C反应蛋白与动脉粥样硬化相关性研究进展

通过综述C反应蛋白与血管硬化指标的相关性及其对中医脉诊研究的影响,多项研究显示C反应蛋白直接参与炎症,与动脉粥样硬化等心血管疾病有关,而且是心血管疾病强有力的预示因子与危险因子之一,炎症在动脉粥样硬化及心血管相关疾病的发生和发展过程起重要作用。     

老年冠心病患者炎症因子水平与冠状动脉病变严重程度的相关性

炎症反应在动脉粥样硬化形成、发生、发展中起着重要的作用,而慢性、低度炎症是动脉粥样硬化发生、发展的一个重要因素。炎症标志物如高敏C反应蛋白(hs-CRP)作为一种系统炎症的敏感指标,能独立预测冠状动脉事件发展的危险度。本实验通过检测老年冠心病患者血清脂联素及hs-CRP水平,进一步分析其与冠心病患者冠状动脉病变之间的相关性,揭示脂联素及hs-CRP在动脉粥样硬化发生发展中的可能     

早期辛伐他汀治疗对不稳定型心绞痛患者凝血纤溶及高敏C反应蛋白水平的影响

目的观察较大剂量辛伐他汀治疗不稳定型心绞痛患者1周前后凝血纤溶指标及血清高敏C反应蛋白的变化,以了解短期辛伐他汀治疗对不稳定型心绞痛患者的抗凝作用和免疫炎症抑制的影响。方法将不稳定型心绞痛患者随机分为常规治疗组和辛伐他汀组,另设非心血管疾病患者为对照组,测定治疗前后凝血纤溶指标、高敏C反应蛋白和血脂水平的变化。结果常规治疗组和辛伐他汀组治疗前后血脂的变化差异均无显著性。辛伐他汀治疗组治疗后血浆凝血因子Ⅶ、纤维蛋白原和纤溶酶原激活剂抑制物较治疗前明显下降,组织型纤溶酶原激活剂有所升高,而高敏C反应蛋白水平明显降低,且血清高敏C反应蛋白水平下降与血脂变化无相关性。结论在不稳定型心绞痛患者早期予以辛伐他汀治疗,可明显影响血浆炎症因子及凝血纤溶因子的水平,具有独立于降脂作用以外的抗凝抗炎作用,可能有利于动脉粥样硬化斑块的稳定。     

维持性血液透析患者炎症与颈动脉粥样硬化的关系

研究维持性血液透析患者慢性炎症状态与颈动脉粥样硬化的关系 ,选择维持性血液透析患者 2 5例和健康对照者 15例 ,用酶联免疫吸附法检测高敏C反应蛋白和肿瘤坏死因子α来评价慢性炎症状态 ,用高分辨超声技术检测颈总动脉内膜中膜厚度和粥样硬化斑块来评价动脉粥样硬化程度。结果发现 ,维持性血液透析患者血浆高敏C反应蛋白和肿瘤坏死因子α水平均明显高于正常对照组 ,维持性血液透析患者颈总动脉内膜中膜厚度和斑块检出率明显高于年龄、性别匹配的正常对照组。维持性血液透析患者血浆肿瘤坏死因子α水平 (取对数值 )与平均颈总动脉内膜中膜厚度呈显著正相关 (r=0 .792 ,P <0 .0 0 1)。多因素逐步回归分析结果表明 ,影响颈总动脉内膜中膜厚度的因素有血浆肿瘤坏死因子α水平 (对数转化 )、年龄、高密度脂蛋白胆固醇、C反应蛋白、磷、载脂蛋白B、前白蛋白和甘油三酯。结果提示 ,维持性血液透析患者存在慢性炎症状态 ,炎症在动脉粥样硬化的发病机制中起重要的作用。     

