易损斑块的血清标记物研究进展

临床研究证实炎症在动脉粥样硬化损伤的各阶段均有重要作用,包括从脂纹形成到最终易损斑块的破裂。炎症标记物可以反映与急性冠状动脉综合征的各个阶段相关联的动脉粥样硬化进程的不同侧面,还可能与急性冠状动脉综合征的严重性有关。该综述总结了有关炎症标记物的文献,为使用炎症标记物检测易损斑块的可行性提供了一些证据。这些证据可能会促使动脉粥样硬化患者的管理更加完善,包括一级预防和二级预防。     

心血管影像技术在冠状动脉易损临界病变诊断中的应用

早期识别冠状动脉易损斑块是近年来临床研究的热点和难点。绝大部分急性冠脉综合征是因轻到中度的动脉粥样硬化斑块破裂所致。与管腔狭窄程度相比,斑块的组成是决定冠状动脉病变易损性的最重要原因。该文简述目前常用的影像技术在识别冠状动脉易损临界病变中的应用。     

心血管影像技术在冠状动脉易损临界病变诊断中的应用

早期识别冠状动脉易损斑块是近年来临床研究的热点和难点。绝大部分急性冠脉综合征是因轻到中度的动脉粥样硬化斑块破裂所致。与管腔狭窄程度相比,斑块的组成是决定冠状动脉病变易损性的最重要原因。该文简述目前常用的影像技术在识别冠状动脉易损临界病变中的应用。     

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。     

易损斑块的病理生理机制及其检测的研究进展

随着对急性冠状动脉综合征(ACS)病理生理机制的深入研究,目前对易损动脉粥样硬化斑块(简称:易损斑块)有了新的理解。认识易损斑块的内在特性和破裂机制,对于早期检测和处理易损斑块具有重要的临床意义。本文就易损斑块的概念、基本特征、病理生理机制及其检测作一论述。一、易损斑块的最新概念从病理生理角度来讲,ACS最主要的深层原因是易损斑块。易损斑块是指那些不稳定和有血栓形成倾向的斑块,主要包括破裂斑块、侵蚀性斑块和部分钙化结节性病变[1] 。大量的研究表明,约70 %～80 %的ACS是由于轻、中度狭窄的冠状动脉斑块的破裂、继发…     

易损斑块动物模型研究进展

易损斑块在急性冠状动脉综合征的发生发展中起着重要作用,减少易损斑块的破裂对降低不良心血管事件有重大意义。近年来,易损斑块的研究成为心血管领域的热点,但由于动物基因组和人类基因组的差异,以及斑块形成的病理生理过程不同,目前动物模型所形成的斑块与人类易损斑块还有很大差异。因此,建立与人类动脉粥样硬化斑块相似的动物模型成为目前亟待解决的难题。     

18F-NaF正电子发射计算机断层扫描成像在冠状动脉粥样硬化性易损斑块中的应用进展

<正>心血管疾病是人类健康的主要杀手,大部分心血管事件是由动脉粥样硬化斑块引起的,动脉粥样硬化斑块破裂导致的心肌梗死或脑卒中是心血管疾病致死的根本原因~([1])。而有创性冠状动脉血管造影术这些传统的检查方法不能发现这些斑块,近年的研究发现这些高风险斑块(所谓的易损斑块)有某些组织病理学特性。因此,能否利用易损斑块的组织病理学特性,寻找易损斑块无创检测方法是现代成像技术     

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。     

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     

动脉粥样硬化易损斑块的动物模型和检测技术

动脉粥样硬化易损斑块破裂、血栓形成是急性冠状动脉综合征的发病机制已成为共识。由于缺乏理想的易损斑块的动物模型,对斑块破裂前的血清学及影像学特征研究较少,尚缺乏能够早期识别易损斑块及预防斑块破裂的最佳方法。本实验室已成功构建家兔和Apo E-/-小鼠的易损斑块模型。易损斑块的检测技术主要包括非侵入性及侵入性的影像学检测及功能学检测技术。对易损斑块的早期准确识别以便及时干预具有十分重要的临床意义。     

