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《中西医结合心脑血管病杂志》2020,(4)
目的探讨急性冠脉综合征合并糖尿病病人颈部血管斑块与冠状动脉狭窄程度的相关性。方法选取2014年1月—2015年1月就诊于陕西中医药大学附属医院心内科的急性冠脉综合征病人382例,其中合并糖尿病185例,收集颈部血管B超和冠状动脉造影检查结果,分析单纯急性冠脉综合征非糖尿病和急性冠脉综合征合并糖尿病病人颈部血管斑块大小与冠状动脉狭窄程度的相关性。结果急性冠脉综合征非糖尿病病人及急性冠脉综合征合并糖尿病病人冠状动脉狭窄75%时颈部血管斑块大小与冠状动脉狭窄相关性不明显;急性冠脉综合征合并糖尿病病人冠状动脉狭窄≤75%时颈部血管斑块大小与冠状动脉狭窄程度呈正相关(r=0.77,P0.000 1)。结论急性冠脉综合征早期颈部血管斑块大小可间接反映冠状动脉狭窄程度。 相似文献
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目的 评价多层螺旋计算机断层扫描(computed tomography,CT)血管造影(multislice computed tomography angiography,MSCTA)检测冠状动脉易损斑块的可靠性,建立急性冠脉综合征积分(score system of acute coronary syndromes,SACS),用于评估冠状动脉粥样硬化性心脏病(冠心病)患者危险分层.方法 研究20例非急性冠脉综合征及41例急性冠脉综合征且冠状动脉MSCTA发现斑块的患者,比较两组斑块CT值、重构指数(RI)等指标,进而构建急性冠脉综合征发病风险预测模型.结果 两组病变血管99支,可分析斑块1 17个,非急性冠脉综合征组36个,以钙化斑块为主(88.9%,32/36);急性冠脉综合征组81个,以脂质斑块为主(37.0%,30/81).两组正性重构比例比较,差异有统计学意义(61.1% vs.32.1%,P<0.01);负性重构比例比较,差异有统计学意义(25.0%vs.19.8%,P<0.01).由RI建立SACS,所得模型为:SACS=0.003PA+2.255RI-4.22,预测准确率为76.9%(P<0.01),受试者工作曲线下面积为0.815(P<0.01).结论 急性冠脉综合征患者冠状动脉斑块多为脂质斑块,以正性重构为主,SACS对急性冠脉综合征发病具有较高的预测价值,有助于临床指导冠心病危险分层及早期干预. 相似文献
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不稳定斑块破裂血栓形成是急性冠脉综合征的主要发病机制,设计成功的斑块破裂血栓形成的动物模型,有助于今后更深入地研究急性冠脉综合征,本文就国外学者在这方面的研究作一综述. 相似文献
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妊娠相关血浆蛋白-A最先是从孕妇血清中分离出来的一种与妊娠相关联的大分子糖蛋白.近年来,发现妊娠相关血浆蛋白-A和急性冠脉综合征关系密切,是急性冠脉综合征新的标记物.在不稳定的粥样斑块中大量表达,代表斑块的稳定性,在急性冠脉综合征患者早期诊断、预后评估及危险分层中发挥重要作用. 相似文献
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不稳定斑块破裂血栓形成的动物模型概况 总被引:1,自引:0,他引:1
不稳定斑块破裂血栓形成是急性冠脉综合征的主要发病机制,设计成功的斑块破裂血栓形成的动物模型,有助于今后更深入地研究急性冠脉综合征,本文就国外学者在这方面的研究作一综述。 相似文献
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《国际心血管病杂志》2020,(4)
斑块侵蚀与急性冠脉综合征有密切关系,可引发心室颤动和心源性猝死,近年来,随着腔内影像学的发展,斑块侵蚀越来越受到重视。研究显示,斑块侵蚀导致的急性冠脉综合征的临床特点、斑块的形态特征和病理机制等方面均与斑块破裂存在明显差异。深入研究斑块侵蚀的病理机制,对进一步指导临床实施个体化精准治疗有重要意义。 相似文献
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急性冠脉综合征(ACS)是指冠脉粥样硬化斑块破裂或侵蚀,继发完全或不完全性血栓形成为病理基础的临床综合征,包括不稳定型心绞痛(UA)、非ST段抬高的心肌梗死(NSTEMI)和ST段抬高的心肌梗死(STEMI)。ACS是复杂的急性心肌缺血综合征,其病理生理学变化以冠脉斑块裂隙、糜烂和(或)破裂为基础,使斑块内高度致血栓形成物质暴露于血流中, 相似文献
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Hitsumoto T Takahashi M Iizuka T Shirai K 《Journal of atherosclerosis and thrombosis》2007,14(6):294-302
AIM: Recent clinical studies using intra-vascular ultrasound have clarified that coronary artery plaque already exists in subjects with normal coronary artery which is diagnosed by coronary angiography; furthermore, culprit lesion on acute coronary syndrome often occurs in mild to moderate angiographical stenotic lesion. The aim of this study is to clarify relationship between metabolic syndrome and early stage coronary atherosclerosis using a 3-dimensional intra-vascular ultrasound.METHODS: 70 subjects with normal coronary artery diagnosed by coronary angiography were enrolled. Proxymal range of left anterior descending coronary artery was observed by intra-vascular ultrasound using autopullback methods.RESULTS: Subjects with metabolic syndrome had significantly high percent plaque volume (31 +/- 8% vs 21 +/- 8%, p < 0.0001) and frequently detected abnormal plaque quality such as eccentricity, calcification and lipid pool into plaque than those without metabolic syndrome. Multivariate analysis showed that serum adiponectin concentration was the most strongest variable for percent plaque volume (t value= - 3.0, p < 0.01). On the other hand, subjects with hypoadiponectinemia were detected high incidence of mild calcification into plaque.CONCLUSION: Metabolic syndrome needs to be detected and treated as early as possible. Furthermore, measurement of serum adiponectin concentration and appropriate treatment would prevent acute coronary syndrome. 相似文献
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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。 相似文献
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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。 相似文献
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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。 相似文献
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探讨不稳定斑块形成、斑块破裂及急性冠状动脉综合征发生的机制对临床防治急性冠状动脉综合征有重要的指导意义。研究证实血凝素样氧化低密度脂蛋白受体-1作为氧化低密度脂蛋白的主要受体,介导了氧化低密度脂蛋白诱导的细胞凋亡、炎症反应、基质降解及血栓形成等过程,血凝素样氧化低密度脂蛋白受体-1表达增加会引起纤维帽变薄、脂核增大、斑块不稳定及破裂,最终导致急性冠状动脉综合征的发生。 相似文献
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Waltenberger J 《Herz》2001,26(Z1):2-8
