炎症标志物与急性冠状动脉综合征

动脉粥样硬化性疾病是一种慢性、非特异性、炎性疾病。在动脉粥样硬化性疾病的不同临床表现过程中,炎症与其发生和发展的所有阶段有关。急性冠状动脉综合征是冠心病的特殊疾病谱,新近研究证实,炎症在急性冠状动脉综合征患者的粥样斑块破裂与血栓形成中起主要作用。炎症与易损斑块的形成有关;临床试验证据支持炎症在急性冠状动脉综合征发生中的病因学地位;炎症标志物的使用,也提供了一个了解急性冠状动脉综合征病理生理机制的窗口。因此,急性冠状动脉综合征可以认为是一种心血管急性炎症综合征。     

急性冠状动脉综合征患者白细胞介素-18的变化及其临床意义

急性冠状动脉综合征的发生发展与动脉粥样硬化斑块的稳定性密切相关,易损斑块的破裂被认为是急性冠状动脉综合征的主要发病机制。目前研究认为动脉粥样硬化是慢性炎症疾病,越来越多的证据支持炎症反应在动脉粥样硬化的发生发展中起到重要作用。白细胞介素-18是近年来发现的一个促炎细胞因子,其在急性冠状动脉综合征粥样斑块易损性方面发挥了重要作用.并对急性冠状动脉综合征患者的早期诊断和冠状动脉病变的严重程度及对心血管终末事件的发生的预测有重要的临床意义。     

B细胞性淋巴瘤因子-2及其BH4结构域参与的细胞凋亡与动脉粥样硬化疾病

正近年来,动脉粥样硬化疾病的发生率逐年升高,动脉粥样硬化易损斑块是引致急性冠状动脉综合征的主要原因。其发病涉及多种机制,包括炎症,氧化应激,脂质代谢紊乱等,其中血管内皮细胞、血管平滑肌细胞及血小板等多种细胞凋亡既是上述多种因素作用的结果,也是加速动脉粥样硬化易损斑块形成的主要原因,是动脉粥样硬化易损斑块的重     

冠状动脉易损斑块的炎症标志物的研究进展

冠状动脉易损斑块定义为具有血栓形成倾向、极有可能快速进展成罪犯斑块的冠状动脉粥样硬化斑块,稳定斑块常无临床症状或者仅出现稳定性心绞痛,从稳定斑块进展为易损斑块,常常是炎症反应的结果。因此,在易损斑块出现急性心血管事件之前,循环中能找到可靠识别易损斑块的炎症标记物就显得非常重要,目前临床与基础研究中,发现许多炎症标志物可提供易损斑块的诊断及预后价值。本文就冠状动脉易损斑块的炎症标记物最新研究进展作一综述。     

冠状动脉粥样硬化斑块温度异质性及其检测的研究进展

冠状动脉易损斑块的破裂与急性冠脉综合征密切相关,目前对易损斑块的检测有多种方法,包括有创性和无创性检测。研究发现动脉粥样硬化斑块表面的温度与正常血管壁的温度有差异,不同的动脉粥样硬化斑块依据其易损程度的不同其温度异质性也不同。冠状动脉内温度导丝测定仪利用该原理检测斑块表面温度异质性,间接判断动脉粥样硬化斑块的组成和易损程度。     

冠状动脉易损斑块的治疗进展

动脉粥样硬化是全身性、慢性炎症性疾病,以局部突出表现为主。冠状动脉粥样硬化是冠状动脉性心脏病最主要病因,冠状动脉性心脏病患者发生急性冠状动脉事件的后果十分严重,常危及生命,而易损斑块是导致急性冠状动脉综合征主要罪犯病变。因此,对易损斑块的早期识别以及积极干预,对于预防急性心血管事件的发生至关重要,具有非常重要的临床意义。现就冠状动脉易损斑块的治疗最新进展做一综述。     

易损斑块的血清炎症标志物的研究进展

急性冠状动脉综合征是严重威胁人类健康的一种常见病和多发病。急性冠状动脉综合征的病理基础是由于易损斑块的存在,且易损斑块的破裂是急性冠状动脉综合征发生的始动环节。现有临床检测方法仅能监测到急性冠脉事件发生的当时及事后血清学变化,而早期发现易损斑块,及时进行干预,对降低急性冠状动脉综合征的发病率和死亡率具有极其重要的临床意义。现主要就检测易损斑块的血清炎症标志物的研究进展作一综述。     

