老年颈动脉粥样硬化性狭窄的治疗

<正>颈动脉狭窄是缺血性脑卒中的重要危险因素,导致颈动脉狭窄的主要病因有动脉粥样硬化、颈动脉夹层、动脉炎、动脉肌纤维发育不良等,但颈动脉粥样硬化最常见,颈动脉狭窄后引起的脑灌注障碍、动脉粥样硬化斑块破裂产生的栓子栓塞是导致脑卒中发生的重要机制。治疗颈动脉狭窄,预     

高分辨率磁共振成像对颈动脉粥样硬化斑块的研究

<正>目前,脑卒中是导致人类残疾的一个主要疾患,居死亡原因的第二位。其中缺血性脑卒中占80%,主要是由于颈动脉粥样硬化斑块造成颈动脉狭窄后,引起的血流动力学变化或血栓形成,且大部分是因为动脉粥样硬化斑块栓子脱落堵塞导致的动脉动脉栓塞所致。以往认为脑卒中的危险随着血管狭窄的程度而增加,但有文献报道,许多缺血性脑卒中发生在具有中等度狭窄的患者中,动脉粥样硬化斑块的成分可能是脑卒中的危险因素,而不管其狭窄的程度。因此,对动脉粥样硬化斑块及其成分的诊断分析成为目前影像     

IL-18在动脉粥样硬化相关疾病中的研究进展

动脉粥样硬化（atherosclerosis,AS）是心血管系统的慢性炎症性疾病,是缺血性心脏病、脑卒中和周围血管疾病的主要病因之一。越来越多的证据表明,炎症反应是斑块不稳定性及斑块破裂的重要因素,贯穿不稳定斑块的发生、发展及破裂的全过程。白细胞介素18(interleukin-18,IL-18)是一种新型的促炎细胞因子,可以促进炎症反应,是参与动脉粥样硬化炎症进程的重要因子。本文就IL-18在AS发病机制中的作用及其在AS相关疾病中的研究现状作一综述,以期为AS及其相关疾病提供新的检测指标和治疗靶点。     

趋化因子CXCL16与动脉粥样硬化性卒中

颈动脉粥样硬化是缺血性卒中的重要发病机制.炎症在动脉粥样硬化的发生、发展及其引起的并发症中起着关键作用.作为一种新型的趋化因子,人CXC型趋化因子配体16( CXC chemokine ligand 16,CXCL16)参与了动脉粥样硬化斑块的形成和发展,可能与动脉粥样硬化性卒中有关.     

放射治疗所致颈动脉狭窄

颈动脉狭窄是缺血性卒中的重要病因, 其机制主要与动脉粥样硬化斑块形成有关。头颈部放射治疗可能会加速斑块形成, 进而造成颈动脉狭窄。另外, 放射治疗也会造成血管内膜和外膜损伤, 加重颈动脉狭窄程度。这种由放射治疗所致的颈动脉狭窄在病因、发病机制以及预防和治疗方面与动脉粥样硬化性颈动脉狭窄有所不同。因此, 充分了解致病机制, 对于选择合适的预防和治疗方法至关重要。     

固有免疫介导的炎症反应在动脉粥样硬化发病机制中的研究进展

动脉粥样硬化是常见慢性心脑血管疾病的病理基础,其病变始于血管内皮细胞构成的天然屏障功能障碍,由各种损伤因子影响内皮细胞Caspase-1/Sirt1/AP-1、SREBP2/NOX2/NLRP3、KLF2/FoxP1/NLRP3、NFAT5/NLRP3等通路信号转导、相关炎症基因表达,激活内皮细胞,继而单核细胞浸润主动脉壁内膜下并分化为巨噬细胞,引起相应内皮激活的固有免疫反应,在NLRP3/ASC/Caspase-1炎性小体途径激活后,使促炎症细胞因子IL-1β、IL-18释放增加,介导下游炎症因子、趋化因子等表达增加,促进动脉粥样硬化炎症反应;血管壁持续慢性炎症反应使血管平滑肌细胞表型转变,促进动脉粥样硬化斑块形成,还使斑块成分发生改变、易损性增加,斑块微钙化则增加了斑块处血管应力,破裂危险增加。本文综述了固有免疫介导的动脉粥样硬化炎症机制研究现状,为动脉粥样硬化抗炎药物研发提供思路以及促进抗动脉粥样硬化研究的实验设计。     

炎症与动脉粥样硬化关系研究进展

研究表明动脉粥样硬化是一种慢性炎症,在内皮损伤、脂质代谢异常、血流动力学损伤、遗传、感染、物理化学等损伤刺激下,多种炎症因子、免疫机制及相关细胞因子网络交叉样作用于血管壁,形成慢性炎症。炎症反应贯穿于动脉粥样硬化的启动、形成和发展以及不稳定斑块,众多的的炎症标志物为动脉粥样硬化的评估和临床预测提供一条重要途径。抗炎症治疗在动脉粥样硬化的防治中不断取得突破。     

