脂蛋白相关磷脂酶A2与动脉粥样硬化血栓形成性卒中相关性研究

目的 探讨血清脂蛋白相关磷脂酶A2（1ipoprotein-associated phospholipase A2,Lp-PLA2）水平对动脉粥样硬化血栓形成（atherothrombosis,AT）性卒中发生风险的预测价值。方法 采用病例-对照研究,按照肝素治疗急性卒中研究（Trial of Org 10172 in Acute Stroke Treatment,TOAST）分型标准纳入急性AT患者80例为病例组,同期纳入80例体检中心年龄匹配的无心脑血管病的受试者作为对照组。所有纳入对象均记录动脉粥样硬化相关危险因素及影响Lp-PLA2水平潜在危险因素。采用酶联免疫吸附法（enzyme-linked immunosorbent assay,ELISA）检测血清Lp-PLA2水平,比较两组间基线Lp-PLA2水平,进一步将Lp-PLA2水平按四分位数分为4组,采用Logistic回归模型进行多因素分析。应用受试者特征工作曲线（receiver operating characteristic curve,ROC）分析评价Lp-PLA2对AT发生的预测价值。结果 病例组血清Lp-PLA2水平高于对照组,差异有显著性［（1571.9±57.4）ng/ml vs （1143.6±262.5）ng/ml,P＜0.001］。多因素分析校正性别、入院时收缩压、入院时血糖、吸烟史、体重指数（body mass index,BMI）及家族卒中史等因素后,病例组血清Lp-PLA2水平仍高于对照组,差异有显著性［比值比（odds ratio,OR）1.003,95%可信区间（confidence interval,CI）1.001～1.004,P=0.001］。将Lp-PLA2水平按四分位数分为4组,采用Logistic回归分析,结果表明,发生AT事件随Lp-PLA2水平的升高而增加;未校正任何危险因素时,最高四分位Lp-PLA2水平发生AT风险是最低四分位的20.864倍（P＜0.001）;校正相关危险因素后,最高四分位Lp-PLA2水平发生AT风险是最低四分位的9.200倍（P=0.003）。ROC分析结果表明,以Lp-PLA2水平1531.4 ng/ml作为预测AT发生的界点,其灵敏度为48.8%,特异度92.5%,曲线下面积（area under the curve,AUC）为0.76。结论 Lp-PLA2可能是预测AT发生的新型生物标志物,Lp-PLA2水平越高,AT发生风险越高;Lp-PLA2水平≥1531.4 ng/ml对预测AT发生可能有重要预测价值。     

Association between hemostatic markers,serum lipid fractions and progression of cerebral small vessel disease: A 2-year follow-up study

Introduction

Little is known if hemostatic markers and serum lipid fractions can predict further radiological progression beyond vascular risk factors in cerebral small vessel disease (SVD). We investigated whether they are associated with SVD radiological progression and if they are related to different SVD clinical manifestations.

Plasma levels of coagulation and fibrinolysis markers in acute ischemic stroke patients with lone atrial fibrillation

Atrial fibrillation (AF) is a well-defined risk factor for ischemic stroke. Patients with lone AF represent a subgroup of AF patients with the lowest lifelong stroke risk. Nonvalvular atrial fibrillation (NVAF) confers a hypercoagulable state resulting in an increased risk of thromboembolism. This study was performed to determine the contributory role of alteration in the hemostatic markers of thrombin generation and fibrinolysis in patients with lone AF during acute ischemic stroke episode. We studied thrombin-antithrombin complexes (TAT), prothrombin fragments 1+2 (F1+2), tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) concentrations in patients with acute middle cerebral artery ischemic stroke due to atherosclerotic large artery disease (n=50), lone AF (n=24) and cardioembolism (n=21). The values were compared with those of age-matched control subjects with lone AF and sinus rhythm (n=21 and 15, respectively). The mean F1+2 concentration was higher in the control subjects with lone AF in comparison with those without AF (p=0.014). Patients with stroke due to possible cardioembolism, from lone AF or other causes, had higher TAT (and marginally higher F1+2) concentrations than those with atherosclerotic stroke (p<0.001). tPA concentrations were not different among groups (p=0.89). PAI-1 levels were marginally higher in stroke patients with lone AF and atherothrombotic large artery disease compared to the controls without AF (p=0.05). These results suggest that in the acute period of ischemic stroke secondary to lone AF, enhancement of the coagulatory activity occurs as a result of increased thrombin generation, similar to other possible sources of cardioembolism. Observed hemostatic alterations in acute ischemic stroke associated with lone AF may indicate some therapeutic and prognostic implications. Received: 3 April 2000 / Accepted in revised form: 20 September 2000     

