缺血性脑卒中患者胱抑素C与颈动脉粥样硬化的关系

目的探讨急性缺血性脑卒中患者血清胱抑素C与颈动脉粥样硬化(carotid atherosclerosis,CAS)的关系。方法选择急性缺血性脑卒中患者92例,根据颈动脉彩色超声结果分为CAS组67例和非CAS组25例。CAS组根据CAS的严重程度分为:轻度CAS 46例、中度CAS 15例和重度CAS 6例;根据超声检查分为:硬斑块26例、软斑块16例和混合斑块25例;根据颈动脉受累范围分为:单侧斑块33例和双侧斑块34例。分析组间胱抑素C水平与颈动脉斑块严重程度、斑块性质及受累范围间的相关性。结果 CAS组胱抑素C水平明显高于非CAS组,差异有统计学意义(P<0.05)。logistic回归分析,胱抑素C水平升高是CAS形成的独立预测因素(P<0.01)。中度和重度CAS患者胱抑素C水平明显高于轻度CAS患者(P<0.01)。Spearman等级相关分析,CAS严重程度与胱抑素C水平呈正相关(r=0.246,P<0.05)。结论胱抑素C水平的升高能预测CAS的发生,并能评估CAS的严重程度,但尚不能作为评估颈动脉粥样硬化斑块稳定性及受累范围的可靠指标。     

血清胱抑素C浓度与颈动脉粥样硬化的关系

目的探讨血清胱抑素C(cystatin C)浓度与颈动脉粥样硬化的关系。方法选择2012年1月至2014年1月在成都医学院第一附属医院心内科住院的患者1 263例,检测其血清胱抑素C、血脂、血糖等血液生化指标,彩色多普勒超声评价颈动脉内膜中层厚度(inteima-media thickness,IMT)及粥样硬化斑块的情况。根据彩色多普勒超声结果将研究人群分为颈动脉粥样硬化组(IMT≥0.9 mm,伴或不伴有斑块形成)及颈动脉内膜正常组,用t检验分析两组患者血清胱抑素C、血脂、血糖等指标的差异。Spearman相关分析、Logistic回归分析血清胱抑素C与颈动脉粥样硬化的关系。结果 1 263例患者的年龄为(65.2±8.5)岁,男性共439例(34.8%)。颈动脉粥样硬化患者的血清胱抑素C浓度高于颈动脉内膜正常组,差异有统计学意义[(1.16±0.16)mg/L vs.(0.96±0.41)mg/L,P0.001]。相关分析结果显示,血清胱抑素C与颈动脉粥样硬化呈正相关(r=0.293,P0.001)。多因素Logistic回归分析校正性别、年龄等因素后,血清胱抑素C与颈动脉粥样硬化独立相关(OR=2.682,95%CI:1.682~4.277,P0.001)。结论血清胱抑素C浓度与颈动脉粥样硬化相关,血清胱抑素C可能是颈动脉粥样硬化的独立危险因素之一。     

急性脑梗死患者血浆胱抑素C、同型半胱氨酸水平与颈动脉粥样硬化的相关性分析

目的探讨急性脑梗死患者血清胱抑素C、同型半胱氨酸水平与颈动脉粥样硬化的相关性。方法选择2011年3—8月在天津市武清区人民医院神经内科住院的急性脑梗死患者346例,根据颈动脉超声检查结果分为无斑块组135例和斑块组211例。记录两组患者一般资料,检测其空腹血糖、血脂、超敏C反应蛋白、胱抑素C、同型半胱氨酸。结果单因素分析结果显示,两组患者性别,吸烟史、饮酒史、糖尿病病史、高血压病史阳性率,空腹血糖,血清总胆固醇、高密度脂蛋白胆固醇水平比较,差异均无统计学意义(P0.05);斑块组患者年龄大于无斑块组,血清三酰甘油水平低于无斑块组,低密度脂蛋白胆固醇、超敏C反应蛋白、胱抑素C、同型半胱氨酸水平高于无斑块组(P0.05)。Pearson相关分析结果显示,斑块组患者血清胱抑素C、同型半胱氨酸水平均与Crouse积分呈正相关(r=0.141,P=0.01;r=0.142,P=0.01)。多元Logistic回归分析结果显示,年龄、超敏C反应蛋白、胱抑素C、同型半胱氨酸为颈动脉粥样硬化斑块形成的危险因素。结论胱抑素C、同型半胱氨酸是急性脑梗死患者颈动脉粥样硬化斑块形成的危险因素,二者共同参与了急性脑梗死患者颈动脉粥样硬化的发生和发展过程。     

