脂蛋白（a）与脑血管疾病关系的研究进展

脂蛋白（ａ）与脑血管疾病关系的研究进展杜怡峰，韩仲岩脂蛋白（ａ）简称Ｌｐ（ａ），是一种特殊的血浆脂蛋白，它于１９６３年由Ｂｅｒｇ首先发现并命名。其后，世界各地的有关学者就这方面进行了不少探索，目前已逐渐认识到血浆Ｌｐ（ａ）与动脉粥样硬化、脑血管疾病有...     

脑血管疾病分类（1995）（中,英文）

脑血管疾病分类（１９９５）（中、英文）一、短暂性脑缺血发作（４３５）（一）颈动脉系统（二）椎－基底动脉系统二、脑卒中（一）蛛网膜下腔出血（４３０）１．动脉瘤破裂引起２．血管畸形３．颅内异常血管网症４．其他５．原因未明（二）脑出血（４３１）１．高血压性...     

血清维生素A,E,C的浓度与脑血管疾病的关系

血清维生素Ａ、Ｅ、Ｃ的浓度与脑血管疾病的关系赵淑清，马长城，李美琳，刘洪斌，李新兰维生素对人类的健康具有重要的作用，许多神经系统疾病的发生均与维生素的缺乏直接有关［１］，因此，研究血清中维生素的含量与脑血管疾病的关系，也成了人们感兴趣的问题之一，我们...     

老年人收缩期高血压与心,脑血管疾病的关系及其治疗

老年人收缩期高血压与心、脑血管疾病的关系及其治疗韩仲岩一、收缩期高血压的定义１９８８年美国高血压协作委员会对收缩期高血压下的定义为：收缩期血压在１６０ｍｍＨｇ（２１．３ｋＰａ）以上，舒张压在９０ｍｍＨｇ（１２ｋＰａ）以下，或舒张压未满９５ｍｍＨｇ（１...     

载脂蛋白E基因多态性与脑血管疾病关系的研究进展

载脂蛋白E（ApoE）是血浆主要载脂蛋白之一,具有多种生物学活性,与血脂代谢和动脉粥样硬化密切相关,目前发现,载脂蛋白E的e4等位基因可以促进动脉粥样硬化和冠心病的发生。但在脑血管疾病中的作用尚不肯定。近年来国外在这方面的研究与探讨尚无定论,有些研究结论甚至是相反的,故仍需进一步研究。本文就载脂蛋白E与脑血管疾病的关系进行简要综述。     

补体与脑血管疾病

脑血管疾病的发病机制和病理生理过程相当复杂。近年来的研究表明,补体在脑血管疾病的发生发展中有重要作用。脑组织自身可合成补体,脑组织损伤时脑内补体激活,导致一系列损伤。本文就脑内补体的来源、激活、损伤机制及其与脑血管疾病的关系作一综述。     

隐匿性脑血管畸形（附10例报告）

隐匿性脑血管畸形（附１０例报告）胡波，周柏建，常义隐匿性脑血管畸形是指血管造影未能显示而为组织学证实的血管畸形。其中多为动静脉畸形，其次为海绵状血管瘤，而静脉性血管瘤及毛细血管扩张症少见［１、２］。我院１９８１～１９９３年间手术治疗隐匿性脑血管畸形１...     

C反应蛋白与脑血管疾病关系研究进展

脑血管疾病发病率及致残率均较高,可由各种原因引起,传统认为动脉粥样硬化是导致脑梗死的主要病理基础之一。近年来,随着对动脉粥样硬化的临床及病理生理研究的深入,炎症在动脉粥样硬化的发生和发展中起重要作用已成为共识,而C反应蛋白（C—reactive protain,CRP）是血管炎症反应的一个敏感性指标,因此,血清C反应蛋白的水平与脑血管疾病的发生、发展与预后有直接关系。旨在就C反应蛋白与脑血管疾病关系研究现状作一综述。     

