老年脑梗死与颈动脉粥样硬化关系的临床研究

目的　探讨老年脑梗死与颈动脉粥样硬化的关系。方法　应用彩色多普勒超声对 1 0 8例老年脑梗死患者及 86例同龄无明显心脑血管病患者进行对照研究 ,观察其颈动脉内膜 -中膜厚度 (IMT)、斑块结构及管腔狭窄情况。结果　脑梗死组颈动脉斑块发生率为 82 .41 % ,显著高于对照组 (48.84% ) (P<0 .0 0 0 1 )。斑块类型中软斑块及溃疡斑所占的比率、颈总动脉 IMT增厚和颈动脉中度 (50 %～ 70 % )及重度 (>70 % )狭窄的发生率脑梗死组高于对照组 ,差异均有显著性意义。结论　老年人颈动脉粥样硬化斑块类型 ,IMT增厚及管腔狭窄程度与脑梗死密切相关。     

颈动脉粥样硬化斑块稳定性与脑梗死的相关研究

目的探讨颈动脉粥样硬化斑块的稳定性与脑梗死关系。方法对120例脑梗死病人及100例对照组病人行颈动脉超声检查。结果脑梗死组斑块发生率（72．8％）明显高于对照组（56．0％），梗死组不稳定斑块（软斑及溃疡斑）的发生率明显高于对照组（分别为41．1％与18．3％）；梗死侧组软斑及溃疡斑的发生率亦明显高于非梗死侧组，分别为63个（52.1％）与11个（18.6％）（P〈0．05）。脑梗死组〉75％的管腔狭窄数为20例明显高于对照组的3例（，P〈0．05）。结论颈动脉粥样硬化与脑梗死显著相关，颈动脉粥样硬化的程度及斑块的不稳定性是脑梗死的危险因素。     

缺血性脑血管病患者颈动脉粥样硬化斑块和狭窄的超声研究

目的观察缺血性脑血管病患者的颈动脉斑块性质、分布特点及狭窄情况,探讨颈动脉斑块和狭窄的分布规律。方法缺血性脑血管病患者340例,行颈部血管超声检查.其中短暂性脑缺血发作(TIA)患者105例(TIA组),脑梗死患者235例(脑梗死组);又根据年龄分为青年组(54例),中年组(137例)和老年组(149例)。结果随年龄增加,缺血性脑血管病患者危险因素:高血压、糖尿病、冠心病、吸烟、家族史显著增加(P<0.01)。脑梗死组颈动脉内膜中层厚度明显高于TIA组(P<0.01);70%～99%血管狭窄斑块发生率高于50%～69%血管狭窄和<50%血管狭窄(P<0.01);老年组斑块发生率、颈动脉狭窄的发生率高于中年组及青年组(P<0.01)。结论超声检查显示不稳定斑块与缺血性脑血管病的关系更为密切,导致颈动脉狭窄的斑块中,以软斑块和混合性斑块多见。超声检查可以用于颈动脉狭窄患者的诊断及监测。     

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。     

影像学检查对缺血性脑血管病患者颈动脉粥样硬化斑块的研究

目的采用双源CT血管造影(CTA)和高分辨MRI,探讨缺血性脑血管病患者颈总动脉分叉处粥样硬化斑块的性质、成分和动脉管腔狭窄程度与缺血性脑血管病的关系。方法选择缺血性脑血管病患者40例,经颈部CTA检测出颈总动脉分叉处粥样硬化斑块并伴管腔狭窄,再接受MRI扫描;分析颈动脉粥样斑块的性质、成分及管腔狭窄程度。结果 40例患者中,CTA检出斑块61个,其中混合性斑块31个;钙化性斑块18个;软斑块12个。高血压30例,检出斑块49个;无高血压10例,检出斑块12个。MRI检出斑块61个,其中Ⅲ型14个;Ⅳ～Ⅴ型23个,Ⅵ型6个;Ⅶ型18个。斑块内溃疡6例;颈动脉粥样硬化斑块造成同侧急性脑梗死14例,双侧颈动脉斑块造成双侧脑梗死10例,一侧颈动脉检出粥样斑块而对侧发生脑梗死2例。结论缺血性脑血管病患者颈动脉粥样硬化斑块主要以混合性斑块为主,双侧好发;高血压患者斑块发生率高于无高血压患者;颈动脉粥样硬化斑块造成同侧脑梗死发生率较高。     

