糖尿病与血管钙化

血管钙化是糖尿病患者的一个常见并发症,包括血管内膜钙化和中膜钙化,呈进展性,是糖尿病患者心血管疾病及全因死亡的预测因子。糖尿病血管钙化是多种促进和抑制钙化的因素参与的细胞介导的主动调节过程,高血糖、胰岛素抵抗、肾脏疾病、炎症、骨相关蛋白表达异常等多种因素与其相关。对于糖尿病血管钙化,目前尚无有效的治疗手段,及时评价和控制血管钙化的危险因素,进行合理的预防性治疗非常重要。     

高龄男性慢性肾脏病患者冠状动脉钙化及影响因素分析

目的：探讨高龄男性慢性肾脏病（CKD）患者冠状动脉钙化的相关因素。方法选取2011年1月至2012年12月于解放军总医院住院治疗的126例高龄（≥80岁）男性非透析CKD3～5期患者,根据肾小球滤过率（GFR）分为A组[30≤GFR＜60ml/（min＆#183;1.73m2）]、B组[15≤GFR＜30ml/（min＆#183;1.73m2）]和C组[GFR＜15 ml/（min＆#183;1.73m2）]。采用多层螺旋计算机断层扫描（MSCT）确定冠状动脉钙化的程度,对比各组患者冠状动脉钙化积分（CACS）变化,分析冠状动脉钙化的相关因素。结果 C组患者心肌梗死、脑梗死的患病率高于A组和B组患者,差异有统计学意义（P＜0.05）。C组与B组和A组比较,血磷明显升高[（1.74±0.56） vs （1.52±0.39） vs （1.38±0.42）mmol/L,P＜0.01或P＜0.05],钙磷乘积增加[（46.32±14.36） vs （40.08±10.21） vs （38.26±13.28）,P＜0.05];冠状动脉钙化积分增加[（438.56±63.22） vs （316.82±77.30） vs （262.50±81.92）,P＜0.01或P＜0.05],差异有统计学意义。Spearman相关分析显示,CACS与患者年龄（r＝0.2218,P＜0.05）、血磷（r＝0.2313,P＜0.05）和钙磷乘积（r＝0.2450,P＜0.05）呈正相关,与体质量指数（r＝-0.1956,P＜0.05）和GFR（r＝-0.4462,P＜0.01）呈负相关。结论高龄男性CKD患者冠状动脉钙化发生率高。年龄、体质量指数、肾功能和钙磷代谢紊乱均与冠状动脉钙化发生相关。     

慢性肾脏病血管钙化相关研究的进展及回顾

慢性肾脏病(CKD)患者的主要死亡风险来自于心血管疾病(CVD),而血管钙化(VC)是CVD的重要危险因素,也是CKD的常见并发症。因此全面掌握CKD患者血管钙化的分类、发病机制、诊断及治疗显得尤为重要。本文将从上述方面介绍CKD患者血管钙化相关研究的进展及回顾。     

慢性肾脏病血管钙化机制的研究进展

慢性肾脏病（chronic kidney disease, CKD）是世界公认的健康问题,我国CKD的患病率约为10.8%,并且CKD的死亡率也很高。心血管疾病（cardiovascular disease, CVD）是CKD最常见的死亡原因,而血管钙化（vascular calcification, VC)是导致CVD的重要危险因素。因此本文对CKD血管钙化的流行病学现状、病理学特点、危险因素、发病机制等方面进行综述,希望能为血管钙化的防治提供新的思路。     

冠状动脉梗死相关病变钙化与临床表现的关系

目的:探讨冠状动脉梗死相关病变钙化与临床表现的关系。方法:将经血管内超声(IVUS)检查发现有冠状动脉钙化的患者48例分为两组:急性冠状动脉综合征(ACS)组 28 例、稳定型心绞痛(SAP)组 20 例。对两组患者的冠状动脉梗死相关病变钙化进行测量及分析。结果:ACS组患者血管梗死病变处较SAP组患者相对缺乏,钙化两组的最大钙化弧度分别为(85.48±71.52)°,(152.00±103.08)°, P<0.05。ACS组的钙化斑块比例低于SAP组,57.14%∶83.33%,P<0.05;前者偏心斑块多于后者,93.88%∶54.17%, P<0.01;破裂斑块亦多于后者,42.86%∶8.33%,P<0.01。结论:ACS患者血管梗死病变处较SAP患者相对缺乏钙化,这有助于对ACS发病机制的理解,钙化的存在也有助于识别冠状动脉狭窄病变。     