Comparison of levels of inflammatory markers and hemostatic factors in the patients with and without peripheral arterial disease

Introduction

Peripheral arterial disease is one aspect of atherosclerosis, a disease associated with both inflammation and hypercoagulability. Many recent studies have focused on the diversity of mechanisms by which inflammation can promote blood clotting. However, the relationship between plasma concentrations of inflammatory and hemostatic markers and the severity of atherosclerosis is not yet well studied. We want to determine the relations among selected D-dimer, C-reactive protein, fibrinogen, prothrombin time and serum amyloid A, and the ankle brachial index in patients with and without peripheral arterial disease.

Materials and methods

In a prospective cohort study, 45 consecutive patients with peripheral arterial disease of ankle brachial index < 0.90, and 44 patients without peripheral arterial disease of ankle brachial index 0.90 to 1.50 were included. D-dimer, fibrinogen, C-reactive protein, serum amyloid A, and prothrombin time were measured at the recruitment.

Results

Median values of serum amyloid A, D-dimer, and C-reactive protein were significantly higher in the peripheral arterial disease group than in those without peripheral arterial disease group (p < 0.001). The patients with PAD had moderately higher fibrinogen levels than without PAD (p < 0.01). Prothrombin time levels were normal in both groups. In multivariable regression analyses adjusting for all blood factors as well as potential confounders, patients with peripheral arterial disease, levels of serum amyloid A, and C-reactive protein showed a highly significant, inverse association with the ankle brachial index. D-dimer and fibrinogen level increase were also found to be related to lower ankle brachial index, while no association was observed between prothrombin time levels.

Conclusions

Higher C-reactive protein, serum amyloid A, and D-dimer levels are showing positive association with the presence of peripheral arterial disease. C-reactive protein and serum amyloid A levels are direct relations between the ankle brachial index and the extent of vascular inflammation.     

Targeted mutation of Fas ligand gene attenuates brain inflammation in experimental stroke

Inflammation is an important contributing mechanism in ischemic brain injury. The current study elucidates a previously unexplored role of Fas ligand (FasL) in post-stroke inflammatory responses that is independent of its well-known effect in triggering apoptosis. Focal cerebral ischemia was induced for 2 h by right middle cerebral artery occlusion (MCAO) in FasL mutant (gld) and wild-type mice. FasL mutation profoundly reduced brain damage and improved neurological performance from 6 to 72 h after ischemic stroke. The production of inflammatory cytokines in the brain was attenuated in gld mice after ischemia in the absence of dramatic change in inflammatory cell apoptosis. FasL mutation attenuated the recruitment of peripheral inflammatory cells (neutrophil) and inhibited the activation of residential glial cells (microglia and astrocyte). FasL mutation reduced CD8⁺ T cells and turned the Th1/Th2 balance towards Th2 in the brain and peripheral blood after cerebral ischemia. In contrast to cerebral ischemia, the molecular and cellular inflammatory changes induced by intracerebroventricular injection of lipopolysaccharide (LPS) were also attenuated in gld mice. Moreover, the soluble FasL (sFasL) and phospho-SAPK/JNK were decreased in gld mice, suggesting that the inflammatory role of FasL in experimental stroke might relate to sFasL and the c-Jun N-terminal kinase (JNK) signaling pathway. Taken together, our data suggest a novel role of FasL in the damaging inflammatory responses associated with cerebral ischemia. Neutralization of FasL may be a novel therapeutic strategy to suppress post-stroke inflammation and improve the long-term outcomes of stroke.     