C反应蛋白在动脉粥样硬化形成中的机制

动脉粥样硬化(atherosclerosis,AS)是严重危害人类健康的疾病。近年来,随着研究的不断深入,揭示细胞因子和化学因子在动脉粥样硬化作用显得尤为重要,动脉粥样硬化“炎症学说”的观点受到了广泛的重视。C反应蛋白(C-reactiveprotein,CRP)作为非特异性炎症反应中主要的、最敏感的     

肾血管性高血压大鼠血清中血管性假血友病因子和高敏C反应蛋白动变化

目的研究易卒中型肾血管性高血压大鼠血清中血管性假血友病因子和高敏C反应蛋白在高血压病程中的动态变化,并探讨血管性假血友病因子和高敏C反应蛋白在高血压脑动脉粥样硬化及脑卒中发生、发展中的作用。方法双肾双夹法复制肾血管性高血压大鼠模型,酶联免疫吸附试验检测肾血管性高血压大鼠血清中血管性假血友病因子和高敏C反应蛋白的含量,并分别与对照组和假手术组比较。结果术后第4、8、12周末,高血压组血清血管性假血友病因子和高敏C反应蛋白含量均较对照组和假手术组显著升高,且随造模时间延长,不同阶段高血压组血清血管性假血友病因子和高敏C反应蛋白含量也随之升高。结论随着高血压病情进展,血清中血管性假血友病因子含量和高敏C反应蛋白含量也同步升高,两者均参与高血压动脉粥样硬化的发生、发展。高血压时血清中增高的血管性假血友病因子和高敏C反应蛋白均可能是其并发缺血性脑卒中的危险因素。     

高敏C反应蛋白与颈动脉粥样硬化的关系

目的 探讨高敏C反应蛋白和颈动脉粥样硬化的关系.方法 选取在神经内科住院的患者225例(其中脑梗塞患者133例),排除了应激、炎症、自身免疫性疾病等影响高敏C反应蛋白水平的疾病,全部患者行颈部血管彩超检测,观察颈动脉内膜-中膜厚度、斑块的检出情况及斑块评分、管腔的狭窄率,作为评价颈动脉粥样硬化的指标.根据血管彩超的检查结果分为颈动脉粥样硬化组和对照组.用微粒子透射增强免疫法(超敏)检测血浆高敏C反应蛋白的水平.分别比较颈动脉粥样硬化组与对照组高敏C反应蛋白水平的差别,分析高敏C反应蛋白和颈动脉内膜-中膜厚度、斑块评分之间的关系.结果 颈动脉粥样硬化组(130例)与对照组(95例)比较,二者之间的高敏C反应蛋白存在明显差异(P<0.05);偏相关分析显示,高敏C反应蛋白与颈动脉内膜-中膜厚度及斑块评分成正相关,相关系数分别为0.4807和0.3024.结论 颈动脉粥样硬化组较对照组高敏C反应蛋白水平高,高敏C反应蛋白与颈动脉粥样硬化的严重程度成正相关.     

心可舒治疗不稳定心绞痛时趋化因子和高敏反应蛋白的变化

冠心病是危害老年人健康的主要疾病之一，近年来越来越多基础研究和临床提示，炎症、细胞因子与动脉粥样硬化的发生发展有重要关联作用。本文比较趋化因子和高敏C反应蛋白在心可舒治疗前后的变化。     

高敏C反应蛋白在冠心病中应用的新进展

冠心病的病理基础是动脉粥样硬化,炎症在动脉粥样硬化的发生和发展过程中起重要作用。因而高敏C反应蛋白(high-sensitivity c-reactive protein,hs-CRP),作为一项高敏感的炎性反应指标,可用于监测冠心病患者病情变化、预测冠心病的预后以及预报亚健康人群发生冠心病的风险,具有     

血清hsCRP水平与脑梗死关系研究的进展

炎症反应在动脉粥样硬化(AS)的发生、发展中起着重要作用.在众多的炎症标志物研究中,高敏C反应蛋白(hsCRP)与AS及脑梗死(CI)的关系已被广泛研究.本文就hsCRP与CI关系的研究进展作一综述.     