冠状动脉钙化研究进展

冠状动脉钙化越来越受到重视,发现钙化即意味着亚临床动脉粥样硬化的存在,而动脉硬化不一定都有钙化。通常钙化越严重,冠脉管腔狭窄程度也就越高。但有时二者却缺乏很好的相关性。现就冠脉钙化的发生机制,冠脉钙化及积分与冠心病及其严重程度的关系,冠脉钙化检测方法及积分,血管重构在严重的冠脉钙化却没有明显的管腔狭窄中的作用等方面做一综述。     

冠状动脉钙化形成机制与新型评估综述

冠状动脉钙化（coronary artery calcification,CAC）在冠心病患者中普遍存在,严重的钙化病变会增加治疗难度以及并发症的发生,了解CAC的病理生理机制能更好地指导诊疗。冠状动脉钙化分为内膜型和中膜型两种类型,各有相应的形成机制与危险因素,前人已充分论述。过去冠状动脉钙化被认为是一种被动的、与年龄相关的退行性改变,现在更多地被认为是一个主动的、受调控的过程。很少有文献从被动、主动方向论述冠脉钙化形成机制。本文旨在从冠状动脉钙化不同形成过程入手,分析钙化病变的相关遗传因素和调节机制,并且介绍了几种新型潜在的评估钙化的方式,为钙化病变的诊疗提供新思路。     

胎球蛋白A对腹膜透析患者冠状动脉钙化发生起始的影响因素分析

心血管疾病(cardiovascular disease,CVD)是慢性肾脏病(chronic kidney disease,CKD)患者的主要死亡原因.终末期肾病(end-stage renal disease,ESRD)患者由于心血管事件造成的死亡占总死亡原因的50％以上[1].而血管钙化与心血管事件的发生密切相关...     

冠状动脉钙化特征在心血管风险评估中的价值

冠状动脉钙化（CAC）作为亚临床粥样硬化的标记物,可以反映冠状动脉粥样硬化的总体负荷,是对患者进行心血管风险分层和诊疗的重要工具。临床上评估和量化CAC最常用的是Agatston积分,此外,钙化的分布、密度、体积、形态等特征在风险评估及诊疗方面均具有指导意义。本文将从CAC多个特征的临床意义进行总结,为深刻理解CAC在心血管风险评估中的作用提供思路。     

冠状动脉钙化的机制研究进展

冠状动脉钙化在动脉粥样硬化晚期出现,是冠状动脉粥样硬化的标志,也与临床意义上的冠状动脉疾病相关。临床检测到的钙化程度能反映斑块稳定状态,且能预测未来的心血管事件。冠状动脉钙化在病理上始于微钙化,然后生长成较大的钙碎片,最终导致片状沉积,这种演变与斑块的进展同时发生。本综述系统总结了冠状动脉启动钙化的两种细胞机制,并归纳了参与影响钙化进程的调节因素,同时重点讨论脂蛋白(a)和维生素K如何参与调节钙化进程,还总结了现有的特异性药物治疗以及潜在靶点,为防治冠状动脉钙化以及预防心血管事件提供了一定参考价值。     

The combined prognostic significance of alkaline phosphatase and vascular calcification in patients with end-stage kidney disease

