人类软骨糖蛋白-39在冠状动脉粥样硬化性心脏病中的研究进展

冠状动脉粥样硬化性心脏病,指由于冠状动脉粥样硬化使管腔狭窄、痉挛或阻塞导致心肌缺血、缺氧或坏死而引起的心脏病。其病因为动脉粥样硬化,发病机制亦即动脉粥样硬化的发展过程。近年来研究证实动脉粥样硬化是一种慢性炎症疾病,炎症被认为是动脉粥样硬化的核心发病机制,参与了动脉粥样硬化发生、发展以及恶化的所有过程。人类软骨糖蛋白-39又名YKL-40,是一种新的炎症标记物,通过促进血管平滑肌细胞迁移和增殖、诱导新生血管生成、促进细胞趋化、黏附、迁移和调控细胞外基质重建等来发挥作用。血浆高水平的YKL-40与冠状动脉粥样硬化性心脏病的发病相关,而且血浆YKL-40水平的增加与冠状动脉粥样硬化病变进展独立相关,甚至在心肌梗死患者中有更高的YKL-40的表达。     

白细胞介素-6、白细胞介素-1O与冠心病关系的研究进展

随着分子生物学技术的发展和临床应用，炎症在冠心病（CHD）发病机制中的作用目益引起重视，而炎性因子在其中起到了不可忽视的作用。冠心病的病理基础是冠状动脉粥样硬化，大量的研究表明动脉粥样硬化（AS）是一种慢性炎症性疾病，炎症和感染过程参与了AS及其并发症的发生和发展，而炎性因子在机体的免疫应答、炎症反应等方面起着关键作用，炎性因子介导的系统或局部的炎症反应导致AS斑块的形成。     

白细胞介素-6、白细胞介素-10与冠心病关系的研究进展

随着分子生物学技术的发展和临床应用,炎症在冠心病(CHD)发病机制中的作用日益引起重视.而炎性因子在其中起到了不可忽视的作用.冠心病的病理基础是冠状动脉粥样硬化,大量的研究表明动脉粥样硬化(AS)是一种慢性炎症性疾病,炎症和感染过程参与了AS及其并发症的发生和发展,而炎性因子在机体的免疫应答、炎症反应等方面起着关键作用,炎性因子介导的系统或局部的炎症反应导致AS斑块的形成.近年来促炎与抗炎之间的平衡失调导致粥样斑块病变的假说引起了人们的注意.白细胞介素-6(IL-6)在炎症反应中起核心调节作用,是炎症免疫反应的重要介质,其与疾病的活动性相关,是冠心病的一个重要的危险因子,参与动脉粥样硬化的形成和发展.白细胞介素-10(IL-10)是近年来研究的最为广泛的一种抗炎因子之一,其有抑制粥样斑块形成、稳定斑块的作用.本文就与冠心病关系较为密切的细胞因子IL-6和IL-10的研究进展作一综述.     

外泌体在冠心病治疗中应用的研究新进展

正冠状动脉粥样硬化性心脏病(CAHD,冠心病)是冠状动脉(冠脉)血管发生动脉粥样硬化(AS)而引起血管狭窄或阻塞,造成心肌缺血、缺氧或坏死而导致的心脏病,是冠脉疾病中的一种常见疾病。全面了解其发生发展的病理生理学机制,对于改善冠心病患者的预后至关重要[1]。外泌体是细胞外囊泡的一个亚群,其内容物的变化可能提示生理或病理变化,被临床诊断学广泛视为关键生物标志物。本文旨在从外泌体的发生、分泌和摄取为出发点,就其在冠心病的诊断和治疗等方面的应用进行综述。     

脂联素在动脉粥样硬化中的抗炎性作用

脂联素是新近发现的一种由脂肪组织特异性分泌的脂肪因子,具有增加胰岛素敏感性、抗炎、抗动脉粥样硬化等作用,脂联素浓度与诸多炎症性疾病,特别是冠状动脉性心脏病(冠心病)进程密切相关。通过药物干预提高血浆脂联素浓度可能成为一种上述疾病的新的治疗方法。     

冠心病诊断和治疗进展

<正>冠心病即冠状动脉粥样硬化性心脏病,是指冠状动脉发生动脉粥样硬化病变而引起血管腔狭窄或阻塞,造成心肌缺血、缺氧或坏死而导致的心脏病。流行病学资料显示,心血管疾病位居全球因病死亡患者死因首位,全球每年约有1 700万人死于冠心病,我国是冠心病发病率和病死率上升较快的国家之一,近十年来,其发病率男性增加了42.2%,女性增加了12.5%。因此,对冠心病的诊断与治疗已成为临     

脂联素在动脉粥样硬化中的抗炎性作用

脂联素是新近发现的一种由脂肪组织特异性分泌的脂肪因子,具有增加胰岛素敏感性、抗炎、抗动脉粥样硬化等作用,脂联素浓度与诸多炎症性疾病,特别是冠状动脉性心脏病(冠心病)进程密切相关.通过药物干预提高血浆脂联素浓度可能成为一种上述疾病的新的治疗方法 .     