颈动脉粥样硬化与脑梗死复发的关系研究

目的探讨颈动脉粥样硬化与脑梗死复发的关系。方法采用彩色多普勒超声对278例脑梗死患者的颈动脉进行检测,并随访18个月,脑梗死复发64例(复发组),脑梗死无复发214例(无复发组),比较2组患者颈动脉粥样硬化的特征。结果复发组患者高血压、高胆固醇血症、糖尿病明显高于无复发组(P0.05,P0.01)。颈动脉中、重度狭窄及闭塞患者脑梗死复发率明显高于无颈动脉粥样硬化改变及颈动脉轻度狭窄患者(P0.05)。软斑患者脑梗死复发率明显高于无斑块及硬斑患者(P0.05)。结论颈动脉粥样硬化与脑梗死的复发密切相关,颈动脉粥样硬化的严重程度是脑梗死复发的危险因素,可作为脑梗死复发的预测指标。     

颈动脉双源CT血管造影和脑CT动态灌注成像在缺血性脑血管病的应用

目的运用颈动脉双源CT血管造影(CTA)和脑CT动态灌注成像(DCTPI)扫描,探讨缺血性脑血管病患者颈动脉粥样硬化斑块造成管腔狭窄与脑缺血之间的关系。方法临床诊断短暂性脑缺血发作和超急性或急性脑梗死患者40例,急诊行头颅CT或MRI扫描后,立即行颈动脉双源CTA和脑DCTPI扫描,对颈动脉粥样硬化斑块造成管腔的狭窄程度和脑灌注血流参数进行评价。结果 40例患者中,颈动脉无狭窄9例,占22.5%;轻度狭窄9例,占22.5%;中度狭窄12例,占30.0%;重度狭窄8例,占20.0%;完全闭塞2例,占5.0%。15例超急性或急性脑梗死患者梗死中心区患侧脑血流量较对侧明显下降,同时梗死中心区脑血流量较缺血半暗带或边缘区也明显下降,差异有统计学意义(P0.05);梗死中心区与缺血半暗带或边缘区脑血容量、造影剂到达峰值时间、平均通过时间差异无统计学意义(P0.05)。结论颈动脉双源CTA和脑DCTPI联合应用可同时显示颈动脉粥样硬化斑块造成颈动脉狭窄情况和缺血脑组织的部位和范围,为临床治疗缺血性脑血管病提供影像学依据。     

磁共振弥散像血管造影及颈动脉超声对短暂脑缺血发作的诊断价值

目的　评价磁共振弥散加权对比成像、数字减影血管造影术 (DSA)及颈动脉超声对短暂性脑缺血发作 (TIA)的诊断价值。方法　 10 2例颈内动脉及椎基底动脉系统TIA患者分别进行磁共振弥散加权对比成像、DSA及颈动脉超声检查。结果　 4 0例 (39.2 %)TIA患者显示脑梗死或小血管腔隙性梗死 ,其中 12例 (11.8%)患者弥散加权对比成像可显示T2 加权像不能显示的超早期梗死灶 ,有 30例患者行颈动脉多普勒超声及DSA检查 ,管腔中、重度狭窄的 10例 (33.3%)。 2 3例 (76 .7%)TIA患者DSA显示颈动脉狭窄和 (或 )相应脑动脉的狭窄及闭塞。结论　磁共振弥散加权对比成像及DSA是诊断TIA患者中超早期脑梗死和显示动脉狭窄及闭塞的敏感手段 ,颈动脉超声对管腔正常或轻度狭窄诊断的吻合率较高 ,对中、重度狭窄或闭塞诊断的准确性不如DSA。     

Clinical applications of noninvasive carotid artery testing

The management of patients with cerebral transient ischemic attacks and carotid artery stenosis remains controversial. Noninvasive techniques help to determine which patients require surgical intervention without exposing the majority of patients to the risk and discomfort of invasive procedures. Measurement of ophthalmic artery pressure by ophthalmodynamometry or oculoplethysmography gives a representation of perfusion pressure in the internal carotid artery circulation. Doppler ultrasound studies can define the extent of obstruction to flow at the carotid artery bifurcation and assess collateral flow from the external carotid artery. Real time B-mode ultrasonography can detect nonobstructive ulcerated plaque in the carotid artery bifurcation. Employing these examinations in a test battery can identify hemodynamically significant lesions, which are more likely to precipitate a stroke. The information obtained from these studies can be utilized in patients with episodes of cerebral transient ischemic attacks, asymptomatic carotid artery bruits and vertebrobasilar insufficiency. Noninvasive carotid artery testing is also useful in screening patients with nonspecific symptoms, such as dizziness or light-headedness, which may be related to decreased flow in the carotid circulation. Noninvasive carotid artery testing can provide valuable anatomic and physiologic information required in the appropriate management of patients with cerebrovascular disease. It is of particular value in managing patients with heart disease who are at high risk for complications from invasive procedures.     