Background and aimsLittle is known about the interaction between serum alkaline phosphatase (ALP) and vascular calcification (VC) affecting cardiovascular events (CVE) and mortality in end-stage kidney disease (ESKD) patients. This study investigated the combined effect of ALP and VC on prognosis in ESKD patients starting dialysis.Methods and resultsData from 587 ESKD patients treated at a single center between January 2006 and July 2017 were retrospectively evaluated. VC was assessed by the aortic calcification index (ACI) using abdominal computed tomography. Patients were stratified into four groups according to the median ACI (17.18) and serum ALP value (108.0 U/L) as low ACI-low ALP, low ACI-high ALP, high ACI-low ALP, or high ACI-high ALP. The association between ALP and VC and the composite of CVE and death was analyzed. During a median follow-up of 3.1 years (range, 1.5–5.6 years), 140 patients (23.8%) developed CVE and 130 deaths (22.1%) occurred. In the stratified analysis, patients with high ACI-low ALP had a greater risk of the composite endpoint than patients with low ACI-low ALP (adjusted hazard ratio, 2.09; 95% confidence interval, 1.58–2.60; P = 0.004). Patients with high ACI-high ALP had the greatest risk (adjusted hazard ratio, 2.25; 95% confidence interval, 1.77–2.72; P = 0.001). The interaction between ACI and ALP on CVE and mortality was statistically significant (P < 0.05).ConclusionsThe combined effect of VC and higher ALP was associated with a greater risk of CVE and death, and high serum ALP amplified the risk associated with VC in ESKD patients starting dialysis.     

终末期肾病心血管钙化与脉搏波速度

终末期肾病患者的生存质量较低,病死率较高,其中重要原因与心血管钙化及其导致的心血管并发症有关。本文主要阐述终末期肾病患者的心血管钙化的分类、机制及危险因素、促进及抑制因子。并对心血管钙化的预测指标脉搏波速度作一简单介绍。以便对此类患者采取措施提早预测和预防心血管钙化的发生,达到提高其生存质量的目的。     

血管钙化的分子机理与临床展望

Cardiovascular disease is a major consideration in the patients with diabetes and chronic kidney disease （CKD）. Vascular calcification is an important problem among these patients, and contributes to the increased risk of cardiovascular events by a variety of mechanism, including an increase in arterial stiffness by medial calcification or an increase in plaque vul- nerability by a specific type of atherosclerotic calcification.     

Association of the new visceral adiposity index with coronary artery calcification and arterial stiffness in Korean population

Background and aimsThe new visceral adiposity index (NVAI) is an indirect marker of visceral adipose tissue recently developed using a Korean population. Here we examined the association of NVAI with coronary artery calcification and arterial stiffness in asymptomatic Korean patients.Methods and resultsWe analyzed data from 60,938 asymptomatic Korean adults. Odds ratios and 95% confidence intervals (CIs) for coronary artery calcification score (CACS) > 100 and brachial–ankle pulse wave velocity (baPWV) ≥14 m/s were calculated across NVAI tertiles using multiple logistic regression analysis. Receiver operating characteristic (ROC) and area under the curve (AUC) analyses were used to assess the ability of NVAI to predict moderate to high risk of cardiovascular disease. The prevalence of moderate and high risk of cardiovascular disease increased significantly as the NVAI tertile increased. The odds ratio (95% CI) of the highest NVAI tertile for CACS >100 was 5.840 (5.101–6.686) for men and 18.916 (11.232–31.855) for women, after adjusting for confounders. All NVAI AUC values were significantly higher than the AUC values for other visceral adiposity markers.ConclusionsThis study provides the evidence that NVAI is independently and positively associated with coronary calcification and arterial stiffness in asymptomatic Korean adults.     

Coronary artery calcification in chronic kidney disease:An update

Arterial calcification is a well-recognized complication of advanced atherosclerosis.Chronic kidney disease(CKD) is characterized by significantly more pronounced,dis-seminated and fast-progressing calcification of the vascular system,including the coronary arteries.New computed tomography-based imaging techniques al-low for the noninvasive assessment and monitoring of calcification in different vascular sites.Coronary artery calcification(CAC) develops early in the course of CKD and is tightly associated with mineral and bone disor-ders,which include but are not limited to secondary hyperparathyroidism.In this review,recent data on the pathogenesis of CAC development and progression are discussed,with a special emphasis on fibroblast growth factor 23 and its co-receptor,klotho.The prevalence,progression and prognostic significance of CAC are reviewed separately for patients with end-stage renal disease treated with dialysis,kidney transplant recipi-ents and patients with earlier stages of CKD.In the last section,therapeutic considerations are discussed,with special attention paid to the importance of treatment that addresses mineral and bone disorders of CKD.     

