急性脑梗死预后与高血压危险分层的关系

目的分析急性脑梗死预后与高血压危险分层的关系。方法将220例急性脑梗死患者进行高血压危险分层,并分为低中危组30例、高危组80例、极高危组110例,观察入院后第1、3、7及14天神经功能缺损情况,并分析其关系。结果高危组与极高危组入院第1天神经功能缺损评分差异无统计学意义(P>0.05);极高危组其余时间点临床神经功能缺损评分明显高于高危组和低中危组(P<0.01);低中危组临床疗效明显优于高危组和极高危组(P<0.01)。结论高血压危险分层对评估脑梗死急性期患者预后有重要参考价值。     

镁与动脉粥样硬化关系的研究进展

<正>镁是人体健康的重要营养元素,在细胞内镁离子的含量仅次于钾离子,是钙的天然拈抗剂.与细胞内三大物质代谢的300多种酶的活性有关。血浆内镁离子1/3与血浆蛋白结合,2/3为有生物活性作用的自由离子状态。镁作为多种酶的辅基参与机体糖、脂肪、蛋白质的代谢,细胞膜通透性、信号转导及线粒体功能,胰岛素受体活性,磷酸化与去磷酸化以及脱氧核糖核酸、核槠核酸的合成等有关,因此,镁儿乎     

PAS方案治疗动脉粥样硬化血栓形成型脑梗死的疗效

目的 探讨抗血小板、调脂和抗氧化联合治疗(PAS方案)动脉粥样硬化血栓形成型脑梗死患者急性期的疗效及预后.方法 收集2008年3月至2010年7月来我院神经内科住院治疗的550例动脉粥样硬化血栓形成型脑梗死患者,平均年龄(64.54±11.60)岁.入选患者分为三组:抗血小板治疗组、抗血小板联合他汀类调脂治疗组和PAS治疗组.随访12个月,其中10例失访,根据改良Rankin评分(mRS)评价各组患者预后,比较改善率、复发率、预后不良发生率和病死率的差异.结果 PAS治疗组在随访3个月和12个月时预后不良发生率、复发率和病死率明显低于其他两组(P<0.05),而改善率高于其他两组(P<0.05);随访3个月和12个月抗血小板联合他汀类调脂治疗组预后不良发生率和病死率低于抗血小板治疗组,但两者复发率比较无统计学差异(P>0.05).结论 抗血小板、他汀类调脂和抗氧化联合治疗能改善动脉粥样硬化血栓形成型脑梗死患者的预后,明显降低预后不良的发生率和病死率.     

症状性大脑中动脉狭窄的预后和影响因素

目的了解症状性大脑中动脉狭窄的脑卒中复发率及影响因素。方法前瞻性连续登记有症状的大脑中动脉狭窄患者107例,经头颅多普勒和磁共振成像证实,其中脑梗死90例,短暂性脑缺血发作17例。记录患者基线期一般情况及脑卒中危险因素。根据MRI将脑梗死患者分为单发病灶和多发病灶。平均随访(26.1±11.3)个月,评价脑卒中复发率及年复发率,多因素logistic回归分析影响脑卒中复发的因素。结果失访11例(10.3%),随访96例患者中,死亡3例,存活的93例患者中,复发缺血性脑卒中患者23例(24.7%).年复发率14.0%.未规律抗血小板治疗是脑卒中复发的独立影响因素(OR=0.154.95%CI:0.039-0.618,P=0.008),多发病灶患者有脑卒中易复发的趋势(OR=2.592,95%CI:0.681-9.861,P=0.162)。结论症状性大脑中动脉狭窄患者的脑卒中复发率高,未规律服用抗血小板药是复发的独立影响因素;多发病灶有脑卒中复发率高的趋势。     