老年腔隙性脑梗死患者的梗死部位及病因分析

目的了解老年缺血性脑血管病患者中腔隙性脑梗死的疾病特点。方法回顾性收集我科住院的年龄≥65岁腔隙性脑梗死患者146例,并对其危险因素和梗死部位进行分析。结果腔隙性脑梗死的主要危险因素为高血压(76.0%)和糖尿病(29.5%),颅内动脉粥样硬化或狭窄(56.2%)和颅外颈动脉粥样硬化斑块(58.9%)在腔隙性脑梗死中也较多见。腔隙性脑梗死以基底节为主。颅内动脉粥样硬化与后循环腔隙性脑梗死相关性高(HR=2.552,95%CI:0.05～1.35),颈动脉粥样硬化与前循环腔隙性脑梗死相关性高(HR=2.645,95%CI:0.76～17.9);心源性疾病可能是后循环腔隙性脑梗死的原因之一(HR=1.401,95%CI:0.08～1.83)。结论老年腔隙性脑梗死进行二级预防,大动脉粥样硬化仍是干预重点。     

脑梗死患者血纤维蛋白原和脂蛋白(a)水平与颈动脉硬化的关系

目的探讨脑梗死患者血纤维蛋白原和脂蛋白(a)水平与颈动脉粥样硬化的关系。方法应用彩色多普勒超声仪检测130例脑梗死患者的颈动脉内中膜厚度及斑块形成情况,同期检测患者血纤维蛋白原和脂蛋白(a)浓度,观察两者间的关系。结果130例患者中有76例患者存在颈动脉硬化病变,其中29例经超声检查诊断为颈动脉内中膜增厚,47例诊断为颈动脉粥样硬化斑块形成。颈动脉硬化组患者的平均纤维蛋白原和脂蛋白a水平显著高于无颈动脉硬化组(均P<0.01),并且随着平均纤维蛋白原水平和脂蛋白a水平升高颈动脉粥样斑块发生率显著升高(均P<0.05)。结论脑梗死患者血纤维蛋白原,脂蛋白a水平和颈动脉粥样硬化程度之间有密切的相关性。     

脑保护装置下高龄重度颈动脉狭窄患者颈动脉支架成形术的有效性和安全性评价

目的评价脑保护装置下高龄重度颈动脉狭窄患者颈动脉支架成形术(CAS)的有效性及安全性。方法选择2009年1月—2012年1月在青岛大学医学院附属医院行CAS的高龄重度颈动脉狭窄患者37例,术中均应用脑保护装置,观察患者狭窄改善情况、围术期并发症发生情况、回收脑保护装置内脱落栓子情况,随访1年观察患者缺血性脑血管事件发生情况。结果 36例患者脑保护伞均一次性顺利通过狭窄段放置到位成功释放;术后残余狭窄率均30%,平均狭窄程度从(83.0±6.7)%降至(13.0±6.1)%;回收的脑保护装置中有26个发现脱落的组织碎片;围术期均未出现脑出血、症状性脑梗死、支架内血栓形成等严重并发症;37例患者随访1年,无短暂性脑缺血发作(TIA)、卒中、死亡发生。结论脑保护装置下对高龄重度颈动脉狭窄患者行CAS成功率和安全性较高。     

C反应蛋白与脑梗死患者颈动脉粥样硬化病变的关系

目的 探讨C反应蛋白与脑梗死患者颈动脉粥样硬化和预后的关系.方法 筛选94例首次发病的急性脑梗死患者,应用免疫比浊法测定血清C反应蛋白水平,应用颈动脉超声评价颈动脉粥样硬化的特征,并对患者神经功能缺损评分、残疾率和死亡率进行评价.结果 与低C反应蛋白组脑梗死患者相比,高C反应蛋白组脑梗死患者颈动脉内膜中膜厚度和不稳定性斑块的发生率显著增高(P<0.05);高C反应蛋白组脑梗死死亡率、残疾率和神经功能缺失评分均显著高于低C反应蛋白组(P<0.01).结论 C反应蛋白可以反映颈动脉粥样硬化的特征和斑块的稳定性,是了解脑梗死预后的重要指标.     