Association of coronary calcification with obstructive disease in coronary arteries in Indian patients

A total of 1150 consecutive patients (1052 males and 98 females; age 51.2 +/- 10.1 years) with suspected coronary artery disease (Group I) were subjected to fluoroscopy for detection of coronary artery calcification (CAC) and coronary angiography. Another group (Group II) of 120 patients (95 males and 25 females; age 51.4 +/- 9.4 years) catheterized for cardiac diseases other than coronary artery disease (CAD) were subjected to the same protocol of fluoroscopy and coronary angiography to exclude incidental CAD in view of their age. CAC was present in 240 patients (20.0%) in Group I. Of these, 200 (83.4%) had triple-vessel disease (TVD); 20 (8.3%) had double-vessel disease (DVD); 19 (7.9%) had single-vessel disease (SVD); and 37 (15.4%) patients had left main coronary disease (LMCAD). Only one of these patients had insignificant CAD considered as "normal" coronary arteries (NC). Incidence of LMCAD, TVD, DVD, SVD, and NC in patients without CAC was 4.4%, 56.3%, 18.2%, 14.0%, and 11.5%, respectively. Incidence of CAC in patients with LMCAD, TVD, DVD, SVD, and NC was 48.1%, 28.1%, 10.8%, 13.0%, and 1.0% respectively. In Group II (n = 120), 24 patients (20%) had CAD, CAC was present in 5 patients with CAD (20.9%), and in two patients without CAD (2%). CAC is relatively uncommon in Indian CAD patients. Its presence, however, indicates severe multivessel disease.     

Cardiovascular calcification in patients with end-stage renal disease

Vascular calcifications are very frequent extraosseous calcifications in patients with chronic renal disease. They occur in the intima and in the media. They are associated with decreased arterial elasticity and increased mortality. The risk factors are: advanced age, duration of dialysis treatment, diabetes, increased phosphate concentration, the dose of Ca-containing phosphate binders and inflammation. It is now well established that vascular smooth muscle cells actively take up phosphate to form bioapatite. This process is associated with a phenotypic transformation of vascular smooth muscle cells during which they express osteoblast markers. Lipids and inflammatory cytokines also increase bioapatite formation. Calcification inhibitors are matrix Gla protein and fetuin-A. Decreased serum fetuin-A concentration is associated with a higher mortality rate in dialysis patients. An important preventive measure for vascular calcification is the substitution of Ca-containing by non-Ca-containing phosphate binders.     

慢性肾脏病患者发生心脏瓣膜钙化的危险因素

目的观察慢性肾脏病患者心脏瓣膜钙化(CVC)的发生率并分析其危险因素。方法收集2009-09-2011-12在我科住院的慢性肾脏病患者258例,均采用德国西门子ACUSONCV70型彩色多普勒超声仪检测患者CVC情况,并将患者分为CVC组与无CVC组,比较两组临床有关参数的变化,探讨钙化相关危险因素。结果慢性肾脏病患者CVC的检出率为25.2%(65/258),并且随着年龄增长,慢性肾脏病患者CVC的检出率逐渐增加(P<0.05),男性患者CVC的发生率较女性患者明显升高(P<0.05)。与无CVC组相比,CVC组年龄、男性比例、高敏C反应蛋白(hsCRP)明显增高,而舒张压、高密度脂蛋白胆固醇(HDL-C)、血浆白蛋白明显降低。CVC组虽然血钙、血磷、钙磷乘积、甲状旁腺激素(PTH)与无CVC组差异无统计学意义,但前者应用药物纠正钙磷紊乱的比例明显高于无CVC组。多因素分析显示年龄增大、hsCRP升高和低白蛋白血症是CVC的危险因素,高HDL-C是CVC的保护因素。结论慢性肾脏病患者CVC的发生与年龄、性别、血压、微炎症状态和营养不良有关。