他汀类药物与动脉粥样硬化斑块消退

根据Glagov’s模型,动脉粥样硬化形成可分为两个阶段:代偿阶段和失代偿阶段,前者的动脉壁已有轻、中度的动脉粥样硬化斑块形成,但动脉管腔直径没有改变;后者的动脉管腔出现程度不同的狭窄;斑块的稳定性与其脂质核心的大小和纤维帽的厚薄,以及斑块内炎症细胞的多寡有关,易损斑块的破裂、出血导致的血栓形成是急性冠脉综合征的主要病理基础;冠状动脉内超声检查(IVUS)是目前测定冠状动脉粥样硬化斑块总体积,评价斑块的结构和稳定性的最好方法。本文论述了动脉粥样硬化的进程,动脉粥样斑块的检测方法,替代终点(QCA、IMT,IVUS)研究的结果,即他汀类药物可延缓、阻断、逆转(消退)颈动脉和冠状动脉动脉粥样硬化病变的进展。     

内皮祖细胞在动脉粥样硬化易损斑块中的作用

目的 动脉粥样硬化易损斑块是急性冠状动脉综合征和心脏缺血性猝死的重要病理基础.研究证实易损斑块表面大面积内皮细胞受损和血栓形成,内皮受损后可引起炎症因子瀑布样反应、单核细胞浸润和血管平滑肌细胞增生,进而促发动脉粥样硬化易损班块形成,故修复受损血管内皮、促使血管重新内皮化已经成为防止动脉粥样硬化的重要课题.近年研究认为,...     

辅助性T细胞17/白介素17在动脉粥样硬化发生与发展中的作用

<正>炎症反应贯穿于动脉粥样硬化发生、斑块形成、易损斑块破裂到血栓形成的全过程,与急性冠状动脉综合征(acute coronary syndrome,ACS)的病理生理过程密不可分。大量研究表明,免疫细胞是动脉粥样硬化的直接参与者[1],T细胞在动脉粥样硬化病变进展中起到了关键性的作用,根据所产     

动脉粥样硬化易损斑块的生物学标志物

多种生化分子参与了动脉粥样硬化的发生发展、斑块失稳定性和破裂过程.因此,寻找能识别易损斑块和预测斑块破裂风险的血清生物学标志物,对临床工作具有重要的指导意义.文章综述了近年来有关易损斑块生物学标志物的研究进展.     

动脉粥样硬化易损斑块的生物学标志物

多种生化分子参与了动脉粥样硬化的发生发展、斑块失稳定性和破裂过程.因此,寻找能识别易损斑块和预测斑块破裂风险的血清生物学标志物,对临床工作具有重要的指导意义.文章综述了近年来有关易损斑块生物学标志物的研究进展.     

From vulnerable plaque to vulnerable patient: the search for biomarkers of plaque destabilization

There is a strong need for biomarkers to identify patients at risk for future cardiovascular events related with progressive atherosclerotic disease. Ideally, increasing knowledge of the mechanisms of atherosclerotic plaque destabilization should be translated in clinical practice. Currently, the following commonly followed strategies can be identified with the objective to detect either the local vulnerable plaque that is prone to rupture and gives rise to a thrombotic occlusion, or the systemic vulnerable patient, who has a high probability to suffer from an adverse clinical event. On the one hand, studies are ongoing to determine local atherosclerotic plaque characteristics to predict future local plaque rupture and subsequent vascular thrombosis. Newly developed imaging modalities are being developed and validated to detect these plaques in vivo. On the other hand, systemic approaches are pursued to discover serum biomarkers that are applicable to define patients at risk for future cardiovascular events. We propose a third original approach that is optional but yet unexplored, that is, to use local plaque characteristics as a biomarker not just for local plaque destabilization but for future cardiovascular events due to plaque progression in any vascular system. This review aims to provide an overview of the current standings of the identification of the vulnerable plaque and the vulnerable patient.     

预测颈动脉粥样硬化易损斑块的新型生物标志物研究进展

易损斑块是指动脉壁内稳定性差的斑块,其易破裂、脱落,导致原位血栓或多发微栓子形成。颈动脉粥样硬化易损斑块是缺血性脑卒中的主要致病机制,颈动脉斑块易损性增加脑缺血事件的发生。因此,早期鉴别易损斑块,对干预脑卒中高危因素、改善脑卒中预后具有重要意义。除各类影像技术外,循环生物标志物为识别颈动脉易损斑块提供了辅助手段。本综述回顾以往研究,讨论能够识别颈动脉易损斑块的新型生物标志物。     

Exploring the role of extracellular matrix proteins to develop biomarkers of plaque vulnerability and outcome

Cardiovascular disease (CVD) is the most common cause of death in industrialized countries. One underlying cause is atherosclerosis, which is a systemic disease characterized by plaques of retained lipids, inflammatory cells, apoptotic cells, calcium and extracellular matrix (ECM) proteins in the arterial wall. The biologic composition of an atherosclerotic plaque determines whether the plaque is more or less vulnerable, that is prone to rupture or erosion. Here, the ECM and tissue repair play an important role in plaque stability, vulnerability and progression. This review will focus on ECM remodelling in atherosclerotic plaques, with focus on how ECM biomarkers might predict plaque vulnerability and outcome.     