C反应蛋白对判断冠心病预后价值的研究现状

炎症在冠心病的发生和发展过程中起着重要的作用,C反应蛋白作为炎症反应的标志物,促进动脉粥样硬化形成和血栓形成,但其对冠心病预后是否有预测价值仍存在争议。现就C反应蛋白对冠心病预后的预测价值做一综述。     

Inflammation and coronary heart disease: an overview

About half of the patients presenting with myocardial infarction do not have the classic risk factors. This finding has stimulated a search for other factors that may be responsible and, when present, may help to predict which patients are at greatest risk for myocardial infarction and other cardiovascular events. With improved understanding of the pathogenesis of ischemic heart disease, new insights into potential markers of underlying atherosclerosis and cardiovascular risk have been gained. In recent years, data have accumulated demonstrating that certain markers of inflammation--both systemic and local--play a key role in the development of atherosclerosis. Specifically, elevated levels of one systemic marker of inflammation, C-reactive protein, are associated with an increased risk of cardiovascular disease events. Moreover, potentially important associations have been established between elevated markers of inflammation, such as C-reactive protein and increased efficacy of established therapies; and, in particular, lipid-lowering therapy with the hepatic hydroxymethylglutaryl coenzyme A reductase inhibitor pravastatin. This article discusses the pathogenesis of atherosclerosis, the role of endothelial dysfunction and plaque rupture, and evidence for the role of inflammation and reviews how therapy might reduce vascular inflammation.     

Inflammation and atherosclerosis

Inflammation plays a pivotal role in all stages of atherogenesis, from foam cell to plaque formation to rupture and ultimately to thrombosis. Insight gained from recent basic and clinical data linking inflammation to atherosclerosis has yielded important diagnostic and prognostic information. Low-grade chronic inflammation as measured by high sensitivity C-reactive protein predicts future risk of acute coronary syndrome independent of traditional cardiovascular risk factors. In addition, individuals with higher “inflammatory burden” gain the largest absolute risk reduction with aggressive risk-lowering therapy. The link between inflammation and atherosclerosis provides a new venue for future pharmacologic agents that may slow the progression of atherosclerosis by inhibiting inflammation.     

C-reactive protein and interleukin-6 in vascular disease: culprits or passive bystanders?

Recent advances in basic science have shown that atherosclerosis should be considered as a chronic inflammatory process, and that a pivotal role of inflammation is evident from initiation through progression and complication of atherosclerosis. In the past few years many studies have examined the potential for biochemical markers of inflammation to act as predictors of coronary heart disease (CHD) risk in a variety of clinical settings. Several large, prospective epidemiological studies have shown consistently that C-reactive protein (CRP) and interleukin-6 (IL-6) plasma levels are strong independent predictors of risk of future cardiovascular events, both in patients with a history of CHD and in apparently healthy subjects. These molecules could be useful to complement traditional risk factors, as well as to identify new categories of subjects prone to atherosclerosis development. An intriguing question is whether these inflammatory molecules simply represent sensitive markers of systemic inflammation or if they actively contribute to atherosclerotic lesion formation and instability. In this paper we will review the evidence concerning the cardiovascular prognostic value and the potential direct involvement of CRP and IL-6 in atherogenesis.     

Markers of inflammation and their clinical significance

Inflammation plays an important role in the initiation and progression of atherosclerosis and the development of atherosclerotic events. Understanding the molecular basis of inflammation has led to the identification of markers that may also serve as new targets of therapy in the management of atherothrombotic disease. Inflammatory markers, such as C-reactive protein (CRP), have been shown to predict future cardiovascular events in individuals with and without established cardiovascular disease (CVD). Statins substantially reduce cardiovascular morbidity and mortality, and recently their anti-inflammatory properties have been investigated. In this paper, we discuss biomarkers implicated in the inflammatory process leading to atherothrombosis, including CRP, adiponectin, monocyte chemoattractant protein 1 (MCP-1), CD40 ligand and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), and the effect of statins on these markers and their potential relationship to cardiovascular events.     