缺血性脑卒中患者纤维蛋白原水平与颈动脉粥样硬化关系的研究

目的 探讨缺血性脑卒中患者颈动脉粥样硬化与纤维蛋白原水平的关系.方法 对缺血性脑卒中住院患者,应用颈部多普勒超声检测颈部血管内中膜厚度及斑块形成情况,并同期检测患者血浆纤维蛋白原浓度.结果 125例患者40例发现有颈动脉粥样硬化病变,其中16例患者经超声检查诊断为颈动脉粥样硬化斑块,24例患者诊断为颈动脉内中膜增厚.有颈动脉粥样硬化病变的患者平均纤维蛋白原水平显著高于无颈动脉粥样硬化组患者(P＜0.05),并且随着平均纤维蛋白原水平升高颈动脉粥样硬化病变的发生率升高.结论 缺血性脑卒中患者颈动脉粥样硬化和纤维蛋白原水平之间有密切相关性.     

老年高血压患者血压晨峰与颈动脉粥样硬化及缺血性脑卒中发病的相关性

目的 探讨血压晨峰与颈动脉粥样硬化及缺血性脑卒中发病的相关性.方法 选择260例老年高血压患者行24 h动态血压监测,分为血压晨峰组(136例),非血压晨峰组(124例),并对患者进行2年随访.缺血性脑卒中均经头颅CT或MRI确诊,比较两组颈动脉粥样硬化、缺血性脑卒中发生率.结果 晨峰组与非晨峰组比较,晨峰组颈动脉内-中膜厚度、斑块检出率、颈动脉狭窄、缺血性脑卒中发生率均明显升高(P＜0.05).结论 血压晨峰是缺血性脑卒中的重要危险因素,通过影响颈动脉粥样硬化程度及斑块稳定性增加脑卒中的发生.     

颈动脉粥样硬化与缺血性脑血管病的关系

脑卒中为老年人死亡的三大原因之一 ,颈动脉是脑供血的主要通路 ,颈动脉粥样硬化与缺血性脑血管病具有一定的相关性 ,充分认识二者之间的关系 ,早期发现颈动脉粥样硬化斑块形成 ,并采取适当的干预措施 ,对及时有效地防治缺血性脑卒中有十分重要的意义。1　颈动脉粥样硬化的部位     

缺血性脑卒中患者踝臂指数与颈动脉粥样硬化的相关性观察

目的探讨缺血性脑卒中患者踝臂指数(ABI)与颈动脉粥样硬化的关系。方法 2010年1月至2011年11月在我院住院的缺血性脑卒中患者共516人,进行颈动脉超声和踝臂指数的测量,对有效数据进行统计学处理。结果颈动脉粥样硬化的患者踝臂指数明显减低,多因素回归分析进一步说明踝臂指数与颈动脉粥样硬化独立相关。结论踝臂指数与颈动脉粥样硬化密切相关,是其独立的危险因素。踝臂指数可用于缺血性脑卒中高危患者的筛查。     

高血压伴与不伴缺血性脑卒中患者颈动脉内中膜厚度的研究

目的 :用彩色多普勒超声观察高血压伴与不伴缺血性脑卒中患者颈动脉内中膜厚度 ,探讨颈动脉粥样硬化与缺血性脑卒中的关系。方法 :用HDI 30 0 0彩色多普勒超声观察了 36例无缺血性脑卒中的高血压病患者和 36例伴有缺血性脑卒中的高血压病患者双侧颈动脉内中膜厚度 ,并与 2 8名健康对照进行了比较。结果 :1 3组间空腹血糖、血脂和体重指数及平均年龄无显著性差异 (P >0 0 5 ) ;2 单纯高血压病患者和高血压病伴缺血性脑卒中患者颈动脉内中膜厚度明显高于健康对照者 (P <0 0 1) ,且高血压伴缺血性脑卒中患者颈动脉内中膜厚度明显高于无缺血性脑卒中的高血压患者 (P <0 0 1)。结论 :高血压病患者存在有颈动脉粥样硬化 ,且伴有缺血性脑卒中患者颈动脉粥样硬化程度明显加重 ,提示颈动脉粥样硬化程度可作为预测缺血性脑卒中发生的参考指标。     