同型半胱氨酸与脑血管疾病

自ＭｃＣｕｌｌｙ[1]首次报道1例少见的先天性异常病例,从而促进了一个意外发现,即认识到同型半胱氨酸或称高半胱氨酸(ｈｏｍｏｃｙｓｔｅｉｎｅ,ＨＣＹ)在动脉粥样硬化发病中的重要性以后,高ＨＣＹ血症已被确认为普通人群中脑血管疾病发病的一个重要危险因素[2,3]。现将近年来的有关研究现状简要综述如下。一、ＨＣＹ的生化特性ＨＣＹ是腺苷蛋氨酸酶水解反应的产物,在细胞内有三种代谢途径[4]:(1)以维生素Ｂ6为辅因子,在胱硫醚β合成酶的催化下与丝氨酸聚合成胱硫醚,然后,进一步在γ胱硫醚酶催化下分解为胱氨酸和α丁酮酸;(2)在5甲基四氢叶…     

Lp(a) Lipoprotein in Cerebrovascular Disease and Dementia

Abstract: Lp(a) lipoprotein has been considered an independent risk factor in the development of coronary heart disease (CHD). We examined the role of Lp(a) in patients with cerebrovascular disease (CVD) and those with dementia.
The Lp(a) concentration in patients with CHD, those with cerebral infarction due to a large artery occlusion and those with vascular dementia (VD) was significantly higher than that of age-matched control subjects. However, the Lp(a) concentration was not high in cerebral infarction due to a small artery occlusion, intracerebral hemorrhage and dementia of the Alzheimer type (DAT).
The present results suggest that Lp(a) should cause VD as well as CVD, and that Lp(a) should be one of the indicators that distinguish VD from DAT.     

Lipoprotein (a) in patients with spontaneous venous thromboembolism

INTRODUCTION: Elevated lipoprotein (a) (Lp (a)) has been established as a risk factor of coronary heart disease and stroke. Findings concerning the risk of venous thromboembolism (VTE) in adults are contradictory. The aim of our study was to investigate, whether elevated Lp (a) levels are an independent risk factor of spontaneous symptomatic venous thromboembolism (VTE). Our study was further designed to detect differences in risk profiles between thrombosis patients with and without symptomatic PE. MATERIALS AND METHODS: We investigated Lp (a) in 128 patients with spontaneous symptomatic deep vein thrombosis (DVT, group 1), 105 with spontaneous symptomatic pulmonary embolism with or without DVT (PE, group 2) and 122 healthy controls. Lp (a) was measured with an immunoturbidimetric assay (Tina-quant(R), Roche, Grenzach-Wyhlen, Germany) on a Hitachi-Modular system. RESULTS: Lp (a) levels (mg/L) were not significantly different among groups, median levels (25th-75th percentiles) were 170 (51-386) in group 1, 140 (<20-427) in group 2 and 126 (54-331) in controls, respectively. As continuous variable, odds ratios for VTE for a 100 mg/L increase of Lp (a) were 1.1 [95% confidence interval 0.98-1.2] for group 1 versus controls and 1.1 [0.95-1.2] for group 2 versus controls. The prevalence of Lp (a) above 300 mg/L was not significantly different among patients and controls (group 1: 30%, group 2: 32% and controls: 25%, p=0.4, p=0.2, respectively). CONCLUSIONS: In conclusion we found no association between Lp (a) and VTE regardless whether DVT occurred together with PE or not.     

Lipoprotein (a), LPA Ile4399Met,and Fibrin Clot Properties

Introduction

Elevated lipoprotein(a) (Lp(a)) levels were reported to be associated with dense fibrin clots. The apo(a) component of Lp(a) is encoded by LPA, and the Met allele of the LPA Ile4399Met polymorphism is associated with elevated Lp(a) levels and cardiovascular disease risk. We investigated whether Ile4399Met was associated with fibrin clot properties.

Materials and Methods

We determined plasma Lp(a) levels, fibrin clot permeability and lysis time for 64 LPA 4399Met carriers and 128 noncarriers matched for age, sex, ethnicity, and enrollment site.

