女性冠状动脉微血管功能障碍的研究进展

胸痛发生于男性多表现为心外膜下冠脉闭塞性冠心病(CAD)，女性则不出现明显冠脉闭塞，而是以冠脉微血管功能障碍(例如较冠脉小的阻力血管功能异常)为主要表现。这类患者常年因反复胸痛发作导致入院次数明显增多且多次进行心导管手术，是临床上仍无法彻底解决的难题之一。最近的研究提示这种冠脉微血管功能障碍可能与微循环的分布异常关系密切。现将女性无冠脉闭塞性胸痛的微血管功能障碍研究的最新进展综述如下。     

vW因子与糖尿病微血管并发症

ｖ Ｗ因子 (ｖｏｎＷｉｌｌｅｂｒａｎｄ因子 ,ｖＷＦ)是内皮细胞和巨核细胞合成的一种重要的内皮下粘附蛋白 ,参与血小板粘附、聚集 ,是血小板粘附于受损微血管的一个重要因子 ,在微血管内皮细胞受到刺激时释放至血浆 ,其水平升高已经成为微血管内皮损伤标志之一。糖尿病微血管并发症的发病机理尚不完全清楚 ,目前认为微血栓形成在微血管病变的形成和发展中起着重要的作用 ,而导致微血栓形成的主要机制为微血管内皮细胞的损伤、血小板被激活、凝血纤溶系统的异常和血液流变学的改变[1] 。ｖＷＦ在糖尿病微血管并发症发生中起着重要作用。本…     

冠状动脉微血管疾病研究进展

冠状动脉微血管疾病(CMVD)是指冠状动脉前小动脉和小动脉的结构和(或)功能在各种致病因素作用下发生异常,导致劳力性心绞痛或客观性心肌缺血的临床综合征。CMVD的发病机制尚未完全明确,但是内皮功能障碍、炎症反应和异常伤害感受都可能是其发病机制。CMVD的患病率逐年升高,且女性多于男性,尤其多见于绝经后女性,提示了雌激素缺乏可能为CMVD的潜在致病因素,也将性别视为导致微血管功能障碍的重要影响因素。因此,雌激素替代治疗可能成为CMVD治疗的新靶点。     

脊柱动物胃壁微血管构筑的研究进展

微循环广泛分布于动物体的器官、组织中,是心血管系统在机体内真正发挥重要功能的部位。研究不同器官微血管的构筑特点是微循环研究的重要内容,本文综述了近年来脊柱动物胃壁微血管构筑的研究进展情况,以其为微循环形态学的研究提供较详实的资料。     

冠脉生理学检测技术发展2021年研究进展

心血管疾病是危害人类生命健康最严重的疾病之一,中国每5人中就有2人死于心血管疾病。心肌缺血是重要的心血管疾病之一。心肌血流储备分数(fractional flow reserve, FFR)用于量化心外膜下冠状动脉狭窄是否产生心肌缺血;微血管阻力指数(index of microcirculatory resistance, IMR)是定量评价冠脉微循环状态的有创指标。传统FFR和IMR测量临床上依靠导丝,在最大充血态下进行介入测量,临床上辅助心肌缺血的诊断。基于冠脉造影的caFFR和caIMR(coronary angiography-derived FFR and IMR)无需介入操作、无需血管扩张药物、无禁忌症限制,可以快速同步计算FFR和IMR,进而辅助冠脉介入手术的诊疗。本文总结了近年来基于冠脉造影的caFFR和caIMR以及其他冠脉生理学检测技术的研究进展。进一步开展基于造影的FFR和IMR组合研究,从宏观到微观开展冠脉功能学研究具有重要的临床价值。     

血管活性肠肽对类风湿关节炎作用的研究进展

类风湿性关节炎(rheumatoid arthritis,RA)是一种病因未明的慢性系统性自身免疫病,以多关节的慢性、对称性炎症及渐进性骨和软骨破坏为主要特征,最终可导致不可逆的关节畸形和功能损伤, 是严重威胁人类健康的疾病之一.     