中国缺血性脑卒中住院患者颈动脉粥样硬化病变性别差异的分析

目的:描述我国急性缺血性脑卒中住院患者颈动脉粥样硬化的分布特征,探讨传统危险因素与颈动脉粥样硬化的关系。方法:研究病例来自全国25个省市41家三级甲等医院,连续收集2011年1月至2011年5月,住院的脑梗死患者,对资料完整且年龄≥18岁的12 424例脑卒中患者进行分析。结果:住院缺血性脑卒中患者的颈动脉斑块患病率为76.9%,颈动脉内膜(IMT)增厚率为54.3%,狭窄率≥70%的患者占7.0%,男性的颈动脉粥样硬化患病率高于女性(P0.001),男女两性的颈动脉粥样硬化患病率随年龄的增加呈线性增加(男性:β=8.550,P=0.012;女性:β=11.100,P=0.002),但男女两性间的差异随年龄的增加逐渐减少。多因素Logistic回归分析显示,年龄、高血压和糖尿病,是男女两性脑卒中患者颈动脉粥样硬化患病的共同危险因素,高LDL与男性颈动脉斑块患病率有关,心房颤动病史与男性颈动脉IMT增厚率密切相关,吸烟仅与男性颈动脉斑块和颈动脉IMT增厚率有关。结论:我国缺血性脑卒中住院患者中颈动脉粥样硬化病变普遍存在,男性脑卒中患者的颈动脉粥样硬化患病率高于女性,传统危险因素与颈动脉粥样硬化指标间的关系存在性别差异。     

阿托伐他汀钙对缺血性脑卒中患者颈动脉粥样硬化斑块的影响

目的 探讨阿托伐他汀钙对缺血性脑卒中患者颈动脉粥样硬化斑块、血脂、C反应蛋白的影响.方法 入选80例缺血性脑卒中伴颈动脉粥样硬化斑块患者,随机分为常规治疗组（39例）和阿托伐他汀钙组（41例、20mg/d）,24周为一疗程.分别于治疗前、治疗后采用多普勒超声检测评估颈动脉粥样硬化斑块（斑块数量、斑块直径、斑块面积）、颈动脉内膜厚度（IMT）,检测比较血浆hs-CRP、血脂水平（总胆固醇、甘油三酯、低密度脂蛋白）.结果 与常规治疗组比较,阿托伐他汀钙组治疗后患者颈部血管动脉粥样硬化斑块直径、面积明显缩小,IMT、hs-CRP及血脂显著降低,差异有统计学意义（P＜0.05）.结论 阿托伐他汀钙对缺血性脑卒中伴颈动脉粥样硬化斑块患者具有较好的疗效.     

高敏C反应蛋白和肺炎衣原体感染与颈动脉粥样硬化及缺血性脑卒中的相关性研究

目的探讨高敏C反应蛋白水平、肺炎衣原体抗体与颈动脉粥样硬化及缺血性脑卒中TOAST亚型的关系。方法缺血性脑卒中组135例,对照组135例,测定2组的高敏C反应蛋白水平、肺炎衣原体IgG抗体、颈动脉内膜中层厚度及颈动脉粥样硬化程度。结果(1)高敏C反应蛋白水平升高与颈动脉内膜中层厚度及颈动脉粥样硬化程度相关,OR值分别为3.44和6.82;高敏C反应蛋白水平升高与大动脉粥样硬化性脑卒中危险性升高相关,OR值为10.11。(2)肺炎衣原体抗体的阳性率与颈动脉内膜中层厚度及颈动脉粥样硬化程度相关,OR值分别为1.76和4.89。结论高敏C反应蛋白水平和慢性肺炎衣原体感染与颈动脉粥样硬化密切相关,同时高敏C反应蛋白水平升高,可增加发生大动脉粥样硬化性脑卒中的风险。     

胱抑素C与早期2型糖尿病患者颈动脉内膜中层厚度的相关性

98例早期2型糖尿病患者,分为动脉粥样硬化(AS)组和非AS组,测定空腹血浆胱抑素C水平.结果显示,胱抑素C水平与颈动脉斑块数量显著相关( r=0.432,P＜0.01),胱抑素C是颈动脉内膜中层增厚的独立危险因素之一(OR=2.21,95％ CI1.88 ～3.02).     