抗血小板治疗后血小板高反应性与急性非心源性脑梗死早期神经功能恶化的关系

目的探讨抗血小板治疗后血小板高反应性(HTPR)与急性非心源性脑梗死早期神经功能恶化(END)的关系。方法入选急性非心源性脑梗死患者215例,根据入院72h内神经功能有无恶化分为END组55例和非END组160例。全部患者入院当日开始口服阿司匹林300 mg后6~24h空腹取血,检测血脂及糖化血红蛋白(HbA1c)等,并以二磷酸腺苷为诱导剂测定血小板聚集功能(PAGT),比较2组HTPR发生率,采用多因素logistic回归分析END的独立危险因素,采用ROC曲线评估PAGT对END的预测价值。结果 END组LDL[(3.23±0.75)mmol/L vs(3.02±0.63)mmol/L]、HbA1c[(6.75±0.65)%vs(6.70±0.54)%]明显高于非END组(P0.01)。END组HTPR发生率明显高于非END组,差异有统计学意义(63.34%vs 43.75%,P=0.011),多因素logistic回归分析显示,LDL、HbA1c和HTPR是急性非心源性脑梗死患者END的独立危险因素(OR=9.023,95%CI:3.085~26.387,P=0.000,OR=11.344,95%CI:3.882~33.152,P=0.000,OR=34.364,95%CI:4.422~267.029,P=0.001,),PAGT判断急性非心源性脑梗死END的ROC曲线下面积为0.864(95%CI:0.806~0.922,P=0.000)。结论 HTPR与急性非心源性脑梗死END密切相关。     

药物洗脱支架术后极晚期血栓形成原因及防治进展

药物洗脱支架能有效减少支架再狭窄率和靶血管的再次血运重建,但与金属裸支架相比,药物洗脱支架极晚期血栓（VLST）发生率呈上升趋势。研究显示药物洗脱支架术后再内皮化延迟、抗血小板药物抵抗、PCI操作技术与晚期血栓形成有密切相关。本文就 VLST形成原因、危险因素及防治策略作以下综述。     

氯吡格雷与他汀合用不会使预后恶化

数年前,有研究发现抗凝药氯吡格雷(商品名波立维)和各种他汀类调脂药有着共同的代谢机制。这些药物是通过同一种生化酶进行代谢的,这使得两者     

急性脑梗死患者血小板白细胞聚集体与动脉粥样硬化的关系

目的探讨急性脑梗死患者血清血小板白细胞聚集体与动脉粥样硬化斑块的关系。方法选择脑梗死患者110例,根据高分辨率MRI对颈动脉和大脑中动脉评估结果分为易损斑块组24例,稳定斑块组56例,无斑块组30例,另选择健康体检者30例(对照组)。比较各组血小板白细胞聚集体、血小板单核细胞聚集体、血小板中性粒细胞聚集体、血小板淋巴细胞聚集体水平。结果易损斑块组、稳定斑块组、无斑块组血清血小板白细胞聚集体、血小板单核细胞聚集体、血小板粒细胞聚集体、血小板淋巴细胞聚集体水平明显高于对照组,差异有统计学意义(P0.05)。易损斑块组和稳定斑块组血清血小板白细胞聚集体、血小板单核细胞聚集体水平明显高于无斑块组,差异有统计学意义(P0.05)。与稳定斑块组比较,易损斑块组血小板单核细胞聚集体水平明显升高,差异有统计学意义[(31.34±6.18)%vs(24.67±5.34)%,P0.05]。结论血小板白细胞聚集体与动脉粥样硬化斑块有关,而血小板单核细胞聚集体与斑块易损性密切相关,可作为斑块易损性指标。     

脑梗死急性期降压治疗与14天预后关系的研究

目的观察脑梗死急性期患者血压变化规律,探讨脑梗死急性期降压治疗与14 d预后的关系,为脑梗死急性期血压管理提供临床依据。方法将入选的143例急性脑梗死患者随机分为干预组70例和对照组73例。干预组给予降压治疗,使其1 d内收缩压下降10%～20%,入院7 d时血压降至140/90 mm Hg(1 mm Hg=0.133 kPa)以下,入院14 d内血压稳定在上述水平。动态监测2组患者14 d内的血压变化,采用美国卫生研究院卒中量表(NIHSS),观察2组患者入院时、14 d神经功能缺损程度及死亡/残疾比率。结果 2组入院14 d NIHSS评分呈降低趋势。与对照组比较,干预组患者14 d NIHSS评分、死亡/残疾比率明显降低(P<0.05)。多因素logistic回归分析显示,在调整了年龄、性别、高血压、入院NIHSS评分、入院血压及1 d血压下降幅度等因素后,降压治疗独立影响急性脑梗死14 d预后,降低14 d死亡/残疾的风险(OR=0.338,95%CI:0.136～0.840,P<0.05)。结论脑梗死急性期给予合理降压干预,有利于早期神经功能恢复,可降低14 d死亡/致残的风险。     