老年人冠心病无症状心肌缺血诊断体会

冠状动脉粥样硬化性心脏病指冠状动脉硬化使血管腔阻塞导致心肌缺血缺氧而引起的心脏病，又称为缺血性心脏病，冠心病是动脉粥样硬化导致器官病变的最常见类型，也是严重危害人们健康的常见病，本病多发生在40岁以后，男性多于女性，脑力劳动者较多见，本病发病与患者年龄、职业、体重、饮食习惯，遗传等有密切关系，高血脂、高血压、糖尿病、患者并发冠心病发病机会最多，而无症状心肌缺血是冠心病恶性事件发生的危险因素，[第一段]     

脂多糖对动脉粥样硬化血管内皮细胞及其信号转导通路的影响

细菌脂多糖通过激活血管内皮细胞,引起相关细胞因子的合成和释放,导致动脉粥样硬化的发生。而脂多糖在血管内皮细胞的跨膜信号转导是引起细胞效应的关键。本文着重综述脂多糖对血管内皮细胞的影响、脂多糖与动脉粥样硬化的关系、脂多糖介导的信号转导机制及其与动脉粥样硬化的关系。为进一步明确动脉粥样硬化炎症发病的分子机制,并为开发具有明确治疗动脉粥样硬化的药物提供新的思路。     

迈进动脉粥样硬化抗炎治疗的新时代

尽管他汀类药物能显著降低低密度脂蛋白胆固醇浓度,从而显著减少心血管事件,但冠状动脉粥样硬化性心脏病(冠心病)患者仍存在其他重要的残余心血管风险,例如炎症[1]。炎症在冠心病的发生、发展和表现中起着关键作用,因此医学界一直在艰辛探索将抗炎治疗在临床上应用于动脉粥样硬化性患者[2-3]。     

他汀类药物在急性冠状动脉综合征中的抗炎作用

急性冠状动脉综合征是常见的冠状动脉粥样硬化性心脏病的急症,炎症在动脉粥样硬化过程中起重要作用。3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂他汀类药物现已广泛应用于冠心病的一级、二级预防,越来越多的证据显示他汀类药物具有显著抗炎作用。     

黏附分子细胞间黏附分子-1/E-选择素与冠心病

冠心病是一种高发病率和高病死率的疾病,炎症反应在冠状动脉粥样硬化斑块的形成中起着重要作用。活化的血管内皮细胞分泌的细胞黏附分子,如细胞间黏附分子-1和E-选择素等,它们介导内皮细胞与白细胞、血小板间的起始黏附,促进血液循环中白细胞、血小板黏附于血管内皮,引起炎症反应、血栓形成等,在动脉粥样硬化和冠心病的发生、发展中起重要作用。     

冠心病靶向抗炎疗法的研究新进展

冠心病是威胁我国城乡居民健康的首要疾病之一。近来研究显示,慢性炎症是动脉粥样硬化诱导和发展的核心致病机制,炎症反应的各个通路成为冠心病治疗的靶点。但目前冠心病二级预防尚未推荐靶向抗炎药物。2017年欧洲心脏病学会年会(ESC 2017)公布的CANTOS研究证实,康纳单抗通过抗炎显著降低目标人群心血管病风险。这一里程碑意义的研究揭示了在传统的降脂、抗栓治疗时代后,抗炎疗法这一冠心病治疗的新篇章。近年来,各类冠心病靶向抗炎药物的研究进展迅速,现就冠心病的靶向抗炎疗法的研究进展作一综述。     

Role of IL-37 in Cardiovascular Disease Inflammation

Inflammation is closely related to the pathogenesis and prognosis of cardiovascular disease (CVD). Interleukin-37 (IL-37), an anti-inflammatory IL-1 family cytokine, shifts cytokine expression from pro- to anti-inflammation via regulation of macrophage polarization and lipid metabolism. In macrophages, IL-37 functions through both intracellular and extracellular pathways to regulate the activity of NF-kB and PTEN as well as the expression of cytokines, including IL-1β, IL-6, and IL-10. Moreover, IL-37 levels are increased in the serum of patients with heart failure, atherosclerosis, and acute coronary syndrome with no evidence of anti-inflammatory effects. However, transgenic overexpression of IL-37 improves cardiac infarct and attenuates atherosclerosis plaque expansion. Hence, it is worthwhile to investigate the precise mechanism and role of IL-37 in the pathogenesis of CVD, which may provide deeper understanding of the inflammatory response in this context. This review summarizes the regulatory role of IL-37 in systematic inflammation induced by CVD and highlights recent advancements in the clinical application of IL-37 as a therapeutic agent or biomarker for diagnosis of CVD.     