BACKGROUND: The acute coronary syndrome is the manifestation of a plaque rupture in a coronary artery, which can lead to intermittent or prolonged regional myocardial ischemia. In such a situation, the underlying atherosclerotic lesion is a complex one. Moreover, the mechanisms leading to the instability of an atherosclerotic plaque are complex themselves. This makes it problematic to systematically analyze the nature of the acute coronary syndrome. Moreover, no animal model is available to study this process. PATHOMORPHOLOGICAL AND CLINICAL STUDIES: Substantial insights into the basis of the acute coronary syndrome have been gathered by pathomorphological analyses, which have helped to identify a number of criteria describing a vulnerable plaque. Clinical studies have helped to identify the thrombotic component as an important aspect of the clinical manifestation of the acute coronary syndrome. Based on such data, well-defined antithrombotic strategies play an important role in today's therapy of the acute coronary syndrome. TRIGGERING MECHANISMS: Concerning the triggering mechanisms for an acute coronary syndrome, there is a number of suspected processes, the most important of which is local inflammation of the coronary plaque. Inflammatory processes have recently been recognized as important stimulators of vascular modeling during atherogenesis. These inflammatory mechanisms involve a number of different cytokines, cells of the immune system and other components of the immune systems such as the complement cascade. C-reactive protein may even be a link between systemic and local inflammatory processes, because it has been shown to be systemically elevated in patients with unstable angina, and--most recently--has been shown to be involved in the initiation and progression of early atherosclerotic lesions. Local inflammation of the atherosclerotic plaques induces the expression of a number of growth factors and other potent molecules that contribute to vascular remodeling. These substances are acting on smooth muscle cells, fibroblasts as well as on the extracellular matrix and include growth factors, matrixmetalloproteinases and tissue inhibitors of metalloproteinase. Another component of potential significance within the unstable plaque is the process called plaque-angiogenesis. Plaque-angiogenesis occurs within complicated atherosclerotic plaques, the process of angiogenesis leads to destabilization of the extracellular matrix and, moreover, newly formed capillaries are more likely to rupture and may therefore be an important trigger of plaque rupture and of the acute coronary syndrome. THERAPEUTIC APPROACHES: A number of molecular strategies including inhibition of matrix metalloproteinasis or inhibitors of angiogenesis may turn out to stabilize the vulnerable plaque. Until these therapeutic concepts may be used in the clinic, our therapeutic repertoire will mostly consist of antithrombotic and entire antiinflammatory approaches. 相似文献
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冠状动脉粥样硬化斑块破裂的临床危险因素分析 总被引:9,自引:0,他引:9
目的 研究临床危险因素与冠状动脉粥样硬化斑块破裂的关系 ,探讨斑块破裂的危险因素。方法 选取 1992~ 1998年间的尸检病例 ,急性心肌梗死 (AMI) 2 0例 ,不稳定心绞痛 (UA) 10例 ,稳定心绞痛 (SA) 12例 ,对所有冠状动脉连续取材制片 ,常规及免疫组化染色 ,光镜观察斑块破裂的形态改变及血栓伴随情况 ,并调查 8个相应的临床危险因素。结果 8个危险因素中 ,血浆甘油三酯水平与斑块破裂有关 (P <0 .0 5 )。结论 高血浆甘油三酯是国人急性冠状动脉综合征患者斑块破裂的一个重要危险因素。 相似文献
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HMG Co-A reductase inhibitors(statins) have been shown, in three large randomized trials, to decrease adverse cardiac events in patients with clinically evident coronary artery disease. All of these trials have excluded patients with an acute coronary syndrome within the three months prior to enrollment. Statin therapy is thought to stabilize coronary plaque and decrease the risk of plaque rupture. Statins have been shown to quickly reduce levels of LDL-C in addition to altering systemic inflammatory responses, improving endothelial function, and reducing platelet aggregation and activation. These mechanisms are potentially beneficial in the setting of acute coronary syndromes, a time of profound plaque instability. There is a growing body of evidence supporting the early initiation of statin therapy in the setting of acute coronary syndromes. This paper reviews the available data from randomized-controlled trials and observational studies evaluating the effect of early statin initiation during, or soon following, an acute coronary syndrome. 相似文献