三维益心方对动脉粥样硬化斑块影响的实验研究

大量研究表明血管新生是动脉粥样硬化(atherosclerosis,AS)的重要病理学特点[4],其临床意义可能在于导致斑块不稳定,继而破裂出血,并形成血栓,引发心血管事件。本研究通     

益气滋阴活血通络方对动脉粥样硬化斑块内新生血管的影响

目的 探讨益气滋阴活血通络方对动脉粥样硬化(AS)斑块内血管新生的影响。方法 首先构建动脉粥样硬化ApoE-/-小鼠模型，用高脂饲料喂养雄性ApoE-/-小鼠12周，在造模完成后，将模型小鼠随机分为空白组、高脂对照组、益气滋阴活血通络中药复方组、阿托伐他汀组，并分别予以蒸馏水、益气滋阴活血通络中药复方、阿托伐他汀干预12周，以检测小鼠动脉斑块内新生血管的密度。通过免疫组化检测中药复方对动脉粥样硬化模型动脉斑块内血管新生的影响。结果 与空白组、高脂对照组比较，在益气滋阴活血通络中药复方、阿托伐他汀组中、高剂量组斑块内新生血管密度系数都有明显降低(P<0.05)。免疫组化结果表明，中药复方组和阿托伐他汀组治疗后减少了斑块内新生血管的表达。结论 益气滋阴活血通络方具有稳定AS斑块的作用，益气滋阴活血通络方可以通过抑制血管新生，从而降低新生血管在斑块内的表达，起到稳定斑块的作用。     

超声e-Flow对脑梗死患者颈动脉斑块内新生血管的检测

目的探讨超声e-Flow对脑梗塞患者颈动脉斑块内新生血管的检测中的价值。方法回顾性分析河北燕达医院2008年1月至2009年3月住院的脑梗死患者69例的临床资料,该组患者均采用超声e-Flow对脑部颈动脉斑块进行检测,总结检测结果。结果超声100个斑块中有66个可见新生血管,其中软斑40个,硬斑0个,混合斑块26个。34个超声未见新生血管的斑块中,硬斑块17个,软斑块8个,混合斑块9个。且未显示新生血管组的斑块厚度显著小于显示新生血管组的斑块厚度,P<0.05。结论超声e-Flow对于斑块内新生血管较为敏感,且由于操作更为简便,费用更低,值得临床推广。     

超微血流成像技术评价颈动脉硬化斑块稳定性及预测脑卒中的应用价值

目的探讨超微血流成像技术(SMI)在评价颈动脉硬化斑块稳定性及预测脑卒中风险性中的应用价值。方法对经颈动脉常规超声检查发现有颈动脉粥样硬化斑块的78例患者(脑梗死患者38例,非脑梗死患者40例)进行SMI检查,并同时进行超声造影(CEUS)检查对比分析。结果常规颈动脉超声检查共发现141个斑块,其中低回声斑块38个,低回声为主的混合回声斑块40个,等回声斑块30个,强回声斑块33个。SMI和CEUS在不同性质斑块内新生血管显示率由高到低均为:低回声斑,低回声为主混合回声斑,等回声斑,强回声斑;低回声斑、混合回声斑与等回声斑、强回声斑比较差异均有统计学意义(P<0.05);低回声斑与混合回声斑比较差异无统计学意义(P>0.05)。所检斑块中137个斑块SMI与CEUS检测结果相同,其中80个斑块内均可见血流显像,多分布在近心端底部;57个斑块均未见血流显像;4个斑块CEUS可显示血流,而SMI未显示,经统计学检验差异无统计学意义(χ~2=0.233,P>0.05)。SMI与CEUS检测斑块内新生血管分级情况比较有较好的一致性(Kappa=0.736)。SMI技术显示斑块厚度≥3 mm斑块内新生血管数目较斑块厚度1.5~3.0 mm斑块内新生血管数目增多,差异有统计学意义(P<0.05)。受检者中脑梗死患者与非脑梗死患者斑块厚度比较差异无统计学意义(t=0.208,P>0.05),而脑梗死组SMI技术显示斑块内新生血管分级程度高于非脑梗组,差异有统计学意义(χ~2=10.44,P<0.01)。结论斑块中新生血管密度越高,发生脑卒中风险越大。     