微血管性心绞痛研究进展

微血管性心绞痛（X综合征）临床上并非少见，近年来认为血管内皮及内皮依赖性舒张功能（EDVR）失调致冠脉储备功能障碍，引起局部腺苷堆积，内皮损伤可引起血小板聚集、粘附启动凝血系统形成微血栓，微血管受损的不平衡性引起“窃流现象”，以及氧自由基的损害等均导致心绞痛，而冠脉造影正常。检测EDVR使其功能诊断成为可能，为防治奠定新的理论基础。     

高血压血液微循环功能障碍及其机制研究进展

外周循环阻力增加是原发性高血压发生发展的重要环节,血液微循环中的小动脉侧是阻力血管的主要组成部分,血液微循环功能障碍与高血压密切相关。在高血压中,血液微循环功能的变化主要与微血管数量和微血管结构有关。内皮细胞凋亡,或继发于血管内皮一氧化氮(NO)释放不足导致的血管生成不足,可能造成微血管稀疏,微血管稀疏既作为高血压早期的危险因素出现,也随着高血压进程而加重;血压增加引起小动脉血管壁与官腔比(h/R)增加,可能会放大高血压刺激因素的效果,形成恶性循环,并影响大动脉的结构改变。     

肝癌微血管密度、微血管面积和Piezo1的表达与微血管侵犯的相关性

目的:探讨肝癌组织中微血管密度(microvascular density,MVD)、微血管面积(microvascular area,MVA)以及Piezo1的表达水平预测肝癌微血管侵犯(microvascular invasion,MVI)的临床价值.方法:应用免疫组织化学方法检测38例病理证实为肝癌患者的肝癌组织的CD34以及Piezo1的表达情况,计算基于CD34染色的MVD和MVA,分析MVI与MVD,MVA以及Piezo1因子的表达水平的相关性.结果:38例肝癌中,13例有微血管侵犯,定义MVI(+)组,25例无微血管侵犯,定义MVI(?)组.MVI(+)组的MVA及MVD均高于MVI(?)组,两组间差异有统计学意义(P=0.007,P=0.011).MVD和MVA联合预测MVI的敏感性和特异性为100％和64％,较单一指标效能高.Piezo1在肝癌MVI(+)组阳性率高于MVI(?)组,两组间差异有统计学意义(P=0.032).结论:MVD,MVA以及Piezo1的表达水平均与肝癌MVI具有一定的相关性,可以作为辅助诊断微血管侵犯的指标,Piezo1可以作为潜在的限制MVI的治疗靶点.     

瘦素与2型糖尿病患者微血管病变关系的探讨

目的 :探讨瘦素与 2型糖尿病患者微血管病变的关系。方法 :对照组、糖尿病无微血管病变组及糖尿病微血管病变组各 30例 ,其中糖尿病微血管病变组包括糖尿病肾病 2 5例 ,糖尿病视网膜病变 12例 ,同时合并DN与DR者 7例。检测血清瘦素、胰岛素及血糖浓度 ,分析瘦素水平与其它指标的相关性。结果 :对照组、无微血管病变组及微血管病变组血清瘦素浓度分别为 (7 2 0± 2 11) μl/L、(7 95± 3 78) μg/L及 (10 2 6± 4 37)μg/L ,糖尿病微血管病变组显著高于无微血管病变组 (t=2 .18,P <0 0 5 )及对照组 (t=2 .71,P <0 0 1) ,而后两者间无显著差异 ;瘦素浓度与体重指数、胰岛素呈正相关 (r =0 .2 9,P <0 0 5 ;r =0 .34,P <0 .0 1)。结论 :糖尿病微血管病变组血清瘦素浓度升高 ,瘦素与糖尿病微血管病变的发病密切相关。     

Microvascular heart involvement in systemic autoimmune diseases: The purinergic pathway and therapeutic insights from the biology of the diseases

Heart involvement – often asymptomatic – is largely underestimated in patients with systemic autoimmune diseases (SADs). Cardiovascular events are more frequent in patients with SADs compared to the general population, owing to the consequences of inflammation and autoimmunity and to the high prevalence of traditional risk factors. Coronary microvascular disease (CMD) is a form of cardiac involvement that is increasingly recognised yet still largely neglected. CMD, the incapacity of the coronary microvascular tree to dilate when myocardial oxygen demand increases or when there is a microvascular spasm (or subclinical myocarditis), is increasingly reported because of the widespread use of new cardiac imaging tools, even in a subclinical phase. The assessment of myocardial coronary flow reserve (CFR) emerged as the most effective clinical tool to detect microvascular damage. The potential causes of microvascular damage, molecular and cellular inflammation along with a pathological CD39-CD73 axis, need always to be considered because data show that they play a role in the occurrence of acute coronary syndromes, heart failure and arrhythmias, even in the early asymptomatic stage. Data suggest that controlling disease activity by means of methotrexate, biologic drugs, antimalarial medications, statins and aspirin, according to indication, might reduce the cardiovascular risk related to macrovascular and microvascular damage in most patients with SADs, provided that they are used early and timely to control diseases. The need of new biomarkers and a careful assessment of myocardial CFR emerged as the most effective clinical tool to detect microvascular damage.     

