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。     

冠状动脉易损斑块及其形态学检测技术的新认识

冠心病患者发生严重急性冠状动脉事件约70%是由易损斑块(VP)所致。不稳定斑块的破裂是急性冠状动脉综合征(ACS)发生的核心机制,其较冠状动脉狭窄程度及病变范围更能反映冠心病患者发生急性心血管事件。现代影像学技术的进展,特别是血管内超声(IVUS)及光学相干断层成像(OCT)对识别和判断VP的形态学特征,包括斑块的形态、成分,甚至功能状态提供了快速、可靠的信息支持,在诊断和评价冠状动脉斑块方面,高分辨率的0CT检测水平已近似于组织学检测水平。该文就VP形态学检测技术的进展和认识作一简要综述。     

影像学检查在冠状动脉易损斑块识别中的作用

冠状动脉（冠脉）易损斑块破裂是急性冠脉综合征的主要诱因,对易损斑块的早期发现识别具有重要意义。近年来医学影像技术的发展为早期更准确的识别易损斑块成为可能。目前对冠脉易损斑块的检查方法包括有创性检查（冠脉造影术、血管内超声、激光相干断层显像、冠脉内窥镜）和无创性性检查（多层螺旋CT 、磁共振显像、PET／CT核素闪烁显像与免疫荧光显像）,各种检查方法各有优缺点,对易损斑块特征的识别能力也各不相同,现做一概述。     

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。     

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。     

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。     

循环免疫复合物与冠状动脉粥样硬化斑块的相关性研究

目的 探讨循环免疫复合物(CICs)与冠状动脉斑块特征的相关性.方法 56例急性冠脉综合征(ACS)患者,发病时取血,酶联免疫吸附法(ELISA)检测血浆中CICs和氧化低密度脂蛋白(ox-LDL)等,以及液相蛋白芯片结合流式细胞分析方法 测定几种血管因子;常规冠状动脉造影(CAG).并行血管内超声(IVUS)检测56个靶病变处动脉粥样斑块形态学及性质特征.分析急性心肌梗死(AMI)与不稳定性心绞痛(UA)患者、易损斑块与非易损斑块组、发生斑块破裂时CICs的改变;以及与斑块形态学指标及血管因子的相关性.结果 ClCs和各血管因子浓度在AMI组与UA组之间未见显著性差异(均P>0.05);斑块破裂与非斑块破裂者比较tics浓度有显著性差异(287±26比170±31 mg/L,P=0.018);易损斑块与非易损斑块两组CICs的比较结果 显示,两组之间均无统计学意义(238±29比253±29 mg/L,P=0.78).ACS患者CICs浓度与斑块形态学指标无统计学意义;除组织纤维蛋白溶酶原激活物(t-PA)以外,CICs与其他的动脉粥样硬化形成不同阶段的炎症因子间大部分存在显著相关性;CICs与ox-LDL之间呈明显正相关性(r=0.591,P=0.005).结论 CICs结合其他因素对于ACS患者冠脉斑块破裂和AMI有重要的诊断意义.     

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.     

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。     

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.     

影像学方法检查冠状动脉粥样硬化斑块性质的研究进展

急性冠状动脉综合征(acute coronary syndrome 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。斑块破裂是引起血栓或栓塞的主要原因,因此,易损斑块的早期检出对于临床预防ACS和减少并发症有重要的意义。笔者对近年来各种影像学方法检查易损斑块性质的研究进展进行综述,旨在为临床及早检出易损斑块,减少急性心血管事件提供帮助。     

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.     

Clinical implications and mechanisms of plaque rupture in the acute coronary syndromes

Coronary atherosclerosis complicated by plaque rupture or disruption and thrombosis is primarily responsible for the development of acute coronary syndromes. Plaques with a large extracellular lipid-rich core, a thin fibrous cap due to reduced collagen content and smooth muscle density, and increased numbers of activated macrophages and mast cells appear to be vulnerable to rupture. Plaque disruption tends to occur at points at which the plaque surface is weakest and most vulnerable, which coincide with points at which stresses resulting from biomechanical and hemodynamic forces acting on plaques are concentrated. Reduced matrix synthesis as well as increased matrix degradation predisposes vulnerable plaques to rupture in response to extrinsic mechanical or hemodynamic stresses. Modification of endothelial dysfunction and reduction of vulnerability to plaque rupture and thrombosis may lead to plaque stabilization. These concepts have significant clinical implications that are just beginning to be explored and incorporated into clinical practice. This article reviews the mechanism of coronary atherosclerosis development and the pathophysiology of acute coronary syndromes to provide a framework for understanding how plaque passivation might be accomplished in clinical medicine.     

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.     

Targeting the inflammatory component in atherosclerotic lesions vulnerable to rupture

Thrombosis of the coronary artery following plaque rupture is the commonest substrate of acute coronary events. The detection of atherosclerotic plaques prone to rupture would allow identifying patients at risk for acute coronary events and aggressive intervention. It has been assumed that the plaque morphology happens to be the major determinant for clinical outcome. The risk of plaque rupture depends upon the prevalence of plaques that have a large lipid core, a thin fibrous cap, and a dense inflammation of the fibrous cap. Evaluating monocytes and the lipid core and their proportions in the atherosclerotic lesion by novel radionuclide imaging strategies may predict a likelihood of an acute coronary event.