应用彩色多普勒超声检测缺血性脑血管病与颈动脉粥样硬化的关系

目的探讨缺血性脑血管病与颈动脉粥样硬化病变之间的关系。方法对130例缺血性脑血管病患者进行颈动脉彩色多普勒超声检查，130例患者中56例短暂性脑缺血发作（TIA），74例脑梗死；42例非缺血件脑血管病患者为对照组。检测颈动脉内膜增厚及斑块形成等血管异常发牛率、斑块类型及斑块的分布情况。结果TIA组患者颈动脉内膜-中层厚度（IMT）增厚及颈动脉硬化斑块等异常检出率为73．2％（41／56），脑梗死组异常率为87．8％（65／74），对照组受检者异常率为28．6％（12／42），TIA组及脑梗死组与对照组比较差异有显著意义（P〈0．01）。脑梗死组患者脂质性斑块及混合性斑块的发生率高于TIA组。颈动脉硬化斑块最常见部位为颈总动脉分又处，其次为颈内动脉近段。左右侧差异无显著意义。结论颈动脉硬化与缺血性脑血管病有密切相关性，颈动脉超声有助于预测缺血性脑血管病的发病危险。     

颈动脉粥样硬化对缺血性脑血管病的影响

目的探讨颈动脉粥样硬化斑块对缺血性脑血管病的影响。方法选择我院神经内科住院的缺血性脑血管病患者68例，分为脑梗死组（CI组）43例和短暂性脑缺血组（TIA组）25例，另选同期门诊及病房非脑血管病患者32例（对照组），采用彩色多普勒血流显像技术对两组患者颈动脉粥样硬化斑块进行比较。结果68例缺血性脑血管病患者中，48例（70．6％）有动脉粥样硬化斑块，对照组5例（15．6％）有动脉粥样硬化斑块，两组患者粥样硬化斑块检出率间差异有显著性意义（P〈0．05）。68例缺血性脑血管病患者无症状侧颈动脉斑块检出率高于症状侧斑块检出率。CI、TIA两组患者无症状侧斑块检出率与症状侧斑块检出率间差异亦均有显著性意义（P〈0．05）。结论颈动脉粥样硬化是脑梗死的重要危险因素。对缺血性脑血管病患者，除常规检查颅脑影像学外，还应重视检查颈部血管。     

颈部血管彩超检查对缺血性脑血管病患者的临床意义

目的 探讨颈部血管彩超检查对缺血性脑血管病患者的临床意义.方法 以我院2011年1月-2012年1月收治的缺血性脑血管病患者30例为观察组,无缺血性脑血管病者30例为对照组,对两组患者进行颈部血管彩超检查,比较颈动脉粥样斑块发生率和颈动脉狭窄率.结果 观察组颈动脉粥样斑块发生率为100.0%,颈动脉狭窄发生率为60.0%;对照组颈动脉粥样斑块发生率为16.7%,颈动脉狭窄发生率为10.0%;观察组患者的颈动脉粥样斑块发生率及颈动脉狭窄发生率均明显高于对照组,差异有统计学意义(P＜0.05).结论 颈动脉血管彩超检查可早期发现颈动脉粥样硬化,及时了解颈动脉血管狭窄,对预防或治疗缺血性脑血管病具有重要的意义.     

他汀药对颈动脉粥样硬化影响及其在预防脑梗死复发中作用

目的探讨辛伐他汀对颈动脉粥样硬化的影响,以及其在预防脑梗死患者复发中的作用。方法将622例脑梗死患者分成阿司匹林治疗组与辛伐他汀治疗组,辛伐他汀治疗组在阿司匹林治疗的基础上加用辛伐他汀20mg,每晚1次。随访观察6~36月,观察脑梗死复发情况,并在治疗前及治疗后8~12周应用彩色多普勒超声对脑梗死患者的颈内动脉斑块和狭窄程度进行评估。结果根据随机分组,治疗前两组一般情况和脑梗死复发危险因素无差异(P>0.05),312例阿司匹林组患者在随访期复发61例(19.6%),而辛伐他汀组仅有32例(10.3%)复发,两组在统计学上有差异(P<0.05),在治疗前两组患者在颈内动脉粥样硬化程度、狭窄程度及斑块的超声病理分型等方面的比较,均无差异,治疗后辛伐他汀组颈动脉粥样硬化程度、狭窄程度以及软斑和溃疡斑块的发生率则明显降低,与治疗前比较有差异(P<0.05)。结论阿司匹林治疗的基础上加用辛伐他汀治疗能明显降低脑梗死复发率,辛伐他汀可能通过对颈动脉粥样硬化的影响而起到降低脑梗死复发的作用。     

A four year clinical and echographic follow-up of asymptomatic carotid plaque.

