易损斑块的检测方法现状

如何尽早发现动脉粥样硬化易损斑块一直是临床心脑血管病预防的重点和难点.早发现、早治疗可显著改善患者预后.本文对目前易损斑块的检测方法现状做一综述.     

"从易损斑块到易损患者"的新概念

动脉粥样硬化斑块破损,继而形成血栓,是急性冠状动脉综合征(ACS)共同的病理生理过程。一直以来,斑块的不稳定性在ACS的认识中占主导地位。但相当部分ACS患者在发病前并无先兆。因此,提出了“从易损斑块到易损患者”的新概念,强调从整体观念上来评估患者。本文将就易损斑块、易损血液、易损心肌作一综述,以阐述评估易损患者的整体理念。1易损斑块1.1易损斑块的命名、定义及标准1.1.1易损斑块的命名国内外文献中,易损斑块、高危斑块、危险斑块、不稳定斑块、软斑块、非钙化斑块、AHAⅥ型斑块等名词均不约而同被作为易于形成血栓的粥样病…     

易损斑块组织特征的影像学研究进展

动脉粥样硬化是心脑血管疾病的主要病因.早期、有效地识别易损斑块是目前研究热点,对动脉粥样硬化患者的治疗和判断预后具有非常重要的临床应用价值,而斑块组份及分布与斑块易损性及其破裂后导致的心脑血管事件密切相关.本文主要从易损斑块的组份特征入手,对其影像学检测手段的进展进行简单归纳.     

动脉粥样硬化易损斑块进展机制与临床干预

<正>冠心病的发病率和死亡率居高不下,其快速进展严重威胁人类健康与生命,而动脉粥样硬化(atherosclerosis, AS)是冠心病的病理基础,早期AS没有明显临床症状,而晚期AS斑块容易出现跳跃式阶段性生长,即从轻度损伤迅速发展为重度损伤到极高危状态,导致急性心血管事件。全面了解AS易损斑块的特征、快速进展机制及相关调控因素,早期识别并干预AS的发生、发展,有利于合理评估AS相关风险因素,早期阻断AS向晚期进展,进行精准医疗。     

外膜滋养血管在动脉粥样硬化易损斑块中的研究现状

随着对动脉粥样硬化(As)的深入研究,促进易损斑块的稳定性成为As新的治疗理念。在As"由内而外"学说中血管内膜的病理改变成为始动因素,然而近年研究表明外膜新生滋养血管(VV)在As"由外向内"发病机制中起到关键作用,总之,对于As的治疗已从保护血管内膜转变为调节外膜VV。     

动脉粥样硬化易损斑块与易损患者

易损斑块指易于形成血栓或可能迅速进展为罪犯病变的斑块。“高危斑块”、“危险斑块”和“不稳定斑块”可以接受但不推荐使用。建议不再采用“软斑块”、“无钙化斑块”和美国心脏病协会“Ⅳ型斑块”。     

易损斑块的中医药治疗

现代医学对动脉粥样硬化易损斑块的相关研究为中医药应用干预易损斑块的措施提供了科学依据,本文就与易损斑块相关的中医病机、治则、方药作一综述.     

易损斑块的中医药治疗

现代医学对动脉粥样硬化易损斑块的相关研究为中医药应用干预易损斑块的措施提供了科学依据,本文就与易损斑块相关的中医病机、治则、方药作一综述。     

易损斑块研究进展

自1844年学者们首次对动脉粥样硬化破裂斑块的组织学进行描述以来,一些领先的研究者和临床医师进行了大量研究,使当今不稳定的斑块导致斑块破裂的观点得到普遍接受.     

动脉粥样硬化易损斑块动物模型的建立

动脉粥样硬化进展、易损斑块破裂导致主要不良心血管事件发生。易损斑块形成机制和干预措施的研究一直备受瞩目。建立与人体斑块相似的进展性斑块是对易损斑块进行研究的基础及热点。目前,研究者已在多种动物体内建立了多种易损斑块模型。本文对目前建立的易损斑块动物模型进行综述与评价,为完善易损斑块模型的建立提供新思路。     

动脉粥样硬化不稳定斑块的研究现状

随不稳定斑块发展而继发的血栓形成是导致急性冠状动脉综合征的重要原因。在内外因素的共同作用下,不稳定斑块可能发生破裂、糜烂以及钙化等现象。斑块中存在许多直接和间接的致血栓形成的物质,它们同血液一起促进了血栓的产生。人们已经建立多种自发或诱发的不稳定斑块的动物模型。针对各种不同的影响斑块稳定性的因素,人们正从不同角度寻找能有效的稳定斑块的治疗方法。     