脂联素和动脉粥样硬化易损斑块

脂联素是脂肪组织所分泌的活性物质,其通过改善血管内皮功能、抑制炎症、稳定纤维帽、减少斑块核心、抑制新生血管生成和斑块内出血、抑制增生和血管正性重构等多种途径稳定动脉粥样硬化斑块,预防和减少斑块破裂。本文对脂联素及其稳定动脉粥样硬化易损斑块的机制作一综述。     

三维超声血管斑块定量分析技术对颈动脉粥样硬化斑块稳定性的评估效果分析

目的 ：分析三维超声血管斑块定量分析技术对颈动脉粥样硬化斑块稳定性的评估效果。方法 ：选取2020年5月至2022年5月收治的脑血管疾病颈动脉粥样斑块硬化患者78例,均行三维超声和CT血管造影（CTA）检查。三维超声检查患者颈动脉狭窄程度、动脉内膜-中膜厚度（IMT）、灰阶中位数（GSM）和斑块总体积、表面积、回声类型、均质性及新生血管,并以CTA检查为金标准,对比三维超声和CTA检查结果。结果 ：经CTA检查,78例患者中47例的颈动脉粥样硬化斑块稳定,31例不稳定。经三维超声检查,78例中42例的颈动脉粥样硬化斑块稳定,36例不稳定。三维超声检查的准确率为85.90%(67/78),敏感性为82.98%(39/47),特异性为90.32%(28/31),阳性预测值为92.86%(39/42),阴性预测值为77.78%(28/36),kappa=0.713,一致性优。稳定与不稳定患者间的三维超声影像学特征存在明显差异,不稳定患者的颈动脉狭窄程度、IMT、斑块总体积均大于稳定患者;GSM低于稳定患者;斑块回声不连续、斑内低回声、新生血管、形态不规则的检出率高于稳定患者（P <0....     

胶原代谢对动脉粥样硬化斑块稳定性的影响及中医药论治的研究进展

目的:为中医药防治动脉粥样硬化(AS)及其继发症的研究提供参考。方法:查阅近年来国内外相关文献,对胶原代谢与AS斑块稳定性的关系及中医药论治的研究进展进行归纳、总结。结果与结论:既往中医药治疗多从补益肝脾肾、活血化痰通络、清热解毒等角度对AS进行干预,并多从降脂、抗炎症反应、抗氧化等角度进行作用机制研究,但对AS斑块稳定性的研究与认识不足,有关调节胶原代谢影响AS斑块稳定性的研究报道较为少见。作为影响AS斑块稳定性的重要因素,胶原代谢的平衡可能为中医药防治AS提供一个新的研究方向和思路。     

炎症与不稳定动脉粥样硬化斑块

血浆脂质的增高(高脂血症)是动脉粥样硬化(AS)发生的重要病理因素,这已是大家公认的事实,然而,近年来的研究表明,炎症在AS的发生发展中同样起着不可忽视的作用。ROSS及其他学者发现血管受损伤后产生炎症--纤维增殖反应,其中涉及大量的生长因子、细胞因子及血管调节因子,最终导致AS有发生。AS是冠心病的病理基础,而动脉粥样硬化不稳定斑块的破裂、血小板的聚集及血栓形成造成冠脉急性狭窄或闭塞是导致急性冠脉综合征(ACS)的重要原因。而Luigi纠的研究表     

超声B-Flow血流成像技术对颈部动脉硬化斑块易损性的研究

目的:使用B-Flow成像技术检测颈部动脉血管硬化斑块的新生毛细血管情况来判断颈部动脉血管硬化斑块的易损性.方法:选取85例有颈部动脉血管硬化斑块的患者,进行B-Flow血流成像技术观察颈部动脉血管硬化斑块内有无微血流信号,将颈部动脉血管硬化斑块分两组,一组有微血流信号组(55例)另一组无微血流信号组(30例),比较两组颈部动脉血管硬化斑块患者患脑梗塞比率的情况.结果:颈部动脉血管硬化斑块内有微血流信号组脑梗塞发生率(74％)显著高于无微血流组(35％),比较有微血流信号组与无微血流信号组结果不同有统计学意义(P＜0.05).结论:通过B-Flow血流成像技术对颈部动脉血管硬化斑块内新生毛细血管的检测判断颈部动脉血管硬化斑块的易损性,预测脑梗塞的风险.     