颈动脉超声预测缺血性脑卒中的研究进展

缺血性脑卒中是造成人类致残和死亡的重要原因，颈动脉粥样硬化（carotid atherosclerosis，CAS）则是脑实质缺血性病变的主要原因之一，当粥样硬化斑块致血管腔狭窄〉60％时，临床上往往出现症状。CAS亦是全身动脉粥样硬化的一部分，是反映全身动脉粥样硬化的“窗口”。颈动脉超声是诊断、评估颈动脉壁病变的有效手段之一，在缺血性脑卒中的流行病学调查预防以及治疗的有效性评价中起重要作用。现将近年来颈动脉超声预测临床缺血性脑血管事件的进展综述如下。     

颈动脉粥样硬化斑块内新生血管的研究现状及进展

颈动脉粥样硬化斑块破裂是导致脑卒中的重要原因之一,大量研究证实颈动脉斑块内新生血管是导致斑块内出血、斑块破裂的重要因素。炎症因子及各类细胞通过斑块内新生血管进入斑块,导致斑块稳定性破坏,但影响斑块内新生血管形成的重要相关因子和主要机制目前尚未完全明确,因此识别斑块内新生血管、探索斑块内新生血管形成的相关因子及机制是研究斑块内新生血管致斑块不稳定性的关键。抑制斑块内新生血管生成,可能成为防治颈动脉斑块破裂、降低脑栓塞事件发生的新策略。本综述旨在探讨颈动脉斑块内新生血管形成的相关因子、机制以及检测成像的最新研究进展,为动脉粥样硬化的诊疗提供支持。     

氯吡格雷稳定易损斑块

动脉粥样硬化是缺血性卒中最重要的病因之一，而易损斑块在脑动脉粥样硬化性血栓形成中起重要作用。动脉粥样硬化是一个炎症过程，血小板的活化和聚集在其发生和发展以及斑块破裂后的血栓形成过程中起重要作用。因此，抗血小板治疗是预防卒中的重要手段。氯吡格雷和阿司匹林减少有症状颈动脉狭窄栓子（Clopidogrel and Aspirin for Reduction of Emboli in Symptomatic Carotid Stenosis，CARESS）研究表明，氯吡格雷可有效稳定易损斑块，从而预防早期卒中。     

The role of carotid plaque vulnerability and inflammation in the pathogenesis of acute ischemic stroke

BACKGROUND: Increasing evidences show that disruption of carotid plaque followed by arterio-arterial thromboembolism is an important mechanism in the generation of ischemic stroke. Inflammatory mechanisms play a key role in transforming structurally vulnerable plaques into functionally unstable ones. The purpose of the present study is to evaluate the roles of carotid plaque vulnerability and inflammation in the pathogenesis of acute ischemic stroke. METHODS: Fifty-two patients with acute ischemic stroke affecting the anterior circulation (stroke group) and 44 with asymptomatic carotid stenosis (asymptomatic group) were investigated. Duplex ultrasonography was used to evaluate the characteristics of carotid plaque and grading the degree of carotid stenosis. Plaque echogenicity was assessed as echolucent, predominantly echolucent, predominantly echogenic, or echogenic. Plaque surface was classified as smooth, irregular, or ulcerated. All subjects had duplex-determined 50% to 99% carotid stenosis. Serum levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitors of metalloproteinases (TIMP-1), soluble CD40 ligand (sCD40L) and high-sensitivity C-reactive protein (hsCRP) were measured. RESULTS: Plaques in the stroke group were echolucent or predominantly echolucent, whereas those of the asymptomatic group were predominantly echogenic or echogenic plaques (P<0.05). Irregular and ulcerated plaques were frequently found in stroke patients, while smooth plaques were frequently detected in asymptomatic patients (P<0.05). Serum levels of MMP-9, sCD40L, hsCRP were higher in stroke than in asymptomatic patients. By contrast, serum TIMP-1 levels were significantly higher in the asymptomatic than in the stroke group. CONCLUSIONS: The results suggest that inflammation plays a crucial role in carotid plaque vulnerability and, together with carotid plaque morphology, in the pathogenesis of acute ischemic stroke.     

颈动脉狭窄的影像学评价

颈动脉狭窄是缺血性卒中的一种重要的可干预性危险因素,对其进行全面的诊断,包括狭窄程度、斑块稳定性以及头颈部血管的全面了解,对于防治缺血性卒中有着重要的指导意义.文章对数字减影血管造影、超声检查、磁共振血管造影和CT血管造影在颈动脉狭窄中的诊断价值进行了综述.     

The Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) study. Aims and results of quality control.