Results

Elevated Lp(a) levels were associated with reduced clot permeability and prolonged lysis time (P < 0.0001). Carriers of 4399Met had higher Lp(a) levels compared with noncarriers (P = 0.0003). However, this association differed by ethnicity (P = 0.003 for interaction between genotype and ethnicity): compared with noncarriers, 4399Met carriers had 2.89 fold higher Lp(a) levels among Caucasians while no difference was observed among non-Caucasians (primarily East Asians and Hispanics). Among all subjects, no association was observed between Ile4399Met and clot properties, but this relationship also differed by ethnicity: among non-Caucasians, 4399Met carriers had increased clot permeability and shorter lysis time; whereas among Caucasians, the trend was for decreased permeability and longer lysis time (P < 0.01 for interactions between genotype and ethnicity).

Conclusions

We confirmed that elevated Lp(a) levels are associated with dense fibrin clots, and found that the association of LPA 4399Met carriers and clot permeability as well as lysis time differ by ethnicity.     

脑梗塞患者血清脂蛋白（a）测定及其临床意义

应用酶标法测定58例脑梗塞患者和56例健康对照者血清脂蛋白(a)[LP(a)]含量,并同时测定了其他脂代谢指标,对其中26例脑梗塞患者还测定了血浆纤维蛋白溶解(简称纤溶)指标。结果表明脑梗塞组存在显著的脂代谢和纤溶功能紊乱。LP(a)含量增高,与所测脂代谢、纤溶指标无显著相关,是脑梗塞发病独立的危险因素。     

Apolipoproteins B and AI and the risk of ischemic cerebrovascular events in patients with pre-existing atherothrombotic disease

BACKGROUND AND PURPOSE: The role of blood lipids and lipoprotein-related variables in the prediction of ischemic stroke is less clear than that for coronary heart disease. Apolipoprotein B (Apo B), which reflects the concentration of potentially atherogenic lipoprotein particles, and apolipoprotein AI (Apo A-I), which reflects the corresponding concentration of the anti-atherogenic HDL, represent additional lipoprotein-related variables that may indicate vascular risk. We examined the association between serum concentrations of Apo B, Apo A-I, and the Apo A-I/Apo B ratio and the risk of incident ischemic cerebrovascular events in patients with pre-existing atherothrombotic disease. METHODS: Patients with documented chronic coronary heart disease and measured Apo B and Apo A-I concentration, screened for but not included in a clinical trial of lipid modification were followed over 4.8 to 8.1 years for hospitalized incident cerebrovascular events. RESULTS: Among 3,434 patients 266 (7.7%) developed an incident ischemic cerebrovascular event. Adjusting for potential confounders, the hazard ratios (HR) for incident ischemic cerebrovascular events associated with the top versus bottom quartile of Apo B was 1.68 (95%CI, 1.18-2.40), of Apo A-I 0.71 (95%CI, 0.50-1.00), and of Apo A-I/Apo B ratio 0.51 (95%CI, 0.35-0.74). CONCLUSIONS: These findings support the hypothesis that Apo B, Apo A-I and the Apo A-I/Apo B ratio predict incident ischemic stroke among patients with preexisting atherothrombotic disease. The potential clinical role of measuring these apolipoproteins for ischemic stroke prediction warrants further study.     

Apolipoprotein (a) mediates the lipoprotein (a)-induced biphasic shift in human platelet cyclic AMP

Lipoproteins are known to influence platelet cyclic adenosine monophosphate (c-AMP) levels. Lipoprotein (a) (Lp(a))'s impact on platelet c-AMP levels has never been assessed. Increasing levels of purified human Lp(a) (1–100) mg/dl were incubated with washed human platelets. Lp(a) concentrations of 1–25 mg/dl resulted an initial statistically significant increase of platelet c-AMP above basal levels and decreased collagen-stimulated platelet aggregation levels. Higher concentrations progressively returned the platelet c-AMP concentrations to basal levels accompanied by further decreases in platelet aggregation. Increasing concentrations of purified apolipoprotein (a) (apo(a)) also resulted in a similar biphasic c-AMP response while Lp(a) without apo(a) was without impact. One antibody directed against apo(a) in intact Lp(a) removed the biphasic c-AMP pattern and eliminated Lp(a) platelet aggregation. Antibodies directed against apo B in intact Lp(a) gave results similar to intact Lp(a) in terms of the biphasic response of c-AMP upon platelet exposure to increasing levels of Lp(a). It is concluded that apo(a) mediates the Lp(a)-induced biphasic response in platelet c-AMP as the result of platelet exposure to increasing levels of Lp(a). The biphasic response in c-AMP assists in platelet aggregation decreases up to a concentration of 25 mg/dl Lp(a), such assistance being lost at higher Lp(a) concentrations.     