微小核糖核酸-146a与心血管疾病关系研究进展

微小核糖核酸-146a是微小核糖核酸的一员,其具有调节免疫应答、炎症、肿瘤、细胞增殖分化以及凋亡的作用,并在心血管疾病的病理生理过程中扮演着重要角色。应用微小核糖核酸-146a抑制动脉粥样硬化炎症,将成为治疗动脉粥样硬化新靶点。     

Proteína C reativa de alta sensibilidade como biomarcador de risco na doença coronária

Vascular inflammation plays a crucial role in the pathogenesis of atherosclerosis and mediates various stages of atherosclerotic plaque development, from lipid streak formation to the plaque rupture and destabilization that precedes the clinical syndromes of cardiovascular disease. Inflammatory biomarkers constitute valuable tools to study this process, enabling the effects of different therapeutic interventions to be assessed. Currently, C-reactive protein (CRP) determined by high-sensitivity methods (hs-CRP) is the most extensively studied biomarker. Data regarding hs-CRP and cardiovascular risk, though largely consistent, are of unclear clinical relevance. This article provides a comprehensive review of current knowledge concerning cardiovascular risk and hs-CRP, and concludes with an evidence-based analysis of the current role of hs-CRP in cardiovascular risk assessment.     

The role of C-reactive protein in cardiovascular disease risk

Over the past few years, a flurry of data in the medical literature has strongly implicated C-reactive protein (CRP) as a marker of inflammation in coronary artery disease (CAD). Recognizing the likely integral role that inflammation plays in the pathogenesis of atherosclerosis, many hospital laboratories have tests to measure CRP concentration in the clinical setting. However, the clinical use of these tests still need definition. To date, of the plasma-based markers investigated, CRP provides the strongest risk prediction for cardiovascular disease in men and women. Questions remain regarding the degree to which CRP can improve risk stratification beyond that of the traditional risk factors of CAD.     

Systemic inflammation as a cardiovascular disease risk factor and as a potential target for drug therapy

Inflammation-related processes play a key role the current etiologic model of atherosclerosis and its acute complications. Recent evidence suggests that blood-based biomarkers that reflect systemic inflammation may contribute to our ability to predict future risk of cardiovascular disease. Global markers of inflammation, such as C-reactive protein and fibrinogen, have been well studied as potential cardiovascular risk factors. A variety of additional markers that reflect various elements of the complex systems governing inflammation, including proinflammatory and antiinflammatory cytokines, mediators of cellular adhesion, and matrix degradation enzymes, are also worthy of study. Although many previous studies have examined the relation of inflammation to myocardial infarction, emerging evidence suggests that other cardiovascular phenotypes such as ischemic stroke and early-stage atherosclerosis may also be related to inflammation. Further elucidating the role of inflammation in cardiovascular disease may lead to the identification of new targets for preventive or therapeutic interventions. In addition, markers of inflammation may be useful as a means to predict or monitor an individual's response to currently available cardiovascular therapies, such as aspirin or HMG coenzyme A reductase inhibitors, that may act via antiinflammatory mechanisms.     

A review of high-dose statin therapy: targeting cholesterol and inflammation in atherosclerosis.

Lipid lowering with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors or 'statins' has dramatically reduced morbidity and mortality in patients with established cardiovascular disease. Recently, there have been multiple studies investigating the role of high-dose statin therapy with more aggressive lipid lowering in this setting. Concomitantly, there is increasing evidence implicating a role of inflammation in the pathogenesis of atherosclerosis. These high-dose statin trials and other studies have also provided a wealth of data suggesting that statins have anti-inflammatory and anti-oxidant properties that go beyond their lipid-lowering effects. In this review, we will provide a brief overview of recent, large-scale, randomized, placebo and active controlled trials of high-dose statin therapy in the setting of stable and unstable coronary artery disease and percutaneous coronary intervention. Further, we will discuss the evidence for effects of high-dose statin therapy on inflammation and C-reactive protein.