微观结构在易损斑块进展中的作用

急性冠状动脉综合征常常导致严重的心血管事件,而冠状动脉粥样硬化斑块破裂是绝大多数急性冠状动脉综合征发生的原因,因此检测高破裂风险的易损斑块,对筛选和干预急性冠状动脉综合征具有重要意义。随着研究的不断进展,易损斑块内的一些微观结构如斑块内新生血管、微小钙化、胆固醇结晶,在易损斑块的进展中起到重要的作用。因此,本文以易损斑块内最常见的3种微观结构为重点,综述斑块内微观结构在易损斑块进展中的作用。     

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。     

虚拟组织学血管内超声检测冠状动脉易损斑块的临床应用进展

<正>动脉粥样硬化易损斑块(vulnerable plaque)破裂和继发血栓形成是导致急性心血管事件的主要原因。易损斑块具有薄纤维帽、大脂质核心及包含大量巨噬细胞在内的炎症细胞浸润的主要病理特征,即薄纤维帽粥样斑块(thin-cap fibroatheroma,TCFA),其易于破裂。易损斑块的早期识别和干预对于急性心血管事件的预防具有十分重要的意义。虚拟组织学血管内超声(virtual histology intravascular ultra-     

炎症与急性冠状动脉综合征

冠状动脉不稳定性粥样斑块的破裂、表面破损或裂隙 ,随后继发的血小板聚集和血栓形成 ,引起冠状动脉急性完全或不完全堵塞 ,是导致包括不稳定型心绞痛 (UA)、急性心肌梗塞 (AMI)和心源性猝死的急性冠状动脉综合征 (Acutecoronarysyndromes,ACS)的主要病理机制。不稳定粥样斑块的标志是斑块内脂质丰富、炎症反应活跃、胶原与血管平滑肌细胞少 ,且纤维帽薄 ,容易破裂[1 ] 。目前认为 ,炎症反应在粥样斑块的不稳定性和破裂中起重要作用。因此 ,认识炎症与ACS的关系 ,对预防、诊断和治疗ACS非常重要。1　炎症反应参与急性冠状动脉综合征的…     

急性冠状动脉综合征治疗

急性冠状动脉综合征（acute corohary syndrome，ACS）的发生是炎症细胞介导的动脉粥样斑块破裂（或糜烂）引起出血及血栓阻塞冠状动脉血流所致。斑块有两种：（1）稳定性斑块，特点是：纤维帽厚、血管平滑肌细胞多、胶原含量高，脂质核心，小炎症细胞少，不易破裂，也称硬斑块；（2）不稳定性斑块，特点是脂质含量多，纤维帽薄，胶原与平滑肌细胞少，炎症细胞多，     

光相干层析成像系统在冠状动脉易损斑块检测中的应用

粥样斑块的自发破裂及继发的血栓形成是急性冠状动脉事件和猝死的主要原因。目前将那些濒临破裂 ,进而发生血栓和 (或 )迅速进展的斑块称为易损斑块 (vulnerableplaque) [1 ] 。如何正确识别易损斑块已成为当前急性冠状动脉综合征诊治中面临的重要挑战。目前 ,多种成像技术已被     

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。     

膜连蛋白V和乳凝集素与早期检测易损斑块的关系

易损斑块受侵蚀或破裂继发血栓形成是发生急性冠状动脉综合征的主要原因,早期发现并干预易损斑块是防治的关键.研究证实,细胞凋亡常发生于易损斑块内的平滑肌细胞及巨噬细胞.因此,通过膜连蛋白V或乳凝集素与凋亡细胞膜表面外翻的磷酯酰丝氨酸特异性结合,可用于冠状动脉易损斑块的早期检测.     

血管紧张素Ⅱ、巨噬细胞与急性冠状动脉综合征

斑块破裂并继发血栓形成是急性冠状动脉综合征 (ACS)的主要病理基础。单核细胞移行并聚集于斑块部位 ,成为巨噬细胞 ,表达组织肾素 血管紧张素系统 (RAS)多种成分 ;所释放的血管紧张素Ⅱ (AngⅡ )又从脂质代谢、炎症和细胞促凝活性等多角度调节巨噬细胞功能。两者相互作用 ,共同参与ACS病理过程。血管紧张素转化酶抑制剂 (ACEI)、血管紧张素Ⅱ受体拮抗剂(ARB)减少心血管事件的发生 ,其稳定斑块的作用与以上机制有关。     

转化生长因子β与动脉粥样硬化斑块稳定性的关系

<正> 动脉粥样硬化(atherosclerosis,AS)是多种因素作用下的慢性炎症过程,随着AS的进展,可导致急性冠状动脉事件的发生。有研究表明,急性冠状动脉事件通常是由斑块破裂并发出血造成的,而不是由于纤维斑块逐渐进行性增大引起血管阻塞所致,导致急性血栓形成和心肌梗死等临床事件的"罪犯病变"血管造影通常并不显示明显病变。大量的研     

内质网应激与不稳定性斑块的研究进展

急性冠状动脉综合征通常由不稳定斑块突然破裂导致的血栓形成和血管闭塞所引起,其病因涉及多种病理生理通路,但具体机制尚未完全阐明.近年来,内质网应激在斑块不稳定性方面的作用越来越受到关注.适度的内质网应激是细胞的一种自我保护性机制,然而过强或长时间的内质网应激反应可以引起细胞功能的障碍.内质网应激可能通过在细胞凋亡、脂代谢异常、炎症反应中起的作用,导致斑块不稳定性增加.现就内质网应激与不稳定斑块的研究进展作一综述.     