脑微出血与脑卒中

目的探讨脑微出血与脑卒中发生、发展的联系。方法卒中患者83例，分为脑缺血组（43例）和脑出血组（40例），以同期住院的50岁以上非脑卒中患者设立对照组（32例）。采用T2加权梯度回波MRI观察各病例脑微出血、卒中病灶、腔隙性梗塞以及白质疏松情况，同时记录卒中患者的高血压、糖尿病、高脂血症、卒中病史以及阿司匹林使用史。结果微出血在缺血组和出血组的发生率分别为34．9％、75．0％，对照组9．4％。各组微出血均最常见于基底节区。微出血与高血压、卒中病史相关（P〈0．01），与高脂血症、糖尿病病史及使用阿司匹林无关（P〉0．05）。微出血的严重程度与腔隙性梗塞、白质疏松的严重程度相关（P〈0．01）．．微出血在卒中病灶区域同侧或对侧分布无显著性差异（P〉0．05）。出血组微出血在卒中病灶区域的分布率明显高于缺血组。结论微出血与脑卒中．特别是与出血性脑卒中有密切关系，对卒中患者出血性转化具有预测意义。     

Heart rate variability and markers of inflammation and coagulation in depressed patients with coronary heart disease

BACKGROUND: Depression is associated with an increased risk for cardiac morbidity and mortality in patients with coronary heart disease (CHD). Cardiac autonomic nervous system (ANS) dysregulation, proinflammatory processes, and procoagulant processes have been suggested as possible explanations. METHODS: Heart rate variability (HRV), an indicator of cardiac autonomic regulation, and markers of inflammation [C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)] and coagulation (fibrinogen) were assessed in 44 depressed patients with CHD. RESULTS: Moderate, negative correlations were found between fibrinogen and four measures of HRV. IL-6 also negatively correlated with one measure of HRV (total power) and was marginally related to two others (very low frequency and low frequency power). Neither CRP nor TNF-alpha was significantly related to any measure of HRV. CONCLUSIONS: The finding that fibrinogen and IL-6 are moderately related to HRV suggests a link between these factors in depressed CHD patients. The relationship between ANS function and inflammatory and coagulant processes should be investigated in larger mechanistic studies of depression and cardiac morbidity and mortality.     

Brain inflammation is induced by co-morbidities and risk factors for stroke

Chronic systemic inflammatory conditions, such as atherosclerosis, diabetes and obesity are associated with increased risk of stroke, which suggests that systemic inflammation may contribute to the development of stroke in humans. The hypothesis that systemic inflammation may induce brain pathology can be tested in animals, and this was the key objective of the present study. First, we assessed inflammatory changes in the brain in rodent models of chronic, systemic inflammation. PET imaging revealed increased microglia activation in the brain of JCR-LA (corpulent) rats, which develop atherosclerosis and obesity, compared to the control lean strain. Immunostaining against Iba1 confirmed reactive microgliosis in these animals. An atherogenic diet in apolipoprotein E knock-out (ApoE^−/−) mice induced microglial activation in the brain parenchyma within 8 weeks and increased expression of vascular adhesion molecules. Focal lipid deposition and neuroinflammation in periventricular and cortical areas and profound recruitment of activated myeloid phagocytes, T cells and granulocytes into the choroid plexus were also observed. In a small, preliminary study, patients at risk of stroke (multiple risk factors for stroke, with chronically elevated C-reactive protein, but negative MRI for brain pathology) exhibited increased inflammation in the brain, as indicated by PET imaging. These findings show that brain inflammation occurs in animals, and tentatively in humans, harbouring risk factors for stroke associated with elevated systemic inflammation. Thus a “primed” inflammatory environment in the brain may exist in individuals at risk of stroke and this can be adequately recapitulated in appropriate co-morbid animal models.     