脑微出血部位和负荷与脑梗死抗血小板治疗的相关分析

目的探讨脑微出血(CMB)发生部位和负荷对脑梗死抗血小板治疗风险及获益的影响。方法选择伴CMB的急性脑梗死患者214例,根据CMB发生部位分为单纯脑叶组39例,深部/幕下组62例,混合部位组113例,随访各组新发脑梗死、脑出血情况,并比较各组治疗前及治疗1年后CMB的变化。结果深部/幕下组既往脑梗死、高血压和糖尿病比例明显高于单纯脑叶组和混合部位组(P<0.05)。混合部位组基线CMB数高于单纯脑叶组和深部/幕下组[(8.69±2.75)个vs(6.65±2.47)个、(6.58±3.17)个,P<0.05]。单纯脑叶组脑出血比例明显高于深部/幕下组和混合部位组(12.8%vs 3.2%、2.7%,P<0.05),且发生脑出血患者中4例基线CMB数>5个。深部/幕下组再发脑梗死比例明显高于单纯脑叶组和混合部位组(24.2%vs 7.7%、9.7%,P<0.05)。3组治疗1年后仅部分患者复查头颅MRI,其中单纯脑叶组28例,深部/幕下组40例,混合部位组56例。单纯脑叶组CMB进展比例明显高于深部/幕下组和混合部位组,差异有统计学意义(35.7%vs 12.5%、10.7%,P<0.05),且病灶以脑叶为主。结论抗血小板治疗风险与CMB部位和负荷相关,单纯脑叶CMB抗血小板治疗的脑出血风险增加,治疗后CMB更易进展。深部/幕下CMB患者脑梗死复发风险更高。     

急性缺血性脑卒中进展与预后关系的前瞻性研究

目的探讨缺血性脑卒中进展情况及其与预后的关系。方法前瞻性连续登记569例急性缺血性脑卒中患者的临床资料,根据欧洲进展性卒中研究小组定义的进展性卒中诊断标准判定卒中有无进展,并进行定期随访;采用单因素和多因素Logistic回归分析研究卒中进展与预后的关系。结果127例（22．3％）患者诊断为进展性卒中,其3、6个月死亡、死亡／残疾发生率均显著高于非进展者（P〈0．05）;卒中进展是3、6个月死亡、死亡／残疾的独立危险因素。结论急性缺血性脑卒中患者中约有20％病情呈进展性,卒中进展是预后不良的独立危险因素。     

氯吡格雷在短暂性脑缺血发作后脑卒中二级预防中的应用

目的探讨氯吡格雷在短暂性脑缺血发作(transient ischemic attack,TIA)后预防缺血性脑卒中发作的疗效。方法选择TIA患者279例,随机分为2组:氯吡格雷组158例(氯吡格雷75 mg,1次/d),长效阿司匹林组121例(拜阿司匹林100 mg,1次/d)。患者随访1.5～3.0(2.3±0.3)年,评估2组的安全性。结果氯吡格雷组患者缺血性脑卒中复发率明显低于长效阿司匹林组,差异有统计学意义(5.06% vs 12.40%,P0.05)。全部患者在TIA后缺血性脑卒中复发的危险比为0.4031,氯吡格雷组为0.1284,长效阿司匹林组为0.8129,差异有统计学意义(P0.05)。氯吡格雷组患者发生次要事件概率和胃肠道出血事件明显低于长效阿司匹林组,差异有统计学意义(1.90% vs 8.26%,1.27% vs 6.61%,P0.05)。结论氯吡格雷对TIA患者的缺血性脑卒中的预防,优于长效阿司匹林。     