稳定斑块——治疗急性冠状动脉综合征的新策略

急性冠状动脉综合征主要由于不稳定的冠状动脉粥样硬化斑块受侵蚀或破裂继发血栓引起。不稳定斑块的特征包括巨大的脂核、炎症细胞和炎症介质的增多以及较薄的纤维帽。对此进行干预可望达到稳定斑块的目的,从而给急性冠状动脉综合征的防治带来新的前景。     

Thrombosis formation on atherosclerotic lesions and plaque rupture

Atherosclerosis is a silent chronic vascular pathology that is the cause of the majority of cardiovascular ischaemic events. The evolution of vascular disease involves a combination of endothelial dysfunction, extensive lipid deposition in the intima, exacerbated innate and adaptive immune responses, proliferation of vascular smooth muscle cells and remodelling of the extracellular matrix, resulting in the formation of an atherosclerotic plaque. High‐risk plaques have a large acellular lipid‐rich necrotic core with an overlying thin fibrous cap infiltrated by inflammatory cells and diffuse calcification. The formation of new fragile and leaky vessels that invade the expanding intima contributes to enlarge the necrotic core increasing the vulnerability of the plaque. In addition, biomechanical, haemodynamic and physical factors contribute to plaque destabilization. Upon erosion or rupture, these high‐risk lipid‐rich vulnerable plaques expose vascular structures or necrotic core components to the circulation, which causes the activation of tissue factor and the subsequent formation of a fibrin monolayer (coagulation cascade) and, concomitantly, the recruitment of circulating platelets and inflammatory cells. The interaction between exposed atherosclerotic plaque components, platelet receptors and coagulation factors eventually leads to platelet activation, aggregation and the subsequent formation of a superimposed thrombus (i.e. atherothrombosis) which may compromise the arterial lumen leading to the presentation of acute ischaemic syndromes. In this review, we will describe the progression of the atherosclerotic lesion along with the main morphological characteristics that predispose to plaque rupture, and discuss the multifaceted mechanisms that drive platelet activation and subsequent thrombus formation. Finally, we will consider the current scientific challenges and future research directions.     

冠状动脉易损斑块形成机制研究进展

心血管疾病已经成为全世界致死率最高的疾病。急性冠脉综合征作为危害性极大的心血管事件之一,多由斑块破裂后继发血栓形成所致。深入了解易损斑块形成机制和影响因素,对急性心血管事件的预防和治疗具有非常重要的临床意义。本文将结合近年来有关易损斑块的研究结果,就易损斑块的概念、基本特征、病理生理机制的研究进展作一综述。     

急性冠状动脉综合征患者易损斑块的临床病理分析

目的 观察易损斑块在急性冠状动脉综合征患者( ACS)中的病理组织学特点。方法 本研究回顾了北京医院1992-2006年尸检患者127例,分为ACS组67例;与其年龄、性别相匹配的临床表现无ACS的病例60例,从斑块的形态如有无血栓、粥池最大横切面占斑块面积、纤维帽最小厚度、炎细胞浸润密度等10个方面进行形态学观察,观...     

Inflammation and plaque vulnerability

Atherosclerosis is a maladaptive, nonresolving chronic inflammatory disease that occurs at sites of blood flow disturbance. The disease usually remains silent until a breakdown of integrity at the arterial surface triggers the formation of a thrombus. By occluding the lumen, the thrombus or emboli detaching from it elicits ischaemic symptoms that may be life‐threatening. Two types of surface damage can cause atherothrombosis: plaque rupture and endothelial erosion. Plaque rupture is thought to be caused by loss of mechanical stability, often due to reduced tensile strength of the collagen cap surrounding the plaque. Therefore, plaques with reduced collagen content are thought to be more vulnerable than those with a thick collagen cap. Endothelial erosion, on the other hand, may occur after injurious insults to the endothelium instigated by metabolic disturbance or immune insults. This review discusses the molecular mechanisms involved in plaque vulnerability and the development of atherothrombosis.     

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.     

Strategies to achieve coronary arterial plaque stabilization.

Acute coronary syndromes result from fissure, erosion or rupture of a vulnerable atherosclerotic plaque. The characteristics of a vulnerable plaque include a large lipid pool, an abundance of inflammatory cells and mediators, a reduced smooth muscle cell and collagen content and a thin overlying fibrous cap. Potential therapeutic strategies at achieving plaque stabilization have targeted these features. Lipid lowering agents, beta-adrenergic blockers, angiotensin converting enzyme inhibitors and antioxidants have been shown to reduce the incidence of acute coronary syndromes, presumably through plaque stabilization. Matrix metalloproteinase inhibitors as well as macrolide antibiotics and gene therapy approaches show promise in achieving plaque stabilization. The evidence supporting plaque stabilization by these agents and the mechanisms by which these agents stabilize plaques are discussed in detail in this review.     

斑块侵蚀的诊疗进展

急性冠状动脉综合征(ACS)是危害人类健康的最严重心血管疾病之一。长期以来,动脉粥样硬化斑块破裂(PR)导致的斑块内容物释放伴随附壁血栓形成被认为是ACS形成的主要机制。随着光学相干断层成像(OCT)的应用,人们认识到除了PR,斑块侵蚀(PE)是ACS的另外一种重要而且常见的病理学机制。近年来对于PE的研究已经取得了一定进展,文章将对PE的诊断以及治疗的研究进展做一综述。