急性重症脑卒中患者单核细胞免疫抑制与炎性标志物的相关性

目的 探讨急性重症脑卒中患者单核细胞免疫抑制与C-反应蛋白(CRP)和纤维蛋白原(Fg)的关系,了解卒中患者免疫抑制的可能机制.方法 研究连续入选的24h内入住神经重症监护病房(NICU)的急性脑卒中患者(53例),以同期神经内科普通病房住院的头晕患者(均经头颅MRI排除急性脑卒中)作为对照组(39例).检测脑卒中患者人院后第1、2、4、6和14天的单核细胞人类白细胞抗原-DR(HLA-DR)表达水平和卒中组、对照组入院后第2天CRP和Fg的浓度.采用GraphPad PRISM4.0 demo软件进行因素之间的关联分析.结果 与对照组比较,卒中组CRP、Fg的水平增高,差异有统计学意义(P<0.05).卒中组CRP和Fg与不同时间点的单核细胞HLA-DR表达水平有不同程度的负相关性.CRP与入院后第2天HLA-DR表达负相关性最明显(r=-0.419,P=0.001).Fg与入院后第4天HLA-DR表达负相关性最明显(r=-0.434,P=0.001).结论 急性重症脑卒中患者单核细胞免疫抑制机制与卒中后炎症反应有关.     

Association between inflammation, lipid and hemostatic factors in patients with stable angina

INTRODUCTION: Dyslipidemia and thrombotic processes are both clearly involved in atherogenesis and its secondary complications. Moreover, inflammation has also been shown to play an important role in the pathophysiology of atherosclerosis. Our objective was to determine the association between inflammation, lipids and thrombosis in a group of patients with stable angina. PATIENTS AND METHODS: 295 patients (217 males and 78 females) with a mean age of 65.69+/-11.24 years. Levels of C-reactive protein, total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, lipoprotein(a), apolipoproteins A1 and B100, fibrinogen and D-dimer were determined for each. RESULTS: Arithmetic and geometric means of C-reactive protein in the sample were 10.7 and 1.4 mg/l, respectively. Distributing the sample by quartiles of C-reactive protein, we found a positive correlation between C-reactive protein, fibrinogen and D-dimer levels (p<0.000), and an inverse correlation for HDL cholesterol and apolipoprotein A1 (p<0.000). In multivariate analysis, fibrinogen (p<0.000) and D-dimer (p<0.01) levels were independently associated with high levels of C-reactive protein. Of the lipid factors, only apolipoprotein A1 (p<0.000) was independently and inversely associated with high levels of C-reactive protein. CONCLUSIONS: These data confirm the association between prothrombotic and inflammatory states and suggest the anti-inflammatory effect of apolipoprotein A1.     

Association of inflammatory markers with hearing impairment: The English Longitudinal Study of Ageing

BackgroundHearing impairment is common at an older age and has considerable social, health and economic implications. With an increase in the ageing population, there is a need to identify modifiable risk factors for hearing impairment. A shared aetiology with cardiovascular disease (CVD) has been advanced as CVD risk factors (e.g. obesity, type 2 diabetes) are associated with a greater risk of hearing impairment. Moreover, low-grade inflammation is implicated in the aetiology of CVD. Accordingly, our aim was to investigate the association between several markers of inflammation – C-reactive protein, fibrinogen and white blood cell count – and hearing impairment.MethodsParticipants of the English Longitudinal Study of Ageing aged 50–93 were included. Inflammatory marker data from both wave 4 (baseline, 2008/09) and wave 6 (2012/13) were averaged to measure systemic inflammation. Hearing acuity was measured with a simple handheld tone-producing device at follow-up (2014/15).ResultsAmong 4879 participants with a median age of 63 years at baseline, 1878 (38.4%) people presented hearing impairment at follow-up. All three biomarkers were positively and linearly associated with hearing impairment independent of age and sex. After further adjustment for covariates, including cardiovascular risk factors (smoking, physical activity, obesity, diabetes, hypertension, cholesterol), memory and depression, only the association with white blood cell count remained significant: odds ratio per log-unit increase; 95% confidence interval = 1.46; 1.11, 1.93.ConclusionsWhile white blood cell count was positively associated with hearing impairment in older adults, no relationships were found for two other markers of low-grade inflammation.     