AIM: The results of the Asymptomatic Carotid Atherosclerosis Study (ACAS) study have provided the first scientific evidence that in patients with asymptomatic carotid stenosis greater than 60% carotid endarterectomy reduces the risk of stroke from 2% to 1% per year. The implications are that approximately 20 operations need to be performed in order to prevent 1 stroke in 5 years. The aims of the Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) study are to identify a subgroup or subgroups at a risk for stroke higher than 4% and a group at a risk for stroke less than 1% per year using systemic and local risk factors (plaque characterization) in addition to the degree of stenosis. The aim of this paper is to present the protocol and the results of the quality control. METHODS: The ACSRS is a multicentre natural history study of patients with asymptomatic internal carotid diameter stenosis greater than 50% in relation to the bulb. The degree of stenosis is graded using multiple established ultrasonic duplex criteria. In addition, ultrasonic plaque characterization is performed and clinical risk factors and medications are recorded. Training is provided centrally. All carotid ultrasound examinations are recorded on video-tape which together with CT-brain scans and ECG are analysed at the coordinating centre with feedback information to partner centres. RESULTS: The video recordings and analysis of data centrally with feed back information have provided quality control with a significant improvement not only in the completion of data forms but also in the grading of internal carotid stenosis and plaque recordings using ultrasound. CONCLUSION: The high level of quality of data collected will add credibility to the results of the ACSRS study and may eventually promote the development of international standards of plaque imaging and characterization.     

Evidence-based management of carotid artery disease

Stroke is a major cause of disability and mortality, and a major cause of stroke is carotid artery stenosis. This stenosis is caused by carotid atherosclerotic plaques, the prevention and management of which are the key to avoiding many resultant strokes. The plaque can either embolize to a cerebral artery or build up in a carotid artery, ultimately resulting in thrombosis and total occlusion. Noninvasive testing can now make the diagnosis of carotid stenosis. Medical management with plaque stabilization and platelet inhibition plays a key role in stroke prevention. Carotid endarterectomy and invasive carotid angioplasty stenting are also important for lesions with extensive progression, and patients with a very high overall risk may especially benefit from the latter procedure. A medical-surgical team approach is now greatly contributing to the avoidance of stroke and its devastation.     

Inflammation as a marker for the prediction of internal carotid artery restenosis following eversion endarterectomy--evidence from clinical studies

The role of inflammation is well established in the pathogenesis of atherosclerosis and an increased level of circulating inflammatory markers may predict the future risk of atherosclerosis progression and plaque rupture. C-reactive protein (CRP) identification by hypersensitive methods (high-sensitivity CRP [hsCRP]) has become a clinical and laboratory inflammation marker. Carotid endarterectomy (CEA) is a well-established procedure for carotid stenosis treatment which can reduce stroke rate. Internal carotid artery (ICA) restenosis reduction may be prevented by the anti-inflammatory effect of statins. This review considers the recent findings on the presence of hsCRP and C3 complement concentration and inflammatory plaque composition as well as their effects on ICA restenosis rate, following eversion CEA with emphasis on human studies.     

颈动脉粥样硬化及斑块的性质、部位与缺血性卒中的关系:回顾性病例对照研究

目的 探讨颈动脉内膜-中膜厚度(intime-media thickness,IMT)、颈动脉粥样斑块性质、部位以及颈动脉狭窄程度与缺血性卒中的关系.方法 回顾性收集行彩色多普勒超声检查的首发急性缺血性卒中患者(缺血性卒中组)和同期门诊和住院的非缺血性卒中患者(对照组),对两组人口统计学资料、血管危险因素和颈动脉粥样硬...     

150例颈动脉粥样硬化斑块患者相关危险因素的分析

目的对颈动脉粥样硬化斑块患者的相关危险因素进行分析。方法经颈部血管彩色超声证实,颈动脉粥样硬化斑块患者1 50例,男91例,女59例;颈动脉狭窄<50%80例,颈动脉狭窄50%～70%49例,颈动脉狭窄>70%21例;合并脑卒中45例,无脑卒中105例。采用Essen脑卒中风险评分量表(ESRS)对危险因素进行评估。结果颈动脉粥样硬化斑块男性患者ESRS为(3.1 98±1.701)分,女性患者ESRS为(2.441±1.643)分,男性明显高于女性,差异有统计学意义(P<0.05);颈动脉狭窄<50%患者ESRS为(2.658±1.632)分,颈动脉狭窄50%～70%患者ESRS为(2.612±1.742)分,颈动脉狭窄>70%患者ESRS为(4.429±1.121)分,颈动脉狭窄>70%患者ESRS评分明显高于其他2个狭窄段患者,差异有统计学意义(P<0.05);合并脑卒中患者ESRS为(4.578±1.305)分,无脑卒中患者ESRS为(2.215±1.332)分,合并脑卒中患者ESRS评分明显高于无脑卒中患者,差异有统计学意义(P<0.05)。结论颈动脉粥样硬化斑块患者的危险因素与性别、颈动脉狭窄程度及是否合并脑卒中相关。     