Eighty-five patients with asymptomatic carotid plaque--a diagnosis revealed by B-mode high-resolution echotomography--were followed up for four years; the echoplaque changes were compared with the clinical history. Eight patients died (2 from stroke, 4 from myocardial infarction, and 2 from lung tumor) and were excluded from the follow-up. Three patients underwent carotid thromboendarterectomy (TEA) (1 bilateral), and these 4 carotids were not considered in the total series. At the first echo Doppler evaluation of 150 carotids, plaques were observed in 112; 38 vessels were free of lesions. Of the 150 carotids, 8 revealed a new plaques. In regard to the echogenic pattern, 95 of the 112 plaques (84.8%) remained unchanged, 16 (14.3%) progressed, and regression of a small homogeneous plaque was observed in 1 patient (0.9%). An increase of the degree of vascular stenosis, was observed in 23 of the 150 carotids (15.3%). Cerebral ischemic symptoms occurred in 5 patients. In 1 patient who suffered from stroke, a new, soft, dyshomogeneous plaque in the carotid of the side of the lesion was observed. In 3 patients (2 with strokes, 1 with transient ischemic attack) the occlusion of a previous severe stenosis was observed. The fifth patient had a stroke on the side of an unchanged, ulcerated hemodynamic lesion. A valid criterion for identifying a risky plaque should be the joint evaluation of the echostructural characteristics and the degree of stenosis.     

Morphologic and dynamic changes of atherosclerotic plaque at the carotid artery bifurcation: sequential imaging by real time B-mode ultrasonography

Occurrence of new symptoms of focal cerebrovascular disease, including completed cerebral infarction, transient cerebral ischemic attack and amaurosis fugax, was correlated with changes in size and morphology of atherosclerotic plaques at the carotid artery bifurcation visualized by real time B-mode ultrasonography. Bilateral serial images of 246 plaques in 123 patients were made in a time interval of 9 to 35 months between initial and follow-up studies. There was a significantly higher incidence of symptoms ipsilateral to plaques that grew [30 (25%) of 121] than of symptoms ipsilateral to plaques that diminished or remained unchanged [8 (8%) of 98] (p less than 0.001). Plaques that became hemodynamically obstructive by causing disruption of laminar flow or reduction of distal perfusion pressure at the ophthalmic artery were associated with a higher frequency of symptoms [12 (40%) of 30] than were nonobstructive plaques [26 (13%) of 201] (p less than 0.001). There was also a strong association between symptoms and plaque configuration. Mural plaques growing in a crescentic configuration along the wall of the carotid bifurcation between the first and second examination had a higher incidence of symptoms [22 (40%) of 56] than did plaques that grew but maintained a nodular configuration [8 (12%) of 65] (p less than 0.001), although the same proportion of each became hemodynamically obstructive. Sequential visualization of atherosclerotic plaques by real time B-mode ultrasonography of the carotid bifurcation may provide a method for studying the pathogenesis of arterial thrombosis.     

Interrelation between the extent of atherosclerosis in the thoracic aorta, carotid intima-media thickness and the extent of coronary artery disease

Intima-media thickness (IMT) of the common carotid artery and atherosclerosis of the thoracic aorta have been shown to correlate with coronary artery disease (CAD). This study compares the relation between wall changes in the thoracic aorta and the carotid arteries and the angiographic severity and extent of atherosclerotic lesions in the coronary arteries in patients with verified CAD. Atherosclerotic wall changes in the carotid arteries and the thoracic aorta were measured by B-mode ultrasonography and transesophageal echocardiography (TEE), respectively, in 37 subjects aged 65+/-10 years with angiographically verified CAD. The mean value of the common carotid IMT of the right and left sides was 0.87+/-0.21 mm. All subjects had carotid plaques. TEE detected grades II-IV atherosclerotic plaques in the thoracic aorta in 32 of the 37 (86%) patients. A significant correlation was seen between the extent of coronary artery stenosis and aortic plaques score (r=0.46, p=0.008). Mean carotid IMT was also significantly correlated with coronary artery stenosis extent score (r=0.44, p=0.007). Moreover, a significant correlation was seen between the aortic plaque score and the mean carotid IMT (r=0.39, p=0.02). In conclusion, we found a clear and significant relationship between wall changes in the thoracic aorta, common carotid IMT and the angiographic extent of coronary artery stenosis in patients with severe CAD. These findings indicate a potential of B-mode ultrasonography of the carotid arteries and transesophageal echocardiographic aortic examination in the diagnostic and prognostic evaluation of patients with suspected CAD.