Lipoprotein(a) concentration increases during treatment with carbamazepine

PURPOSE: Treatment with carbamazepine (CBZ) is known to affect apolipoprotein B-containing lipoprotein concentrations in serum. However, little is known about the effects of anticonvulsant drugs (AEDs) on lipoprotein(a) [Lp(a)], although Lp(a) has been characterized as independent cardiovascular risk factor. We investigated prospectively the effect of CBZ on lipoprotein(a) concentration in normolipidemic healthy adults. METHODS: Twenty male volunteers were included in the study. Lp(a) levels were determined before and 69 +/- 19 days after CBZ administration by using an enzyme-linked immunoassay. RESULTS: CBZ (mean plasma concentration, 6.6 +/- 0.6 microg/ml) caused a significant increase in Lp(a) concentrations, with a median change of +19.5% (95% CI: +8.2, +53.3; p < 0.001). Total cholesterol, low density lipoprotein (LDL) cholesterol, and triglycerides also increased significantly. CONCLUSIONS: Although the precise mechanism of action of CBZ on Lp(a) elevation remains uncertain, it might be related to its enzyme-inducing properties. During treatment with CBZ, special focus should be given to elevated LDL cholesterol and Lp(a) concentrations with regard to increased risk for atherosclerotic vascular diseases.     

Association of levels of lipoprotein (a) and other lipoproteins with cerebrovascular disease in the Turkish population

Lipoprotein (a) [Lp (a)] is a cholesterol-rich lipoprotein that structurally resembles the low density lipoprotein cholesterol (LDL-C) particles, but contains a molecule of apolipoprotein (a) attached to apolipoprotein B by disulfide bond. Because of the fact that high plasma levels of Lp (a) have been shown to be associated with cerebrovascular disease (CVD), we determined plasma Lp (a) levels in CVD for the Turkish population, and compared them with previous findings of some developed countries. Plasma Lp (a) levels were evaluated in CVD and control groups. The mean plasma Lp (a) levels in the CVD group was found to be approximately two-fold higher than that of the control group (0.21 g/1 vs 0.38 g/1). Also, it was found to be higher than the mean levels of CVD group in the other populations described in previous reports. But CVD prevalence in the Turkish population is lower than in those of developed countries, especially United States and Japan. Therefore, we believe that each of those populations should determine their plasma Lp (a) levels to observe the risk for CVD.     

血清脂蛋白（a）与缺血性脑卒中关系的临床研究

目的探讨脂蛋白（a）（Lp（a））是否为缺血性卒中的危险因素,以及Lp（a）水平与缺血性脑卒中类型和预后的关系。方法将缺血性脑卒中患者按急性卒中治疗低分子肝素试验．TOAST）分型标准分为心源性脑栓塞（CE）、大动脉粥样硬化性卒中（LAA）、小动脉卒中（SAA）、其他原因引发的缺血性卒中（SOE）和原因不明的缺血性卒中（SUE）。以同期入院的非脑卒中患者（经头颅CT或磁共振排除）作为对照组。病例组和对照组均于入院次日清晨空腹抽取静脉血,测定Lp（a）及其他各项血脂指标,并于入院及病程两周时分别行NHISS评分评估神经功能缺损程度,分析Lp（a）与卒中类型及NIHSS评分之间的关系。结果缺血性脑卒中组Lp（a）浓度及异常率均高于对照组（P〈0．05）,Lp（a）进入大动脉粥样硬化卒中患病因素的回归方程Lp（a）水平与卒中患者的NIHSS评分无相关性（P〉0．05）。结论高浓度Lp（a）可能参与了缺血性脑卒中的发生,并且可能是大动脉粥样硬化性卒中发生的危险因素,但与神经功能缺失程度和早期功能修复无关。