Nailfold avascular score and coronary microvascular dysfunction in systemic sclerosis: A newsworthy association

Background and aims

We aimed to assess the relationship between nailfold videocapillaroscopy (NVC) abnormalities and coronary flow reserve (CFR), a marker of coronary microvascular dysfunction (CMD) in patients with systemic sclerosis (SSc).

Increase in systemic vascular resistance during acute mental stress in patients with rheumatoid arthritis with high-grade systemic inflammation

Patients with rheumatoid arthritis are at increased risk for myocardial infarction. It has been hypothesized that mental stress-induced cardiovascular reactions may play a role in the triggering of myocardial infarction. Cardiovascular activity was measured during rest, stress, and recovery in rheumatoid arthritis patients with high systemic inflammation (C-reactive protein >8 mg/l), rheumatoid arthritis patients with low systemic inflammation (C-reactive protein 相似文献   

Cardiovascular involvement in systemic autoimmune diseases

Autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), primary antiphospholipid syndrome (APS), systemic sclerosis and systemic vasculitis, affect a large number of people in whom one of the leading causes of morbidity and mortality is cardiovascular disease. Cardiovascular disease is associated with the development of accelerated atherosclerosis. It seems to occur at a younger age than in the general population, is often asymptomatic and, in addition to traditional risk factors, also involves specific risk factors as chronic inflammation, the duration and activity of the autoimmune disease, and immunosuppressive therapy. The early phases of cardiovascular involvement in patients with autoimmune diseases may be clinically silent, with only a microcirculation disorder present. There are various means of detecting morphological cardiac damage: coronary angiography remains the gold standard for diagnosing coronary stenosis, but new, non invasive and more reliable methods have been introduced into clinical practice in order to detect subclinical microcirculation abnormalities.     

Inflammation: a pivotal link between autoimmune diseases and atherosclerosis

Premature coronary heart disease has emerged as a major cause of morbidity and mortality in systemic autoimmune diseases. Recent epidemiologic and pathogenesis studies have suggested a great deal in common between the pathogenesis of prototypic autoimmune disease such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and that of atherosclerosis. Some of the most remarkable data in support of a link between autoimmunity and atherosclerosis comes from epidemiological studies of patients with autoimmune disorders (RA and SLE). Many epidemiologic observations have linked systemic inflammation with the cardiovascular events in autoimmune disease such as RA and SLE. Inflammation is increasingly being considered central to the pathogenesis of atherosclerosis and an important risk factor for vascular disease. Systemic inflammation may be regarded as accelerating the atherosclerotic process. Systemic levels of soluble inflammatory mediators such as C-reactive protein (CRP) have been associated with cardiovascular risk in the general population. CRP, or more specifically high sensitivity-hsCRP, is a marker of systemic inflammation that has been identified as a valid biomarker of cardiovascular risk. Furthermore, the immunomodulatory and anti-inflammatory actions of statins may affect their utility in the context of chronic inflammatory autoimmune disease. Thus, effective control or dampening of inflammation, with such agents, should be included in the therapeutic armamentarium of autoimmune diseases with the aim of protecting against cardiovascular disease.     

Matrix Metalloproteinase-9 and Autoimmune Diseases

Matrix metalloproteinases (also named matrixin or MMPs) are a major group of enzymes that regulate cell-matrix composition by using zinc for their proteolytic activities. They are essential for various normal biological processes such as embryonic development, morphogenesis, reproduction tissue resorption, and remodeling. Metalloproteinases also play a role in pathological processes including inflammation, arthritis, cardiovascular diseases, pulmonary diseases and cancer. Herein we review the involvement of MMP-9 in a variety of autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, systemic sclerosis, rheumatoid arthritis, multiple sclerosis, polymyositis and atherosclerosis. MMP-9 plays either a primary or secondary role in each one of those autoimmune diseases by its up or down-regulation. It is not expressed constantly but rather is induced or suppressed by many regulating molecules. This feature of MMP-9 along with its involvement in disease pathogenesis turns it into a target for therapy of autoimmune diseases.     