颈动脉斑块超声血管造影分级与病理微血管密度的相关性

目的 探索超声血管造影(CEUS)检测到的颈动脉粥样硬化斑块内新生血管是否与斑块病理检测的微血管存在相关性.方法 前瞻性入组行颈动脉内膜剥脱术(CEA)的20例患者,所有患者术前行CEUS检查,并按照检测到的斑块内增强情况分为0～3级,术后对患者斑块标本行常规HE染色及CD31单克隆抗体标记的免疫组化染色,并根据CD3...     

Rosiglitazone promotes atherosclerotic plaque stability in fat-fed ApoE-knockout mice

Type 2 diabetes is considered a "risk equivalent" for cardiovascular disease, rosiglitazone, as an insulin sensitizer, has been explored as a novel therapeutic drug for the prevention of cardiovascular disease, but whether it can stabilize vulnerable atherosclerotic plaques is still unknown. Our study aims to investigate the effect of rosiglitazone on plaque stability in fat-fed ApoE-knockout mice. Our findings showed that rosiglitazone can stabilize the vulnerable atherosclerotic plaques in fat-fed ApoE-knockout mice by modifying the plaque composition as well as decreasing the number of buried fibrous caps and its anti-inflammatory effect probably is the key mechanism through which promotes the plaque more stable.     

Analysis of contrast-enhanced intravascular ultrasound images for the assessment of coronary plaque neoangiogenesis: another step closer to the identification of the vulnerable plaque

Atherosclerotic cardiovascular disease (CVD), primarily manifested as heart attacks and strokes, remains the main cause of death in the developed countries and is rapidly increasing in the developing world. Early detection and aggressive treatment of hidden (asymptomatic) atherosclerotic plaques that cause heart attack or stroke are most needed. However, existing clinical tools are not sufficient to address this need. Intravascular ultrasound (IVUS) is a catheter-based medical imaging tool that is capable of providing cross-sectional images of arteries. It is by far the most powerful clinical tool available for characterization of atherosclerotic plaques. However, existing IVUS is unable to detect plaque inflammation which is a key factor in complications of atherosclerotic plaques. Contrast enhanced IVUS (CE-IVUS) for detection of Vasa Vasorum (VV), microvessles that feed the vessel wall, can indirectly image plaque inflammation and thereby significantly increase the diagnostic power of IVUS. Several studies have shown that the density of VV in the atherosclerotic plaques is strongly correlated with the intensity of plaque inflammation and related processes which lead to plaque destabilization and rupture (the Vulnerable Plaque). Therefore the detection and measurement of VV in plaque, and leakage of blood from VV into plaques using CE-IVUS, can enable the development of an index for plaque vulnerability. In this paper, we present a review of our original work on coronary VV imaging, discuss subsequent reports by others, and also present the latest on the detection of VV based on CE-IVUS.     

The importance of reendothelialization after arterial injury

Atherosclerosis is still the principal cause of morbidity and mortality in Western countries and although a significant progress has been made in the understanding of its pathophysiology, the determinants of atherosclerotic plaque instability are still poorly understood. The endothelium plays a pivotal role for the development, progression, and complication of atherosclerosis. Endothelial dysfunction is widely recognized as one of the early alteration in the vessel wall preceding the development of the plaque. However, considering the plethora of vascular functions which are regulated by endothelium, it plays a pivotal role throughout the atherosclerotic process and indeed the loss of endothelial cells, leading to plaque denudation, is one of the main causes of plaque complication. It is therefore conceivable that the maintenance of the endothelial layer physical continuity and function is crucial for the prevention of atherosclerosis. In the presence of cardiovascular risk factors, endothelial cells are continuously injured and repaired by the proliferation of resident cells and circulating endothelial progenitor cells. Indeed the number of circulating endothelial progenitor cells has been identified as an predictor of cardiovascular events. The increase in bone marrow release of endogenous progenitor cells or the enhancement of their homing in arterial denuded sites or in intravascular stent surface, are currently pursued to reduce atherosclerosis development/complication and intrastent restenosis, respectively. However, some challenges may arise from procedures enhancing endothelialization, including unwanted angiogenesis which may favor neoplasia progression and paradoxically atherosclerotic plaque expansion and complication.     