急性缺血性脑卒中患者血清TIGAR mRNA水平及其与预后的关系

目的探讨急性缺血性脑卒中患者血清tp53诱导的糖酵解和凋亡调节因子(TIGAR)mRNA水平及其与预后的关系。方法选取247例急性缺血性脑卒中患者为研究对象。收集患者年龄、性别、体质指数、高血压、高脂血症、糖尿病、冠心病、吸烟、脑卒中分布、脑卒中发病时间、TOAST病因学分型、严重程度、脑卒中病灶数、出血转化、同型半胱氨酸(Hcy)、C反应蛋白(CRP)、D二聚体(D-D)、糖化血红蛋白A1c(HbA1c)、血管生成素1(Ang-1)等资料。采用实时荧光定量PCR法(qRT-PCR)检测血清TIGAR mRNA相对表达量,并分析其与预后的关系。结果 247例急性缺血性脑卒中患者90天内预后不良发生率为47.77%。预后良好组TIGAR mRNA相对表达量明显高于预后不良组(P0.05)。TIGAR mRNA评估急性缺血性脑卒中患者预后的曲线下面积AUC、敏感度、特异度分别为0.886、88.14%、80.62%。Logistic多因素回归分析显示脑卒中发病时间、TOAST病因学分型、严重程度、出血转化及TIGAR mRNA与急性缺血性脑卒中患者预后关系密切。结论血清TIGAR mRNA相对表达量越高,急性缺血性脑卒中患者预后越好,检测TIGAR mRNA相对表达量有助于评估患者预后情况。     

FLAIR血管高信号征预测急性缺血性脑卒中患者预后的应用价值分析

目的 探讨MRI中FLAIR血管高信号征在预测急性缺血性脑卒中患者预后的效果.方法 将2017年9月至2020年8月住院治疗的100例急性缺血性脑卒中患者纳入本次研究,据FLAIR是否呈现血管高信号征分为对照组(50例、血管高信号征阴性)和观察组(50例、血管高信号征阳性).对比两组患者血管狭窄程度、侧支循环分级情况、...     

北京地区缺血性脑卒中或短暂性脑缺血发作二级预防的研究

目的对入院的缺血性脑卒中或短暂性脑缺血发作(TIA)患者采取ABCDE策略治疗,分析患者出院后能否维持高水平药物治疗的符合率。方法选择2007年8～12月连续收入北京地区21家医院神经内科病房的缺血性脑卒中和(或)TIA患者1166例,记录患者二级预防中抗血小板、降压、降糖及调脂药物等治疗情况,出院后对患者进行随访,分析出院后90d、6个月和1年二级预防中抗血小板、降压、降糖和调脂治疗的符合率。结果 1166例患者中,复发性脑卒中541例,其抗血小板治疗比例为58.4%,降压、降糖和他汀类药物治疗比例分别为82.3%、85.3%和14.2%。出院后,完成90d、6个月及1年随访的患者分别为1012例、1012例和981例,其二级预防中抗血小板、降压、降糖和调脂治疗的符合率维持在较高水平。结论复发性脑卒中二级预防现状不容乐观,采取ABCDE策略治疗,对入院的缺血性脑卒中或TIA患者进行规范干预后,明显缩小二级预防循证证据与临床实践的差距,患者出院后,二级预防治疗的符合率维持在较高水平。     

Lisinopril for the treatment of hypertension within the first 24 hours of acute ischemic stroke and follow-up