Autoimmune Disease During Pregnancy and the Microchimerism Legacy of Pregnancy

Pregnancy has both short-term effects and long-term consequences on the maternal immune system. For women who have an autoimmune disease and subsequently become pregnant, pregnancy can induce amelioration of the mother's disease, such as in rheumatoid arthritis, while exacerbating or having no effect on other autoimmune diseases like systemic lupus erythematosus. That pregnancy also leaves a long-term legacy has recently become apparent by the discovery that bi-directional cell trafficking results in persistence of fetal cells in the mother and of maternal cells in her offspring for decades after birth. The long-term persistence of a small number of cells (or DNA) from a genetically disparate individual is referred to as microchimerism. While microchimerism is common in healthy individuals and is likely to have health benefits, microchimerism has been implicated in some autoimmune diseases such as systemic sclerosis. In this paper, we will first discuss short-term effects of pregnancy on women with autoimmune disease. Pregnancy-associated changes will be reviewed for selected autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus and autoimmune thyroid disease. The pregnancy-induced amelioration of rheumatoid arthritis presents a window of opportunity for insights into both immunological mechanisms of fetal-maternal tolerance and pathogenic mechanisms in autoimmunity. A mechanistic hypothesis for the pregnancy-induced amelioration of rheumatoid arthritis will be described. We will then discuss the legacy of maternal-fetal cell transfer from the perspective of autoimmune diseases. Fetal and maternal microchimerism will be reviewed with a focus on systemic sclerosis (scleroderma), autoimmune thyroid disease, neonatal lupus and type I diabetes mellitus.     

Obstructive sleep apnea is associated with coronary microvascular dysfunction: A systematic review from a clinical perspective

There is now increasing evidence demonstrating that obstructive sleep apnea (OSA) contributes to microvascular disorder. However, whether OSA is associated with impaired coronary flow reserve is still unclear. Therefore, we conducted this systematic review and meta‐analysis to summarize current evidence. In a systematic review, PubMed, Embase, the Cochrane Library and Web of Science were searched; five observational studies fulfilled the selection criteria and were included in this study. Data were extracted from selected studies and meta‐analysis was performed using random‐effects modelling. In all, 829 OSA patients and 507 non‐OSA subjects were included and assessed for coronary flow reserve (CFR), the clinical indicator of coronary microvascular dysfunction (CMD). For all studies, OSA was significantly associated with reduced CFR. The pooled weighted mean difference (WMD) of CFR was ?0.78 (95% confidence interval [CI] ?1.25 to ?0.32, p ＜ 0.001, I² = 84.4%). The difference in the apnea–hypopnea index (AHI) between studies can explain 89% of heterogeneity (coef = ?0.05, 95% CI ?0.12 to 0.02, p = .078) in a meta‐regression, indicating the CFR tended to negatively correlate with severity of OSA. The Egger regression test did not show statistical significance (p = .49). In conclusion, there are plausible biological mechanisms linking OSA and CMD, and the preponderance of evidence from this systematic review suggests that OSA, especially severe OSA, is associated with reduced CFR. Future studies are warranted to further delineate the exact role of OSA in CMD occurrence and development in a prospective setting.     

Atherosclerosis in Autoimmune Rheumatic Diseases—Mechanisms and Clinical Findings

Atherosclerosis is one of the major entities leading to morbidity and mortality in the western world. It is known now that atherosclerosis cannot be explained merely by the presence of the Framingham traditional risk factors and that autoimmunity takes a significant role in its pathogenesis. It is also known that individuals with autoimmune diseases demonstrate increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. The mechanisms for the assumed accelerated atherosclerosis in diseases such as systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, and systemic sclerosis include the classical risk factors, but may also be due to chronic inflammatory processes and immune dysregulation. Autoantibodies, autoantigens, pro-inflammatory cytokines, and infectious agents play a role in that process. Involvement of autoimmunity in the pathogenesis of accelerated atherosclerosis in rheumatic diseases and the common pathway that leads to this condition may lead to significant change in prevention of treatment.