Current status of vulnerable plaque detection

Critical coronary stenoses have been shown to contribute to only a minority of acute coronary syndromes (ACS) and sudden cardiac death. Autopsy studies have identified a subgroup of high‐risk patients with disrupted vulnerable plaque and modest stenosis. Consequently, a clinical need exists to develop methods to identify these plaques prospectively before disruption and clinical expression of disease. Recent advances in invasive and noninvasive imaging techniques have shown the potential to identify these high‐risk plaques. The anatomical characteristics of the vulnerable plaque such as thin cap fibroatheroma and lipid pool can be identified with angioscopy, high frequency intravascular ultrasound, intravascular MRI, and optical coherence tomography. Efforts have also been made to recognize active inflammation in high‐risk plaques using intravascular thermography. Plaque chemical composition by measuring electromagnetic radiation using spectroscopy is also an emerging technology to detect vulnerable plaques. Noninvasive imaging with MRI, CT, and PET also holds the potential to differentiate between low and high‐risk plaques. However, at present none of these imaging modalities are able to detect vulnerable plaque neither has been shown to definitively predict outcome. Nevertheless in contrast, there has been a parallel development in the physiological assessment of advanced atherosclerotic coronary artery disease. Thus recent trials using fractional flow reserve in patients with modest non flow‐limiting stenoses have shown that deferral of PCI with optimal medical therapy in these patients is superior to coronary intervention. Further trials are needed to provide more information regarding the natural history of high‐risk but non flow‐limiting plaque to establish patient‐specific targeted therapy and to refine plaque stabilizing strategies in the future. © 2009 Wiley‐Liss, Inc.     

Intravascular modalities for detection of vulnerable plaque: current status

Progress in the diagnosis, treatment, and prevention of atherosclerotic coronary artery disease is dependent on a greater understanding of the mechanisms of coronary plaque progression. Autopsy studies have characterized a subgroup of high-risk, or vulnerable, plaques that result in acute coronary syndromes or sudden cardiac death. These angiographically modest plaques share certain pathologic characteristics: a thin, fibrous cap, lipid-rich core, and macrophage activity. Diagnostic techniques for vulnerable-plaque detection, including serologic markers and noninvasive and invasive techniques, are needed. Recent advances in intravascular imaging have significantly improved the ability to detect high-risk, or vulnerable, plaque in vivo by using various features of plaque vulnerability as methods of identification. The characteristic anatomy of a thin, fibrous cap overlying a lipid pool has promoted high-resolution imaging, such as intravascular ultrasound, optical coherence tomography, and intracoronary magnetic resonance. The lipid-rich core is identifiable by angioscopically detected color changes on the plaque surface or by its unique absorption of energy, or "Raman shift," of its cholesterol core, driving coronary spectroscopy. Finally, temperature heterogeneity arising at foci of plaque inflammation has prompted the development of intracoronary thermography. In this review, we will discuss these techniques, their relative advantages and limitations, and their potential clinical application.     

Drug-eluting stents and vulnerable plaque

Coronary artery disease with acute coronary syndromes (ACS) is the leading cause of death worldwide in both men and women. ACS mostly occur as a result of rupture of “vulnerable plaque” with a superimposed thrombus formation, which ultimately leads to distal cessation of blood flow. Vulnerable plaque mostly occurs in mildly obstructive coronary lesions rather than severely stenosed (< 50%) lesions. Support for this conclusion comes from studies of patients with ACS who had a recent prior coronary angiogram; the artery involved in the subsequent ACS was usually only moderately diseased. Whether early treatment of these mildly obstructive lesions with percutaneous coronary interventions may lead to prevention of this deadly malady remains unknown. The long-term efficacy of percutaneous coronary intervention for mildly obstructive coronary narrowing is limited by the occurrence of restenosis, which limits the applicability of this therapy for these lesions. However, use of drug-eluting stents has significantly reduced the incidence of in-stent restenosis, yielding much better long-term outcomes. This article reviews the available data for possible early treatment of mildly obstructive coronary lesions with drug-eluting stents for prevention of ACS.     

Dyslipidemia and the vulnerable plaque

In the last decade, an increasingly sophisticated understanding of the pathogenesis of atherosclerosis and its cardiovascular consequences has emerged. The characteristics of the unstable atherosclerotic plaque, the substrate for the majority of acute coronary events, have been well defined: mild-to-moderate stenosis, a lipid-rich pool, few smooth muscle cells, a friable fibrous cap, and macrophage infiltration. Lipid modification, an important cardiovascular risk reduction strategy, induces a number of effects at the vascular level that may contribute to the clinical benefits seen in large-scale, prospective prevention trials. New developments in imaging technologies may afford improved opportunities to visualize the at-risk plaque and may provide new insights into the optimal management of the unstable plaque. Copyright 2002, Elsevier Science (USA). All rights reserved.     

易损斑块的检测方法及意义

每年突发性心血管事件f包括急性冠状动脉综合征（acute coronary syndrome,ACS）和心脏性猝死]夺去世界上约1900多万人的生命。这些患者大多死于不稳定的冠状动脉粥样斑块破裂,相继发生的血栓形成与心肌坏死。轻、中度狭窄病变（狭窄度40％～70％）往往无临床先兆症状,表明斑块的稳定性（即易损性）预测急性心血管事件比管腔狭窄程度更为重要。     

肝纤维化发生发展机制的研究现状

肝纤维化是多种慢性肝病进展至肝硬化的中间过程,其严重的并发症影响着慢性肝病患者的预后,目前为止肝纤维化仍没有确切的治疗药物。从信号通路和分子机制方面对肝纤维化发生发展进行深入探讨,简述了TGFβ-Smad信号通路、血小板衍生生长因子信号通路、瘦素作用的信号通路、结缔组织生长因子作用的信号通路,及趋化因子、神经内分泌因子和血管生成在肝纤维化发生机制中的最新研究进展,以期增加对肝纤维化发生机制的认识,为基于肝纤维化发生机制的分子靶向药物研究提供理论依据。