Intracoronary Thermography

Arteriosclerosis is an inflammatory disease. Inflammatory processes play a role in the initiation of plaque development and the early stages of the disease as well as in complex plaques and complications such as intraarterial thrombosis. A method to detect inflammation in coronary arteries has the potential to characterize both local and systemic activation of arteriosclerotic plaque disease. It could help to define in more detail what constitutes a vulnerable plaque or vulnerable vessel and thus improve the prediction of acute coronary syndromes. Intracoronary thermography records a cardinal sign of inflammation. Heat is probably produced by (activated) macrophages. Experimental work has suggested that thermal heterogeneity is present in arteriosclerotic plaques and that increased temperature is found at the site of inflammatory cellular-macrophage-infiltration. Preliminary experience in patients undergoing coronary angiography has demonstrated that it is safe and feasible to perform intracoronary thermography using various systems. A graded relationship between thermal heterogeneity and clinical symptoms has been reported, with the greatest temperature elevation in acute myocardial infarction. Increases in thermal heterogeneity appeared to be associated with a comparably unfavorable long-term prognosis. Intracoronary thermography has the potential to provide insights into location and extent of inflammation as well as the prognostic consequences. Currently, this novel method and the underlying concepts are extensively evaluated.     

易损斑块的诊断进展

急性冠状动脉综合征患者具有较高的发病率,预后较差,而冠状动脉内易损斑块破裂伴随血栓形成是其主要原因.因此早期正确诊断易损斑块,对于急性冠脉综合征的防治具有重大意义.现就易损斑块的诊断进展作一综述.     

冠状动脉CT成像与易损斑块

冠状动脉内斑块破裂或侵蚀所致的急性腔内血栓是急性冠状动脉综合征的主要原因。防止急性血栓形成成为了降低冠状动脉粥样硬化性心脏病病死率的唯一有效策略。斑块易破裂的冠状动脉病变与稳定斑块相比,存在不同的形态学改变。因此可以利用特殊的成像方法来识别这些易损斑块。亚毫米空间分辨率和图像质量优良的现代计算机断层扫描方法可以对冠状动脉斑块进行检测、分析和量化。斑块体积较大、低CT衰减、餐巾环征、正性重构以及点状钙化等与斑块容易破裂有密切关系。将冠状动脉斑块的形态学与功能特征等相结合,在未来有可能成为检测易损斑块的新方法。现将就多层螺旋CT与冠状动脉易损斑块的检测做一综述。     

关于脂联素与易损斑块相关性的研究进展

所谓易损斑块是指易于破裂的高风险斑块,有别于引起管腔狭窄,导致稳定型心绞痛的斑块。此种斑块具有独特的组织学特性,由脂质核心、薄纤维帽等构成,并伴有血管壁的正性重构。而脂联素是一种脂肪因子,几乎参与到了从易损斑块形成至破裂的全部过程。目前更有大量研究指出,血清脂联素水平的降低同日益增长的冠状动脉疾病尤其是急性冠状动脉综合征的发病率密切相关。脂联素能够解释冠状动脉疾病病理进程中所涉及的炎症及动脉粥样硬化机制。     

中国人群脂蛋白a与冠状动脉易损斑块相关性的Meta分析

目的：系统评价脂蛋白a[Lipoprotein a, Lp （a）]对冠状动脉易损斑块的预测价值。方法：以脂蛋白a、易损斑块、不稳定斑块、冠状动脉、冠心病、Lipoprotein a、Lipoprotein (a)、vulnerable plaque、unstable plaque、coronary vessel、coronary artery、coronary heart disease、coronary disease等为检索词,检索PubMed,Embase,Cochrane Library,CNKI,CBM以及万方平台从建库到2020年7月的关于Lp （a）与冠脉易损斑块相关性的临床试验研究,。采用NOS质量评分量表对文献进行质量评价,应用RevMan 5.3软件及Stata 12.0软件对纳入的文献进行Meta分析。结果：经筛选后最终纳入文献11篇,1351名患者,易损斑块组717人,稳定斑块组634人。Meta分析结果显示：易损斑块组中患者血清Lp （a）水平较稳定斑块组明显升高（SMD=1.27,95%CI：0.77,1.77）。结论：人血清中Lp （a）可能是冠状动脉易损斑块形成的重要危险因素,其含量的升高可能具有预测急性心血管事件发生的能力。     