BACKGROUND: Hypertension immediately after acute ischemic stroke is associated with impaired morbidity and mortality, although there are few data on antihypertensive use immediately after ictus. This randomized, double-blinded, placebo-controlled, parallel-group study explored the hemodynamic effect and safety of oral lisinopril initiated within 24 h after an ictus. METHODS: Forty hypertensive (systolic blood pressure [BP] >/=140 or diastolic BP >/=90 mm Hg) acute ischemic stroke patients (14 lacunar, 13 partial anterior, 7 total anterior, 6 posterior circulation infarct) were randomized to 5 mg of oral lisinopril (n = 18) or matching placebo (n = 22). Dose was increased to 10 mg (or 2 x placebo) on day 7 if casual systolic BP was >/=140 mm Hg and continued to day 14. After the initial dose, automated BP levels were monitored for 16 h. The BP levels and stroke outcome measures were assessed at day 14, and all patients were followed to day 90. RESULTS: At h 4 after the first dose, systolic/diastolic BP change was -20 +/- 21/-6 +/- 10 mm Hg (mean +/- SE) in the lisinopril group and 1 +/- 11/0 +/- 8 mmHg in the placebo group (group differences: systolic BP, P < .05; diastolic BP, P = .07). With a daily dosing regime, systolic BP, mean arterial pressure (MAP), diastolic BP, and pulse pressure (PP) were significantly lower in the lisinopril group compared to the placebo group at day 14 (P < .01). Neurologic and functional measures were similar between groups at follow-up. CONCLUSIONS: Lisinopril, even at small dosages, is well tolerated and an effective hypotensive agent after acute ischemic stroke, gradually reducing BP by 4 h after oral first-dose administration. Oral lisinopril is now being studied in a larger outcome-based trial in acute hypertensive stroke patients.     

Risk factors for and impact of poststroke pneumonia in patients with acute ischemic stroke

Poststroke pneumonia (PSP) is a common complication of stroke and an important cause of death following stroke. However, the treatment of PSP remains inadequate due to severe impairment to the respiratory system by PSP. Thus, it is crucial to focus on preventing PSP to improve the prognosis of patients with stroke.This prospective single-center Cohort study aimed to investigate the risk factors for pulmonary infection following an ischemic stroke and identify whether PSP significantly influences the prognosis of patients after stroke.Altogether, 451 patients who were treated for acute ischemic stroke in the First Affiliated Hospital of Chongqing Medical University in China between April 2017 and April 2018 were enrolled. Clinical data from the patients from admission to 3 months after discharge were collected. PSP was the primary outcome and poor prognosis or death at 3 months following discharge was the secondary outcome observed in this study. We performed logistic regression analyses to identify the risk factors for PSP and test an association between pneumonia and poor prognosis or death after stroke.Our findings revealed the following risk factors for PSP: atrial fibrillation odds ratio (OR) = 2.884, 95% confidence intervals (CI) = 1.316–6.322), being bedridden (OR = 2.797, 95%CI = 1.322–5.921), subject to an invasive procedure (OR = 12.838, 95%CI = 6.296–26.178), massive cerebral infarction (OR = 3.994, 95%CI = 1.496–10.666), and dysphagia (OR = 2.441, 95%CI = 1.114–5.351). Pneumonia was a risk factor for poor prognosis (OR = 2.967, 95%CI = 1.273–6.915) and death (OR = 5.493, 95%CI = 1.825–16.53) after stroke.Hence, since pneumonia increases the risk of poor prognosis and death following acute ischemic stroke, preventing, and managing the risk factors for PSP may improve the prognosis and reduce the mortality after stroke.     

Association between uric acid and the prognosis of acute ischemic stroke: A systematic review and meta-analysis

AimsMeta-analysis was performed to assess the value of serum uric acid in the prognosis of ischemic stroke.Data synthesisWe searched the databases of PubMed, Embase, and Web of Science. The literature we searched was published from the establishment of the database to January 2021. The references of the included literature were also collected. Two researchers sifted through the literature according to the inclusion and exclusion criteria and extracted the data. Stata 16.0 software was used for meta-analysis, and funnel plots were used to evaluate publication bias. Ten studies fulfilled the research criteria and were eventually included, and the analysis results showed that there was no significant association between serum uric acid and the functional outcome (OR = 0.99, 95% CI; 0.97–1.10), poor outcome (OR = 1.07, 95% CI; 0.99–1.15), vascular events (OR = 0.86, 95% CI; 0.52–1.41), and mortality (OR = 1.08, 95% CI; 0.93–1.24) related to ischemic stroke.ConclusionsThere was no significant correlation between serum uric acid level and prognosis of ischemic stroke.