应用于并存斑块的影像学诊断方法有多种,其中高分辨率磁共振管壁成像有广阔的应用前景。本文将主要针对并存斑块的影像学研究进展方面进行综述。     

脑梗死患者颈动脉颅外段不稳定斑块形成的危险因素

目的 探讨脑梗死(CI)患者颈动脉颅外段不稳定斑块形成的危险因素.方法 根据彩色多普勒超声仪检测结果将205例伴颈动脉颅外段斑块的CI患者分为不稳定斑块组(73例)及稳定斑块组( 132例);对两组患者年龄、性别、文化程度、生活习惯、既往病史、家族史等进行问卷调查,并进行血液生化指标检测.以单因素及多因素非条件Logi...     

Inflammatory mechanisms in Alzheimer's disease

In recent years many studies have indicated an involvement of inflammatory mechanisms in Alzheimer's disease (AD). Acute-phase proteins such as 1-antichymotrypsin and c-reactive protein, elements of the complement system, and activated microglial and astroglial cells are consistently found in brains of AD patients. Most importantly, also cytokines such as interleukin-6 (IL-6) have been detected in the cortices of AD patients, indicating a local activation of components of the unspecific inflammatory system. Up to now it has remained unclear whether inflammatory mechanisms represent a primary event or only an unspecific reaction to brain tissue damage. Therefore, we investigated whether IL-6 immunoreactivity could be found in plaques prior to the onset of neuritic changes, or whether the presence of this cytokine is restricted to later stages of plaque pathology. we confirmed our previous observation that IL-6 is detectable in a significant proportion of plaques in the brains of demented patients. In AD patients IL-6 was found in diffuse plaques in a significant higher ratio as would have been expected from a random distribution of IL-6 among all plaque types. This observation suggests that IL-6 may precede neuritic changes, and that immunological mechanism may be involved both in the transformation from diffuse to neuritic plaques in AD and in the development of dementia.     

Senile plaques do not progressively accumulate with normal aging

Senile plaques (SP) are one of the pathologic hallmarks of Alzheimer's disease (AD). Models of SP formation, particularly the early stages, could provide valuable insight into AD pathogenesis. One such model may be provided by non-demented elderly individuals in whom some SP are a common incidental finding. This study has examined post-mortem brain tissue from a large number of such neurologically normal patients in an attempt to better understand the temporal sequence of SP formation. SP were identified in modified Bielschowsky-stained sections of mesial temporal lobe in 122 (30%) of 402 cases. The prevalence of SP in the temporal neocortex correlated strongly with patient age. Surprisingly, however, neither the mean nor maximum SP density showed any increase with age. This suggests that SP do not progressively accumulate in normal aging but develop over a limited time period after which their number stabilizes at a constant level. In most cases, all SP were of the diffuse type. In 37 cases (9%), however, some neuritic SP (NP) were also seen. Although the NP density did not show a significant increase with age either, the proportion of SP which were neuritic (NP/SP), did. This suggests that changes in SP morphology may be more important than total SP numbers in normal aging.     

Re-evaluation of classic senile plaques by three-dimensional analysis

We evaluated the proportion of classic plaques among all of the senile plaques in four Alzheimer brains (frontal, temporal, occipital and hippocampal areas) by the usual method of two-dimensional analysis using a single methenamine silver-stained section and three-dimensional analysis using a set of serial sections. Three-dimensional analysis showed the number and percentage of classic plaques to be 2–5 times greater than those revealed by two-dimensional analysis. In the hippocampal area of one case, no classic plaques were found by two-dimensional analysis but three-dimensional analysis showed that some classic plaques were present. From these findings, it is suggested that three-dimensional analysis using serial sections is indispensable for sub-classifying senile plaques.     

Interleukin-6 is present in early stages of plaque formation and is restricted to the brains of Alzheimer's disease patients

Interleukin-6 (IL-6) immunoreactivity has previously been shown in plaques in Alzheimer's disease (AD) and elevated IL-6 concentrations have been measured biochemically in brains of AD patients. In this study, we investigated the appearance of IL-6 immunoreactivity in AD plaques according to the stage of plaque formation. Using the Bielschowsky silver-staining method, we were able to differentiate between four types of plaques described earlier: diffuse, primitive, classic and compact. While diffuse plaques represent the early stage of plaque formation, primitive and classic plaques are thought to represent later stages of plaque development. We investigated serial sections of paraffin-embedded cortices of ten clinically diagnosed and histopathologically confirmed AD patients and ten patients with no clinical history of dementia. We found plaques in the brains of both nondemented and demented persons using the silver staining method or immunohistochemistry with antibodies against the amyloid precursor protein. In the group of clinically nondemented persons, diffuse plaques were the predominant plaque type, whereas primitive plaques formed the larger portion of lesions in the group of AD brains. IL-6 could not be detected in plaques of patients without dementia. Many IL-6-positive plaques were found in six of the AD brains and to a smaller extent in the other four AD cases. In the six cases with a large number of IL-6-positive plaques, IL-6 was found in a significantly higher ratio of diffuse plaques than expected from a random distribution of IL-6 in all plaque types. We conclude from these findings that IL-6 immunoreactivity correlates with clinical dementia and that in AD patients, an IL-6-related immunological event may contribute to plaque formation. IL-6 might be involved both in the transformation from diffuse to primitive plaques in AD as well as in the development of dementia.