Increased heart rate and atherosclerosis: potential implications of ivabradine therapy

Despite all the therapeutic advances in the field of cardiology, cardiovascular diseases, and in particular coronary artery disease, remain the leading cause of death and disability worldwide, thereby underlining the importance of acquiring new therapeutic options in this field. A reduction in elevated resting heart rate (HR) has long been postulated as a therapeutic approach in the management of cardiovascular disease. An increased HR has been shown to be associated with increased progression of coronary atherosclerosis in animal models and patients. A high HR has also been associated with a greatly increased risk of plaque rupture in patients with coronary atherosclerosis. Endothelial function may be an important link between HR and atherosclerosis. An increased HR has been shown experimentally to cause endothelial dysfunction. Inflammation plays a significant role in the pathogenesis and progression of atherosclerosis. In the literature, there is data that shows an association between HR and circulating markers of vascular inflammation. In addition, HR reduction by pharmacological intervention with ivabradine (a selective HR-lowering agent that acts by inhibiting the pacemaker ionic current If in sinoatrial node cells) reduces the formation of atherosclerotic plaques in animal models of lipid-induced atherosclerosis. The aim of this editorial is to review the possible role of ivabradine on atherosclerosis.     

Ischemic cardiopathy: inflammation markers and the cardiovascular risk

In recent years it has been established that inflammation is a key mechanism in the pathogenesis of atherosclerosis and in coronary artery disease progression. Inflammation is a host response to a wide variety of tissue injuries. A persistent or continually repeated insult will lead to chronic inflammation which may result in tissue destruction and/or loss of normal organ function. Atherosclerosis and other pathologies involving inflammation are associated with increased levels of cytokines, which in turn raise acute-phase proteins levels in blood (acute inflammation markers, i.e. fibrinogen and C-reactive protein). It has been shown recently that concentrations of these proteins are higher in individuals at increased risk of developing cardiac events in the years to come. This is true both in apparently healthy men and women and in ischaemic heart disease patients. CRP is currently the inflammatory marker which appears to have captured the investigators' attention around the globe. In this report we review the current data on the relationship between atherosclerosis and inflammation, with special attention to cytokines and acute phase reactants. The use of acute phase reactants as prognostic risk markers in ischaemic heart disease is also discussed.     

单核细胞/高密度脂蛋白胆固醇比值与冠心病关系研究进展

近年来冠心病发病率和死亡率逐渐增高,冠状动脉粥样硬化（AS）是冠心病的主要原因。AS的基本病理机制为炎症反应,单核细胞在炎症反应中起关键作用。高密度脂蛋白胆固醇（HDL-C）有抗炎、抗氧化、抗血栓等作用,单核细胞/HDL-C比值（MHR）作为新近出现的炎症指标,其方便、容易检测,在预测冠心病短期和长期不良事件中有重要意义。     

Inflammation as a Mechanism and Therapeutic Target in Peripheral Artery Disease

Peripheral artery disease is 1 of 3 major clinical manifestations of atherosclerosis, the other 2 being coronary artery and cerebrovascular disease. Despite progress in surgery, antithrombotic therapy and therapies that modify conventional risk factors (lipid-, blood pressure-, and glucose-lowering interventions), patients with peripheral artery disease have an unacceptably high risk of vascular complications. Additional strategies to reduce this residual risk are needed. The accumulated evidence that inflammation plays an important role in the pathogenesis of atherosclerosis has spurred recent efforts to evaluate anti-inflammatory agents as an additional therapeutic approach for atherothrombosis prevention and treatment. In this review, we examine the evidence supporting the role of inflammation in atherosclerosis, review recent trials of anti-inflammatory approaches to reduce cardiovascular complications, and offer insights into the opportunities for novel anti-inflammatory strategies to reduce the burden of cardiovascular and limb complications in patients with peripheral artery disease.     

Role of blood platelets in coronary artery disease

Over the past decade, research in blood platelet physiology has led to the suggestion that platelets play an important part in the pathogenesis and complications of coronary artery disease. Occlusive intravascular platelet aggregates have been shown to cause ischemic myocardial damage in the experimental animal and to be present in some patients who die suddenly. The interplay between endothelial damage and platelet aggregation has been implicated in the etiology of atherosclerosis. Products released from platelets during aggregation may cause arterial spasm. Patients with overt ischemic heart disease and with the risk factors associated with coronary artery disease have been found to have abnormally reactive platelets.

Clinical studies of drugs that inhibit platelet aggregation have been reported to show a beneficial effect in preventing cardiac deaths or myocardial infarction; other studies have been negative or shown only a trend toward benefit. This report reviews the theoretical and experimental basis for the platelet hypothesis and the current data on the use of antiplatelet drugs in patients with coronary disease.     

炎症与冠心病关系的研究进展

通过综述炎症反应对动脉粥样硬化(AS)的作用及炎症的血清学标志物、抗炎治疗等方面的研究进展,以探讨炎症在AS斑块的发生、演变及破裂过程中的作用.