脉粥样硬化血栓形成性卒中与幽门螺杆菌感染的相关性

Previous studies have demonstrated that Helicobacter pylori infection is associated with coronary atherosclerotic heart disease, but the correlation between Helicobacter pylori infection and ischemic stroke remains unclear. The present study assessed the effects of Helicobacter pylori infection on atherothrombotic stroke. This study included 115 individuals with atherothrombotic stroke, all of whom were patients receiving treatment at the Department of Neurology, Aerospace Central Hos-pital (Aerospace Clinical Medical College Affiliated to Peking University) in China, from March 2006 to July 2009. In addition, 131 controls without the history of cardiovascular disease, cerebrovascular disease or atherothrombosis were also enrolled in the study. Results show that the Helicobacter pylori-IgG positive rate was greater in the atherothrombotic stroke patients than in the controls, but the difference was not statistically significant (67.8% vs. 61.8%, OR = 1.301, 95%CI: 0.769–2.203, P = 0.327). After correction for potential risk factors for Helicobacter pylori infection and known risk factors for ischemic stroke, no significant difference was detected between them (OR = 1.278, 95%CI: 0.667–2.449, P = 0.459). These results indicate that there is no specific correlation between Helicobacter pylori infection and atherothrombotic stroke. This finding requires further verification in large-sample prospective studies.     

缺血性脑卒中的病因分型与危险因素

目的探讨缺血性脑卒中病因分型与不同危险因素的关系。方法回顾性分析连续登记的急性缺血性卒中患者,记录其危险因素,并按急性卒中治疗试验（TOAST）标准将缺血性卒中分为5种类型分析相关危险因素对其发生风险的影响。结果在纳入分析的205例患者中,大动脉粥样硬化性卒中（LAA）100例（48．9％）、心源性卒中（CE）17例（8．3％）、小动脉闭塞性卒中（SAO）38例（18．5％）、其他原因所致卒中（SOE）12例（5．8％）、不明原因卒中（SUE）38例（18．5％）。分析显示,高血压与LAA的发生有关（OR=2．40,P=0．0028）;心房颤动对CE发生有显著作用（OR=365．90,P〈0．0001）;饮酒与SAO的发生可能有一定关联（OR=2．73,P=0．036）,而白细胞则在CE患者显著升高（OR=8．00,P=0．0013）。结论不同类型缺血性脑卒中与不同的危险因素有关。该结果对临床个体化预防与治疗有一定提示意义。     

Activated factor XI and tissue factor in chronic obstructive pulmonary disease: links with inflammation and thrombin generation

Introduction

Increased cardiovascular mortality and risk of venous thromboembolism are serious extra-pulmonary complications of chronic obstructive pulmonary disease (COPD). Previously, circulating active tissue factor (TF) and factor XIa (FXIa) have been reported to be associated with acute coronary syndromes.

Objective

To measure plasma FXIa and active TF, prothrombin fragment 1.2 (F1.2), and markers of systemic inflammation (C-reactive protein [CRP], interleukin-6 [IL-6], tumor necrosis factor α [TNFα] and matrix metalloproteinase 9 [MMP-9]) in 60 patients with documented stable COPD free of previous thromboembolic events.

Methods

In-house clotting assays using inhibitory monoclonal antibodies against FXIa and TF.

Results

FXIa was detected in 9 (15%) and TF activity in 7 (11.7%) COPD patients. Subjects positive for FXIa and/or TF (n = 10; 16.7%) had higher F1.2 (median [interquartile range], 398 [216] vs 192 [42] pM, p < 0.000001), fibrinogen (5.58 [2.01] vs 3.97 [2.47] g/L, p = 0.0007), CRP (14.75 [1.20] vs 1.88 [2.95] mg/L, p < 0.000001), IL-6 (8.14 [4.74] vs 2.45 [2.24] pg/mL, p = 0.00002), and right ventricular systolic pressure (47 [15] vs 38 [12] mmHg, p = 0.023), and lower vital capacity (66 [15] vs 80 [17] % predicted, p = 0.04) than COPD patients without detectable FXIa and TF. COPD severity was not associated with the presence of circulating FXIa and active TF.

Conclusions

This is the first study to show that active FXIa and TF are present in stable COPD patients, who exhibit enhanced systemic inflammation and thrombin generation. Our findings suggest a new prothrombotic mechanism which might contribute to elevated risk of thromboembolic complications in COPD.     

Association between site of lesion and driving performance after ischemic stroke

Abstract

Background:

Stroke presents with heterogeneous recovery periods, severity, and manifestation of deficits, all of which may adversely impact fitness-to-drive. Little is known about the association between site of lesion and driving performance after stroke.