Molecular imaging of plaques in coronary arteries with PET and SPECT

Coronary artery disease remains a major cause of mortality. Presence of atherosclerotic plaques in the coronary artery is responsible for lu-men stenosis which is often used as an indicator for determining the severity of coronary artery disease. However, the degree of coronary lumen stenosis is not often related to compromising myocardial blood flow, as most of the cardiac events that are caused by atherosclerotic plaques are the result of vulnerable plaques which are prone to rupture. Thus, identification of vulnerable plaques in coronary arteries has become increas-ingly important to assist identify patients with high cardiovascular risks. Molecular imaging with use of positron emission tomography （PET） and single photon emission computed tomography （SPECT） has fulfilled this goal by providing functional information about plaque activity which enables accurate assessment of plaque stability. This review article provides an overview of diagnostic applications of molecular imaging tech-niques in the detection of plaques in coronary arteries with PET and SPECT. New radiopharmaceuticals used in the molecular imaging of coro-nary plaques and diagnostic applications of integrated PET/CT and PET/MRI in coronary plaques are also discussed.     

冠状动脉CT血管造影综合评估易损斑块的进展

急性冠状动脉综合征（ACS）是以冠状动脉粥样硬化斑块破裂或侵袭,继发完全或不完全闭塞性血栓形成为病理基础的一组临床综合征。与稳定斑块相比,容易破裂的斑块具有明显的影像学特征：大斑块体积,低衰减斑块,餐巾指环标志,正性重构和点状钙化,这为在导致临床事件之前运用非侵入性成像识别易损斑块提供了独特的机会。随着影像技术的发展,冠状动脉CT 血管造影（CCTA）无创性评价冠状动脉易损斑块的作用已成为国内外研究热点。笔者就CCTA在评估冠状动脉斑块易损性方面的临床应用现状与进展等方面作一综述。     

Proteomics of acute coronary syndromes

Acute coronary syndromes (ACS), such as unstable angina, acute myocardial infarction, and sudden cardiac death, are commonly associated with the presence of vulnerable plaques in coronary arteries. Rupture or erosion of vulnerable plaques results in the formation of luminal thrombi due to the physical contact between platelets and thrombogenic elements within the atherosclerotic lesions. Considering the socioeconomic burden of ACS, it is imperative that the scientific community achieves a clear understanding of the multifaceted pathophysiology of vulnerable atheroma to identify accurate prognostic biomarkers and therapeutic targets. The analytical power of modern proteomic technologies could facilitate our understanding of vulnerable plaques and lead to the discovery of novel therapeutic targets and diagnostic biomarkers.     

The percutaneous assessment of regional and acute coronary hot unstable plaques by thermographic evaluation (PARACHUTE) study: a prospective reproducibility and prognostic clinical study using thermography to predict future ischemic cardiac events

Intravascular thermography is currently being considered as a valuable tool in assessing macrophage‐rich plaques. Since it is unknown what the prognostic value is of non‐obstructive atherosclerotic plaques showing temperature heterogeneity, we designed the PARACHUTE study, a prospective, reproducibility, and prognostic clinical study using thermography in patients presenting with an unstable coronary syndrome. The primary endpoint of the study is the predictive value of temperature heterogeneity towards the occurrence of ischemic coronary events and hospitalization for ischemia and/or angina. The secondary endpoints are the predictive value of high‐risk plaques associated with the development of future cardiac events, assessment of safety of the procedure, assessment of temperature reproducibility and heterogeneity in coronary arteries, as defined by the total thermal burden towards the occurrence of any cardiac event. Based on an event rate of death and myocardial infarction at 1 year of 10%, a sample size of 260 patients with presumed coronary artery disease, and positive troponin level who are scheduled to undergo an intervention will be included. All three main epicardiac vessels will undergo angiography and thermography at baseline after revascularization of the flow‐limiting vessel. At 12 months, angiography of all vessels and thermography of the vessel with the highest thermographic burden will be performed. Independent core laboratories will assess outcomes and a clinical endpoint committee will assess clinical events. (Int J Cardiovasc Intervent 2004; 2:?69–75)     

Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction

OBJECTIVES: This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL). BACKGROUND: Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques. METHODS: We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL. RESULTS: An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively. CONCLUSIONS: This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.