Statins and their use in preventing carotid disease

Carotid disease may be evaluated by surrogate outcomes, such as intima-media thickness and carotid plaque features, and by clinical end points. Statins stop progression or may induce regression of intima-media thickness, and statins may also stop plaque growth or even induce reduction of plaque volume. Areas rich in lipids within plaques may be reduced in size and/or in number of inflammatory cells. Ultrasound reflectivity may be reduced by statin treatment, indicating less lipid/inflammatory content. Finally, statins appear to reduce the risk of all cardiovascular events (eg, stroke, myocardial infarction, need for revascularization) in patients with carotid stenosis. This review summarizes and discusses the existing data.     

Surgical management of asymptomatic carotid artery stenosis. Authors' experience, problems and prospectives]

BACKGROUND: Some trials have demonstrated effectiveness of carotid endarterectomy (CEA) for preventing stroke in patients with severe symptomatic carotid stenosis. Although some researches, indication to surgery for asymptomatic carotid stenosis is debated up today. Based on personal experience and literature, the main problems of CEA for asymptomatic stenosis are discussed. METHODS: DESIGN: Retrospective study. SETTING: Section of Vascular Surgery, University Department. PATIENTS: CEA was performed in a consecutive series of 63 cases with asymptomatic stenosis (59 patients, 40 males and 19 females, ages ranging from 46 to 80 years, mean 67.9). INTERVENTIONS: CEA was performed under general anesthesia, with primary closure of arteriotomy in 37 cases and patch angioplasty using PTFE in 24, using eversion technique in 2 cases. Pruitt-Inahara shunt was used in 10/63 cases (15.9%), according to the mean velocity of the middle cerebral artery at carotid clamping/mean velocity of the middle cerebral artery pre-clamping ratio x 100 equal to or lesser than 15%, evaluated with transcranial Doppler, or stump pressure lesser than 50 mmHg, when transcranial Doppler examination was not possible. MEASURES: Operative mortality and postoperative morbidity. RESULTS: Operative mortality plus postoperative stroke were 1.6% (1/63). Operative mortality was precisely 0.0%. Postoperative complications were two: one was a neurologic deficit (monoparesis of the arm) and the other was myocardial ischemia. CONCLUSIONS: Four main problems have been shown in CEA for asymptomatic stenosis: 1. Identification of asymptomatic stenosis: 2. Assessment of risk for stroke: 3. Role of CEA: 4. Questions about surgical treatment. For the first problem, it is important to consider possible indicators for carotid stenosis (contralateral carotid stenosis, coronary artery disease, aortic aneurysm, peripheral arterial disease, etc.). With regard to the second problem, it is important to know the natural history of the carotid stenosis, which shows a stroke rate of 1-2% per year. Regarding the third problem, the role of CEA is conditioned by: trials, patient conditions, lesion characteristics and ability of the surgeon. Further studies should identify some groups of patients (with severe carotid stenosis, dyshomogeneous plaque, progression of plaque, etc.), who can profit from CEA. Finally (fourth problem), CEA for asymptomatic carotid stenosis carries all common problems of carotid surgery (preoperative assessment, evaluation of cerebral ischemia due to carotid clamping, shunt, closure of arteriotomy, etc.). Some of these problems can receive ultimate solutions from some studies in next years.     

脑梗死患者颈动脉斑块及其稳定性

探讨脑梗死患者颈动脉粥样硬化病变特点及其与脑梗死之间的关系 ,寻找不稳定性颈动脉斑块的血清标志物。通过对 12 0例定位于颈内动脉系统的动脉粥样硬化性脑梗死患者进行颈动脉超声检查 ,根据颈动脉超声结果分为软斑组、硬斑组和无斑块组 ,对符合入选标准的 84例患者于入院 3周后 ,用酶联免疫吸附测定法测定血清基质金属蛋白酶 9水平。结果发现 ,颈动脉粥样硬化斑块检出率为 72 .5 % (87例 ) ,颈动脉重度狭窄发生率为 4 .17%。梗死侧颈动脉软斑发生率 (32 .9% )高于非梗死侧 (16 .9% ) ,软斑组和硬斑组基质金属蛋白酶 9水平均明显高于无斑块组 ,而软斑组基质金属蛋白酶 9水平又高于硬斑组 (P <0 .0 5 )。结果提示 ,缺血性脑卒中患者颈动脉粥样硬化病变特点可能以斑块居多 ,而重度狭窄发生率较低 ,软斑为脑梗死重要危险因素 ,基质金属蛋白酶 9可能是不稳定性粥样斑块的一个潜在的血清标志物。