Objective:

To investigate the association between site of stroke lesion and driving performance.

Method:

Seventy-three participants (age?=?56?±?11 years; 66 men) underwent a detailed battery of visual, cognitive, and on-road tests to determine fitness-to-drive at about 10 months after ischemic stroke. Associations between stroke location and driving performance were calculated using rank biserial (r _rb) correlation coefficients. Correlations were considered weak below 0.10, moderate between 0.10 and 0.49, and strong above 0.50. Wilcoxon rank sum tests were employed to discern differences in on-road driving performance between participants whose performance was of concern to the driving assessor and those who exhibited no major difficulties on the road.

Results:

In all, 28 (38%) out of the 73 participants exhibited major difficulties on the road. Those who showed difficulties on the road performed worse in all driving skills (P?<?0.05). Correlation analysis showed moderate to strong correlations between site of lesion and performance in several visual, cognitive and on-road tests. Lesions in the parietal lobe showed correlations ranging between 0.23 and 0.25 with driving skills including vehicle control and speed adaptations. Lesions in the occipital lobes correlated strongly with visual field (r _rb?=?0.53) and moderately with visual neglect (r _rb?=?0.28).

Conclusions:

Our results suggest that cortical lesions in the parietal and occipital lobes are associated with driving deficits after stroke. Further advances in our understanding of the neural correlates of driving performance may provide prognostic markers of fitness-to-drive and lead to early, targeted rehabilitation.     

Reperfusion following focal stroke hastens inflammation and resolution of ischemic injured tissue

Previously, we described cellular changes following Permanent Middle Cerebral Artery Occlusion (PMCAO) in spontaneously hypertensive rats. Ischemic changes following PMCAO included a time-related focal pan necrosis, inflammatory cell infiltration, gliosis, and eventual loss of necrotic tissue postPMCAO. We have now characterized changes which occur after Temporary Middle Cerebral Artery Occlusion (TMCAO; 80 or 160 min) followed by reperfusion and compared these changes to those which occur following PMCAO. TMCAO with reperfusion results in cortical infarcts which vary in size in an occlusion-time-dependent manner. After 1 h of reperfusion, ischemic changes were observed histologically, including microhemorrhages and the beginning of a slight inflammatory infiltration in and around the meningeal vasculature. This infiltrate consisted primarily of neutrophils, which by 6 h of reperfusion was significant with infiltration from deep blood vessels into brain tissue, including the presence of some monocytes adhering within blood vessels. Neutrophil infiltration occurred sooner and to a greater extent in reperfused tissues than in permanently occluded tissues, where it only began at 12 h postPMCAO. As occurred following PMCAO, increased Glial Fibrillary Acidic Protein (GFAP) immunoreactivity indicating astrogliosis was first observed at 12 h postTMCAO. Over 1–3 days of reperfusion, a heavy macrophage infiltrate was observed in the reperfused tissues in addition to a continued influx of neutrophils. Following 5 days of reperfusion, the lesion was completely replaced with inflammatory cells, of which macrophages predominated. Unlike PMCAO, which resulted in focal spots of neutrophil accumulation, neutrophils were more distributed throughout the infarcted cortex following TMCAO. Another apparent difference was in the great number of fibroblast-like cells seen in the fibrous connective tissue, especially adjacent to the meninges, following TMCAO. Finally, by 15 days after TMCAO few scattered macrophages were present within a loose fibrous connective tissue matrix that was once the lesion. This matrix continued to contain an abundance of fibroblasts and astroglia. In contrast, at this time after PMCAO, macrophages were observed within a diminished infarct area. The data indicate that reperfusion following focal ischemia alters the timing and extent of the inflammatory response that leads to resolution of the necrotic tissue.     