Anti-atherosclerotic effect of microbial hyaluronate lyase from group B streptococci

The effect of the microbial hyaluronic acid splitting enzyme hyaluronate lyase produced by Streptococcus agalactiae was investigated in vitro in human atherosclerotic plaque specimens and in vivo on Watanabe heritable hyperlipidaemic rabbits (WHHL) as an animal model for familiar hypercholesteraemia. The in vitro presence of the enzyme caused a partial destruction of the atherosclerotic plaque surfaces as well as releasing of glucuronic acid and solid calcium-containing materials from pieces of atherosclerotic plaques in human arteries. Accordingly hyaluronic acid seems to be the main component for anchoring of calcium deposits on the plaque surfaces. Repeated intravenous injections of hyaluronate lyase in WHHL rabbits resulted in a tendency of decreased formation of atherosclerotic plaques. The observed effects are discussed to be primary the result of the splitting of hyaluronic acid in the vessels.     

清除斑块胆固醇结晶治疗动脉粥样硬化的研究进展

动脉粥样硬化是导致心脑血管疾病的主要诱因。主动脉血管内皮下斑块的形成是动脉粥样硬化的病理特征,而在斑块中胆固醇结晶的出现不仅会加剧斑块炎症反应,还会造成斑块去稳定和破裂,最终导致心脑血管事件。因此,清除斑块胆固醇结晶将有利于动脉粥样硬化的归转。本文综述了斑块中胆固醇结晶的形成过程和特点、胆固醇结晶促进动脉粥样硬化的作用机制以及清除斑块胆固醇结晶的策略,为开发以斑块胆固醇结晶为靶点的抗动脉粥样硬化药物提供理论依据和参考。     

Effects on Coronary Atherosclerosis by Targeting Low-Density Lipoprotein Cholesterol with Statins

A correlation exists between circulating levels of low-density lipoprotein cholesterol (LDL-C) and risk of cardiovascular disease (CVD). Evidence from clinical trials indicates that reducing LDL-C levels can result in beneficial clinical outcomes in patients at risk of CVD and in high-risk patients with clinical symptoms of CVD. Lipid-lowering agents, of which HMG-CoA reductase inhibitors (statins) are the most effective, protect against the vascular changes seen in the development of atherosclerotic plaque formation. Clinical trials assessing the effects of statins on coronary atherosclerosis using quantitative coronary angiography or intravascular ultrasound showed that statins can reduce progression or even cause regression of atherosclerotic plaque. This improvement of vascular structure after statin treatment is correlated with reductions in LDL-C levels. This appears to be the principal mechanism by which statin therapy reduces cardiovascular risk, with emerging evidence for statin-mediated changes in high-density lipoprotein and C-reactive protein levels contributing to modification of the atherosclerotic plaque.     

Chemokines and atherosclerotic plaque progression: towards therapeutic targeting?

Atherosclerosis is currently viewed as an inflammatory disease in which the initiation and progression of the atherosclerotic plaque towards a rupture prone, unstable plaque is driven by leukocyte recruitment mediated by various inflammatory mediators. Recently, interest in chemotactic cytokines or chemokines with regard to atherosclerosis has been growing as chemokines mediate the influx of leukocytes that is typical of atherothrombosis. The activity of the majority of chemokines is overlapping and chemokines are not only produced by the various cellular constituents of the atherosclerotic plaque but also by activated platelets. Consequently, the direct influence of individual chemokines on plaque destabilisation and rupture is widespread and rather unclear. Experimental research has already established the role of a number of chemokines in advanced atherosclerosis. Nevertheless, given the complexity and size of the chemokine family, further screening of cardiovascular disease for chemokine level and genetic polymorphisms for chemokines will be warranted as the search for viable biomarkers of plaque destabilization as well as novel therapeutic targets for specific atheroregressive therapeutic compounds is ongoing. With regard to the latter, clinical trials with specific chemokine inhibitory strategies, like chemokine receptor antagonists, are already underway in other inflammatory disorders. Summarizing, chemokine inhibition likely constitutes an important therapeutic option next to already established drugs in the management of cardiovascular disease.     