血浆半胱氨酸蛋白酶抑制剂C与缺血性卒中患者颈动脉粥样硬化的关系

目的 探讨血浆半胱氨酸蛋白酶抑制剂C（cystatin C,CysC）水平与缺血性卒中患者颈动脉粥样硬化斑块的相关性.方法 回顾性分析急性缺血性卒中患者的临床资料,根据颈部血管超声检查结果分为无斑块组和斑块组,再将斑块组分为稳定斑块组和易损斑块组,采用多变量logistic回归分析和Pearson相关分析,探索颈动脉粥样硬化斑块的危险因素.结果 共纳入226例急性缺血性卒中患者,其中172例存在颈动脉斑块,54例无斑块.存在颈动脉斑块的患者中,94例为稳定斑块,78例为易损斑块.斑块组年龄[（71.82 ±9.94）岁对（60.74±13.81）岁;t=6.160,P=0.014]、缺血性心脏病患者比例（11.6％对1.9％;6.169,P=0.020）、收缩压[（148.770± 21.007）mm Hg对（142.240 ± 19.404） mm Hg;t=2.029,P=0.044;1 mm Hg=0.133 kPa]和血浆CysC浓度[（1.046±0.438） mg/L对（0.860±0.214） mg/L;t=3.006,P=0.003]以及颈动脉IMT[（1.122±0.278）mm对（0.878 ±0.250） mm;t =5.762,P=0.000]显著性高于无斑块组.多变量logistic回归分析显示,年龄[优势比（odds ratb,OR）1.079,95％可信区间（confidence interval,CI）1.044 ～1.116;P =0.000]和IMT（OR 31.450,95％ CI 6.233 ～ 158.692;P =0.000）是颈动脉斑块的独立危险因素,而血浆CysC水平与颈动脉斑块无显著独立相关性（P=0.217）.稳定斑块组仅IMT显著性高于易损斑块组[（1.176±0.285） mm对（1.058±0.258） mm;t=-2.824,P=0.005],而且IMT（OR0.195,95％ CI0.059～0.064;P =0.007）是颈动脉斑块稳定性的独立保护因素.Pearson相关性分析显示,血浆CysC水平与年龄（r =0.375,P=0.000）和血清肌酐水平（r=0.462,P=0.000）呈正相关,但与颈动脉IMT（r=0.075,P=0.264）无显著相关性.结论 在缺血性卒中患者中,未发现血浆CysC水平与颈动脉粥样斑块、斑块稳定性以及IMT之间存在相关性.     

主动脉弓粥样硬化性病变与缺血性卒中

由于检测技术的局限和医生认识的不足,人们公认的常见栓子来源仍为心源性栓子、颈动脉和椎动脉病变,而对主动脉弓粥样硬化病变这一重要的栓子来源未引起足够重视.文章简要阐述了主动脉弓粥样硬化性病变的特征、检测方法及其与缺血性卒中风险的相关性.     

Relationship of Von Willebrand Factor with carotid artery and aortic arch calcification in ischemic stroke patients