The impact of inflammation on the pathogenesis and prognosis of ischemic stroke

The inflammation plays a critical role in the stroke onset and even in the worsening of the lesions. Therefore, the investigation of inflammatory response in the acute stage may contribute to improve the treatment of ischemic stroke. High-sensitive CRP (hsCRP), IL-6 and TNFalpha were measured as inflammatory markers on admission and in the 28th day after the onset. Oxidized LDL was measured simultaneously, since it can be a marker of reactive oxygen species which reflect the activity of inflammation. Ischemic stroke patients within 24 h after the onset (n=105) were included in this study. All patients were classified into cardioembolism, large-artery atherosclerosis, lacunar infarction, branch atheromatous disease and arterial dissection groups based on the findings of MRI and MRA and clinical records. Oxidized LDL was significantly increased in the acute phase of all cases. The amplified level of IL-6 was related to the worse outcome. The increase of TNFalpha in lacunar infarction was statistically correlated to the neurological severity on admission. In conclusion, IL-6 may predict not only the severity of the stroke lesions but also the outcome of patients. TNFalpha may suggest the small arterial lesions.     

Association between pneumonia in acute stroke stage and 3-year mortality in patients with acute first-ever ischemic stroke

The influence of pneumonia in acute stroke stage on the clinical presentation and long-term outcomes of patients with acute ischemic stroke is still controversial. We investigate the influence of pneumonia in acute stroke stage on the 3-year outcomes of patients with acute first-ever ischemic stroke. Nine-hundred and thirty-four patients with acute first-ever ischemic stroke were enrolled and had been followed for 3 years. Patients were divided into two groups according to whether pneumonia occurred during acute stroke stage or not. Clinical presentations, risk factors for stroke, laboratory data, co-morbidities, and outcomes were recorded. The result showed that a total of 100 patients (10.7%) had pneumonia in acute stroke stage. The prevalence of older age, atrial fibrillation was significantly higher in patients with pneumonia in acute stroke stage. Total anterior circulation syndrome and posterior circulation syndrome occurred more frequently among patients with pneumonia in acute stroke stage (P < 0.001 and P = 0.009, respectively). Multivariate Cox regression revealed that pneumonia in acute stroke stage is a significant predictor of 3-year mortality (hazard ratio = 6.39, 95% confidence interval = 4.03–10.11, P < 0.001). In conclusion, pneumonia during the acute stroke stage is associated with increased risk of 3-year mortality. Interventions to prevent pneumonia in acute stroke stage might improve ischemic stroke outcome.     

赖氨酸蛋白缺乏激酶1基因多态性与维吾尔族人缺血性卒中的关联研究

目的 探索赖氨酸蛋白缺乏激酶1( with no lysine[K]1,WNK1)基因单核苷酸多态性(SNP)与中国维吾尔族缺血性卒中的关系.方法 收集295例维吾尔族缺血性卒中患者和318例其他疾病对照者,进行病例对照研究.用标签SNP( tagging-SNP,tSNP)策略选择WNK1基因10个SNP位点( rs3858703、rs11611246、rs7305065、rs1990021、rs34408667、rs12309274、rs1012729、rs956868、rs12828016、rs953361).SNPs基因分型检测采用SNaPshot平台.用t检验、卡方检验和Logistic回归分析对数据进行统计分析,用Haploview软件进行连锁不平衡分析和单倍型分析.结果 rs11611246位点T等位基因在对照组中的分布(30.0％)高于病例组(25.6％),但是差异无统计学意义.用性别进一步分层分析,发现rs11611246 T等位基因是维吾尔族女性卒中发病的保护因子.显性遗传模型显示T等位基因携带者发生缺血性卒中的风险是对照组的0.448倍(95％ CI 0.269 ～0.746,P＝0.002).调整年龄后差异仍有统计学意义,进一步调整混杂因素年龄、体质量指数、吸烟、饮酒、高血压、糖尿病、高脂血症后,差异仍有统计学意义.除此之外,WNK1基因其余9个SNPs位点未发现同维吾尔族人脑梗死相关.结论 我们首次发现WNK1基因第4内含子rs11611246多态影响缺血性卒中的发生,rs11611246位点T等位基因可能是维吾尔族女性发生缺血性卒中的保护因素.     

Association between mitral regurgitation and clinical outcome after endovascular thrombectomy in stroke patients

ABSTRACT

Objective

Some hyperacute stroke patients have unfavorable outcomes after endovascular thrombectomy (EVT) despite successful recanalization. We hypothesized that a cardiac parameter, moderate-to-severe mitral regurgitation (MR), might decrease the rate of favorable clinical outcome after EVT in patients with atrial fibrillation (AF).