The vulnerable plaque: Current concepts and future perspectives on coronary morphology,composition and wall stress imaging

Cardiovascular imaging plays an important role in the identification and characterization of the vulnerable plaque. A major goal is the ability to identify individuals at risk of plaque rupture and developing an acute coronary syndrome. Early recognition of rupture‐prone atherosclerotic plaques may lead to the development of pharmacologic and interventional strategies to reduce acute coronary events.We review state‐of‐the‐art cardiovascular imaging for identification of the vulnerable plaque. There is ample evidence of a close relationship between plaque morphology and patient outcome, but molecular imaging can add significant information on tissue characterization, inflammation and subclinical thrombosis. Additionally, identifying arterial wall exposed to high shear stress may further identify rupture‐prone arterial segments. These new modalities may help reduce the individual, social and economic burden of cardiovascular disease.     

Biomarkers of Plaque Instability

Atherosclerosis is the proximate cause of arterial thrombosis, leading to acute occlusive cardiovascular syndromes. Thrombosis in atherosclerosis usually results from rupture of the fibrous cap of atherosclerotic plaques with a smaller proportion resulting from superficial endothelial erosion. Ruptured plaques are often associated with intimal and adventitial inflammation, increased size of lipid-rich necrotic core with thinned out collagen-depleted fibrous cap, outward remodeling, increased plaque neovascularity, intraplaque hemorrhage, and microcalcification. By inference, non-ruptured plaques with similar compositional features are considered to be at risk for rupture and hence are labeled vulnerable plaques or high-risk plaques. Identification of vulnerable plaques may help in predicting the risk of acute occlusive syndromes and may also allow targeting for aggressive systemic and possibly local therapies. Plaque rupture is believed to result from extracellular matrix (which comprises the protective fibrous cap) dysregulation due to excessive proteolysis in the context of diminished matrix synthesis. Inflammation is believed to play a key role by providing matrix-degrading metalloproteinases and also by inducing death of matrix-synthesizing smooth muscle cells. Systemic markers of inflammation are thus the most logical forms of potential biomarkers which may predict the presence of vulnerable or high-risk plaques. Several studies have suggested the potential prognostic value of a variety of systemic markers, but regrettably, their overall clinical predictive value is modestly incremental at best, especially for individual subjects compared to groups of patients. Nevertheless, continued investigation of reliable, cost-effective biomarkers that predict the presence of a high-risk plaque and future athero-thrombotic cardiovascular events with greater sensitivity and specificity is warranted.     

DNA damage as a new emerging risk factor in atherosclerosis

Atherosclerosis is the leading cause of illness and death in Western societies. It is now clear that the disease is a result of a chronic fibroproliferative-inflammatory response of the arterial intima leading to the formation of atherosclerotic plaque. There is, however, strong experimental evidence for a "mutation theory of atherosclerosis," underlining the similarity between atherosclerotic and carcinogenic processes. This review provides an overview of the studies that support the role of genetic alterations in the disease. The demonstration of microsatellite instability and loss of heterozygosity in smooth muscle cells of human plaques suggests that genomic destabilization may play a pivotal role in atherosclerotic mechanisms. Furthermore, the use of accepted biomarkers of carcinogenic exposure-such as DNA adducts and cytogenetic end points-recently has provided evidence consistent with the view that somatic cell alterations are critical in atherogenic process. It follows that the study of DNA damage may provide new insights into the pathogenesis of atherosclerosis and lead to the development of novel therapeutic approaches.     

Techniques characterizing the coronary atherosclerotic plaque: influence on clinical decision making?

The composition of the atherosclerotic lesion rather than the degree of stenosis is currently considered to be the most important determinant for acute clinical events. Modalities capable of characterizing the atherosclerotic lesion may be helpful in understanding its natural history and detecting lesions with high risk for acute events. Speaking grossly, three histologic features of the vulnerable plaque have been reported: size of the atheroma, thickness of the fibrous cap, and inflammation. Imaging techniques are currently being deployed and are under development to aid visualization of the vulnerable coronary plaque. Most of these diagnostic modalities have the potential to detect locally one or more of the three histologically defined features of vulnerable plaque. This review will focus on imaging techniques that have been developed to characterize the atherosclerotic lesion. Most catheter-based visualization techniques will provide insight into components of the local atherosclerotic plaque which may limit their predictive value for the occurrence of a clinical event. Therefore, the clinical relevance of these imaging tools will be discussed.