Immune-mediated mechanisms in atherosclerosis: prevention and treatment of clinical manifestations

Accumulation of inflammatory cells identifies atherosclerotic plaque at risk for rupture. Typically, activated immune cells occupy the rupture-prone areas of the atherosclerotic lesion. These cells are an appealing therapeutic target for novel strategies of plaque stabilization. Biologic consequences of plaque inflammation ultimately depend not only on the cellular players populating the lesion but also on triggers of immune activation originating from within the plaque or arriving from the circulation, and immune effector mechanisms that mediate cellular damage and plaque destabilization. Recent studies have provided insights into particular immune mechanisms in the atherosclerotic plaque that contribute to plaque vulnerability. This knowledge provides the basis for potential immunomodulatory therapies in cardiovascular disease. These therapeutic approaches can be classified as (1) immunomodulatory effects of existing therapies, (2) therapies targeting inflammatory triggers, and (3) agents inhibiting specific immune mechanisms.     

Recognition, pathophysiology, and management of acute myocardial infarction.

New insights into the pathophysiology of atherosclerotic plaques leading to acute myocardial infarction (MI) are discussed, along with new diagnostic and treatment strategies. Ischemic heart disease represents a continuum from stable angina to unstable angina to non-Q-wave MI to Q-wave MI. Patients whose angina becomes unstable are classified as having acute coronary syndrome (ACS). It was formerly believed that thrombosis leading to critical occlusion of coronary arteries at the site of atherosclerotic plaque rupture was the common cause of ischemic heart disease. It is now thought that even lesions that do not critically occlude coronary arteries can cause MI. ACS can be caused by the rupture of an unstable atherosclerotic plaque. Vulnerable plaques are usually those causing only mild to moderate stenosis and having a lipid-rich core and a thin, macrophage-dense, collagen-poor fibrous cap. Factors affecting plaque rupture include mechanical injury, circadian rhythm, inflammation, and infection. Progressive thrombosis and vasospasm may follow plaque rupture. The diagnosis of MI starts with the recognition of symptoms of myocardial ischemia that are new or different from the usual pattern. Agents used to prevent or treat plaque rupture and its complications include thrombolytics, antiplatelet agents, antithrombotics, beta-blockers, angiotensin-converting-enzyme (ACE) inhibitors, and nitrates. Once patients survive the acute phase of MI, long-term therapy for prevention of future events begins. Post-MI patients should receive aspirin, beta-blockers, and an ACE inhibitor indefinitely; modification of cardiovascular risk factors is also important. Greater understanding of the pathophysiology of ACS has led to strategies to limit the progression of atherosclerosis and to improve survival and function after an acute event.     

二十碳五烯酸乙酯胶囊降低缺血性心血管事件的研究进展

动脉粥样硬化性心血管疾病发病率逐渐上升，并呈年轻化趋势。血脂异常是动脉粥样硬化发生和进展的重要危险因素。其中甘油三酯水平升高是缺血性心血管事件风险增加的独立危险因素。既往降甘油三酯药物：贝特类、烟酸和混合ω-3多不饱和脂肪酸无明确减少缺血性心血管事件发生的作用，近年研究发现二十碳五烯酸乙酯胶囊除了可降低甘油三酯水平外，同时还可通过延缓斑块进展、减小低衰减斑块体积、稳定斑块形态等机制降低缺血性心血管事件的发生率。目前完成的动物实验和临床试验均证明了其有效性、安全性和良好的耐受性。本文主要对二十碳五烯酸乙酯胶囊降低缺血性心血管事件研究的新进展进行综述。