BackgroundLarge population studies have revealed that increased von Willebrand Factor (VWF) levels are associated with an increased risk of ischemic stroke. In previous studies VWF was associated with atherosclerosis in healthy individuals. However, it is yet unknown what the association is between atherosclerosis and VWF levels in patients with ischemic stroke.ObjectivesThe aim of our study was to determine the association of atherosclerosis, measured with recent developed techniques, and VWF levels in a large, well characterized, cohort of ischemic stroke patients and to determine the prognostic value.MethodsWe included 925 consecutive patients with transient ischemic attack (TIA) or ischemic stroke. Calcification volumes (mm³) were scored in the aortic arch and both carotid arteries using multidetector computed tomography (CT) angiography. VWF antigen (VWF:Ag) levels were measured using ELISA.ResultsMean VWF:Ag levels were significantly higher in the presence of calcification in either the aortic arch (1.47 vs. 1.37 IU/ml [P = 0.039]) or the carotid arteries (1.49 vs. 1.34 IU/ml [P = 0.001]). Patients with a large artery atherosclerosis ischemic stroke had significantly higher VWF:Ag levels then the other TOAST subtypes (P < 0.0001). High VWF:Ag levels were associated with an unfavorable outcome (modified Rankin Scale >2 vs. ≤2; 1.64 vs. 1.41 IU/ml, [P < 0.0001]).ConclusionOur study showed a strong association between the extent of atherosclerosis in both the aortic arch and the carotid arteries and VWF levels in patients with TIA or ischemic stroke. Higher VWF levels are found in large artery atherosclerosis and are associated with a poor outcome.     

Relationship between mitral annular calcification and severity of carotid atherosclerosis in patients with symptomatic ischemic cerebrovascular disease

OBJECTIVES: Many studies have reported the association between mitral annular calcification (MAC) and stroke. MAC has been speculated to be a direct embolic source of stroke. Recently, the association between MAC and atherosclerosis in the coronary artery, aorta, and carotid artery has been reported. This prospective study investigated the association between MAC and severity of carotid atherosclerosis in patients with symptomatic ischemic cerebral disease to evaluate the association between MAC and atherosclerosis as a cause of stroke. METHODS: We studied 377 patients with ischemic cerebral disease (253 men, 124 women, mean age 68 +/- 11 years) who underwent echocardiography to determine the presence of MAC and carotid ultrasonography to determine the severity of carotid atherosclerosis. Plaque score was the sum of the maximum intimamedia thickness in the common carotid region, the bifurcation bulb region, and the internal carotid artery region, including both right and left arteries. RESULTS: MAC was found in 86 patients, and was more frequent in women, the elderly, and patients with diabetes or hyperlipidemia (p < 0.05). Plaque score was higher in patients with than without MAC (8.3 +/- 5.8 vs 5.2 +/- 5.2 mm, p < 0.001). Multivariate regression analysis identified MAC (r = 0.26, p < 0.0001), female sex (r = -0.12, p = 0.03), and age (r = 0.23, p < 0.0001) as independently associated with plaque score. CONCLUSIONS: MAC is independently associated with severity of carotid atherosclerosis in patients with symptomatic ischemic cerebral disease. This association suggests MAC may be indirectly related to cerebrovascular disease as a marker of the presence of progressive arteriosclerosis for thromboemboli causing stroke.     

Carotid atherosclerosis and ischemic stroke in young patients.

BACKGROUND: Epidemiological studies indicate a high prevalence of carotid atherosclerosis in elderly patients with ischemic stroke. The aim of this study was to investigate the presence of early carotid atherosclerotic lesions in young subjects with ischemic stroke, in the absence of the common atherosclerotic risk factors. METHODS: We studied 98 young patients with first ischemic stroke (54 males and 44 females; mean age 41.2 years; range 32-50) and 96 healthy controls. All subjects underwent ultrasonographic scanning of the carotid arteries according to a standardized protocol. RESULTS: The carotid intima-media thickness was significantly increased in the patient group (p<0.001) compared with controls. In addition, the prevalence of carotid atherosclerotic plaques was greater in the patients than in the controls (p<0.001). In particular, we detected 18 non-occlusive carotid plaques and 16 thrombotic occlusions. In 8 patients, the lesions were bilateral. The echographic pattern of the plaques was hard in 8 cases, soft in 5 cases, and mixed in the remaining 5 cases. CONCLUSIONS: We detected an increased wall thickness of the carotid arteries and an increased prevalence of carotid atherosclerotic lesions and carotid thrombotic occlusions in young patients with ischemic stroke, with a relative low incidence of cardiovascular risk factors. This finding suggests that arterial intima-media thickness per se is an important determinant of vascular disease in young patients. The data also provide indirect support for the potential role of genetic factors in the genesis of atherosclerosis in young patients.